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Spaceflight muscle wasting - AA metabolites essential for muscle maintenance?
According to the following article the people without AA in their
bodies should suffer from severe sarcopenia. Perhaps Mead acid can
supply the PGF2a function as well since Ray Peat as well as Monty are
still able to move around :-)
Taka
NASA Discovers the Anabolic Properties of Prostaglandins
In the January 1999 issue of the American Journal of Physiology, a new
study performed on astronauts during spaceflight demonstrates the key
role played by prostaglandins in maintaining the strength of muscles.
A major problem during spaceflight is the rapid loss of lean muscle
mass in both animals and humans. This prevents the space agencies from
sending men into space for extended periods without threatening their
health. It is, of course, the lack of resistance and weight due to the
weightlessness that is the cause of muscle atrophy. The million dollar
question is: how does this lack of resistance alter the intracellular
environment so that muscle wasting is free to take place?
Why are these experiments relevant to bodybuilders? Simply because the
pathways triggering the muscle wasting in space flight are the same
that make our muscle grow when we train. They just work in opposite
directions in each case.
--------------------------------------------------------------------------------
Hormone fluctuations during spaceflight
Hormones are obvious candidates as possible mediators of this wasting
process. The favored hypothesis is that spaceflight induces some major
alterations in our hormone levels. Two main pathways could be
involved. First, the levels of catabolic hormones could rise and so be
the cause of this wasting. Second, the level of the anabolic hormones
could drop so that the constant basal renewal of muscle protein could
not take place at a sufficient rate, resulting in a net negative
balance.
The study by Dr. Peter Stein [1] of the University of Medicine and
Dentistry of New Jersey consisted of measuring the key hormones in
astronauts during a space shuttle mission. Cortisol, a known wasting
hormone, was one of the favorite candidates. Unfortunately, a
consistent pattern of fluctuations in cortisol level was not apparent.
Cortisol increased in some but not all subjects. As all of them
experienced significant muscle loss, cortisol excess does not explain
the consistent wasting. Another paradox is that, once back on the
ground, the astronauts regained lean body mass while cortisol level
was at its peak.
This means that you can waste away while having a normal cortisol
level, and you can put on lean mass despite a high cortisol level. It
should be a major eye-opener for bodybuilders.
Next on the list of candidates were the catecholamines (epinephrine
and norepinephrine). Depending on whom you listen to, catecholamines
are either anti-catabolic or catabolic. Whatever their effect, every
scientist would agree that it is at best mild. The expected drops and
rebounds of catecholamines were detected during the flight and the
post flight periods, respectively. To explain the lean mass
fluctuations, it would mean that catecholamines are very potent
anabolic or anti-catabolic substances -- information that no research
has ever demonstrated even at high doses in humans. So they are not
the mediator the scientists were looking for.
The next substances to be measured were the anabolic hormones and
growth factors such as GH, IGF-1 or insulin. Stein did not find any
significant alteration of their levels taking place during the phase
of wasting or regrowth. He did notice that T3 (an active thyroid
hormone) level dropped during the flight, to rebound after landing. T3
fluctuations concur with the mass loss and regain, so Stein suggests
that T3 could be one of the mediators of the lean mass fluctuation. As
T3 drops during the flight, so would the rate of muscle protein
synthesis. After landing, the increased T3 would boost anabolism and
therefore muscle growth.
I disagree with Stein on this point. I consider the space-induced drop
in T3 as a protective mechanism against excessive muscle wasting
rather than a mediator of the growth inhibition. T3 is both an
anabolic and catabolic hormone. A minimal amount of T3 is required for
muscle to grow at an optimal rate, but as the T3 level increases, its
catabolic actions start to predominate and overwhelm its anabolic
properties.
This is why you'll never meet a bodybuilder claiming to have gained
muscles by taking only T3. In fact, bodybuilders using T3 start to
lose both lean and adipose mass. Studies performed in bed-rested
people which attempt to duplicate weightlessness showed that in this
situation, exogenous T3 promoted protein degradation and not
anabolism. Therefore, T3 is unlikely to be the mass modulator we are
looking for.
Stein's genuine breakthrough came from the fact that he measured the
levels of prostaglandins in both the blood and urine and compared them
with the degree of muscle wasting.
Both measures were used for better accuracy as the levels of
prostaglandins are very hard to evaluate, prostaglandins being mainly
a local and not systemic growth modulator. Skeletal muscles and bones
are both net producers of prostaglandins with muscles being the major
site of manufacture. Those locally produced prostaglandins will
eventually pass into the blood before being quickly destroyed. So the
blood level of prostaglandins roughly reflects the rate of production
of prostaglandins inside the muscles. With urine prostaglandins,
results tend to be harder to interpret as prostaglandins produced in
the kidney tend to bias the figures. Nevertheless, Dr. Stein found out
that both measures agreed anyway.
To the surprise of the scientific community (but not to bodybuilders),
the levels of the prostaglandins measured dropped during the flight --
especially the PGE2.
After landing, there was a significant rebound of the prostaglandin
levels, especially of the PGF2. Those fluctuations closely reflected
the observed changes in lean muscle mass.
The major cause of this drop is the lack of resistance placed on both
the muscles and bones. As we flex our muscles, a local formation and
release of prostaglandins is taking place. The harder we flex, the
more the local level of prostaglandins is elevated. Weightlessness
prevents the astronauts from flexing their muscles against a
resistance. Therefore, a significant drop in muscle prostaglandins can
be expected. As less prostaglandins are produced in our muscles, the
drop will quickly be reflected by the blood measurements.
This may explain the well known development of insulin resistance
occuring during space flight as prostaglandins mediate many of the
actions of insulin on muscles. This resistance also contributes to the
muscle protein loss and again we find prostaglandins as key mediators
of this phenomenon.
Stein's interpretations of these new findings are somewhat less
convincing. Scientists are expected to accurately measure the results
they obtained during an experiment, but also they are also expected to
interpret their results. Sometimes, their discussion is well
researched and documented which provides a worthwhile reading.
Unfortunately, many times it is not so well researched and the
discussion is a big step backward. This is the case in the above
mentioned study. The basic ideas are bright and the results original
but the comments made by the team of scientists is at the very least
poor. Paradoxally, they reached a good conclusion with a biased
reasoning.
The discussion part of this study is based on a very selective reading
of the scientific literature while the bottom line conclusion is very
good. It concludes that "the inflight data support a major role for
decreased prostaglandin production in the protein loss by muscles."
This is very refreshing as the average scientist considers
prostaglandins as mediators of wasting and certainly not of muscle
growth. Stein's conclusion fits very well with his findings. The fall
in muscle prostaglandins induced by the lack of resistance during the
spaceflight results in a sharp fall in protein synthesis.
For a quick recap:
Our muscles are subjected to a constant protein turnover. This means
that the old proteins composing the contractile tissue of each cell
are constantly destroyed (catabolism) and replaced by new proteins
(anabolism).
If you are a sedentary person between 20 to 40 year old, this constant
basal turnover is neutral. The rate of catabolism is roughly equal to
the rate of anabolism.
Young growing adolescents acquire their muscle mass as anabolic rate
exceeds catabolism.
Elderly people slowly waste away as anabolism is slower than
degradation.
During spaceflight, anabolism is reduced, causing the rebuilding
mechanisms to be overwhelmed by the catabolic pathways. A loss of lean
mass ensues.
The big issue is to understand which hormones or factors are involved
in the drop of anabolism.
Stein based his reasoning on the common belief concerning
prostaglandins, i.e., that PGF2 is anabolic and PGE2 is catabolic.
From there, he tries to explain how PGE2, a catabolic factor according
to him, could make our muscle grow. Good luck! Also, if PGE2 is a key
mediator of muscle wasting as many believe, how to explain its drop
while catabolism is intense? This belief concerning the so-called
wasting effect of PGE2 is due to some old, badly conducted, and flawed
studies which other laboratories have been unable to reproduce. Other
newer and more comprehensive studies have shown that PGE2 has an
overall positive influence on the protein turnover [2]. In other
words, PGE2 is an anabolic mediator rather than a catabolic one.
This fits better into the NASA findings. During the flight, muscle
prostaglandins fall, which depresses anabolism. After the flight,
muscle prostaglandin production bounces back as astronaut muscles are
once against submitted to the resistance of gravity. The extra
prostaglandins strongly stimulate anabolism which explains the fast
muscle rebuilding.
--------------------------------------------------------------------------------
Let's speculate a little!
With this major role of prostaglandins in mind, let's try to go a bit
further. Scientists specializing in Aeronautics have spent years
trying to combat space-induced wasting. In fact, the main research on
bodybuilding hormones has mostly been conducted by those scientists.
They have tried to administer hormones such as GH or IGF-1 during
spaceflights in order to combat the muscle loss. They have had little
success -- hardly surprising in light of recent findings. As the
levels of these peptide hormones hardly fluctuate, administering some
more does not appear to be the optimal solution. Usage of anabolic
steroids during weightlessness has achieved some but not exceptional
results. The next step is now to administer prostaglandins during a
flight and see what will happen.
The lack of effects of the tested anabolic hormones on muscles
suggests that their receptors failed to function normally. In other
words, the lack of muscle contractions rapidly produce a receptor
insensitivity. What if it was the level of muscle prostaglandins that
was one of the major controllers of the sensitivity of the main
anabolic hormones? I've mentioned that the potency of steroids was
enhanced by exogenous PGF2. By the same token, PGF2 sensitivity is
enhanced by androgens.
So:
Prostaglandins control androgen and IGF-1 receptor activities.
Androgens control prostaglandin receptor expression.
IGF-1 and anabolics are major controllers of the level of muscle
prostaglandins.
This looks like a righteous anabolic cycle. Therefore, the major issue
for the scientists of the third millennium is to figure out how, at
which part of the cycle and where to enter this anabolic cycle for
maximal effectiveness of our muscle building tools.
--------------------------------------------------------------------------------
References:
Stein TP. 1999 Jan. Endocrine relationships during human spaceflight.
Am J Physiol. 276:E155-62.
Fagan JM, Goldberg AL. 1986 Apr. Inhibitors of protein and RNA
synthesis cause a rapid block in prostaglandin production at the
prostaglandin synthase step. Proc Natl Acad Sci U S A. 83(8):2771-5.
SOURCE:
http://www.mesomorphosis.com/articles/dharkam/anabolic-properties-of-prostaglandins.htm
AND SOME RELATED READING (just to see how prostaglandins are also mis/
used):
http://www.mesomorphosis.com/articles/dharkam/prostaglandins.htm
http://www.mesomorphosis.com/articles/dharkam/how-dharkam-uses-pgf2.htm
bodies should suffer from severe sarcopenia. Perhaps Mead acid can
supply the PGF2a function as well since Ray Peat as well as Monty are
still able to move around :-)
Taka
NASA Discovers the Anabolic Properties of Prostaglandins
In the January 1999 issue of the American Journal of Physiology, a new
study performed on astronauts during spaceflight demonstrates the key
role played by prostaglandins in maintaining the strength of muscles.
A major problem during spaceflight is the rapid loss of lean muscle
mass in both animals and humans. This prevents the space agencies from
sending men into space for extended periods without threatening their
health. It is, of course, the lack of resistance and weight due to the
weightlessness that is the cause of muscle atrophy. The million dollar
question is: how does this lack of resistance alter the intracellular
environment so that muscle wasting is free to take place?
Why are these experiments relevant to bodybuilders? Simply because the
pathways triggering the muscle wasting in space flight are the same
that make our muscle grow when we train. They just work in opposite
directions in each case.
--------------------------------------------------------------------------------
Hormone fluctuations during spaceflight
Hormones are obvious candidates as possible mediators of this wasting
process. The favored hypothesis is that spaceflight induces some major
alterations in our hormone levels. Two main pathways could be
involved. First, the levels of catabolic hormones could rise and so be
the cause of this wasting. Second, the level of the anabolic hormones
could drop so that the constant basal renewal of muscle protein could
not take place at a sufficient rate, resulting in a net negative
balance.
The study by Dr. Peter Stein [1] of the University of Medicine and
Dentistry of New Jersey consisted of measuring the key hormones in
astronauts during a space shuttle mission. Cortisol, a known wasting
hormone, was one of the favorite candidates. Unfortunately, a
consistent pattern of fluctuations in cortisol level was not apparent.
Cortisol increased in some but not all subjects. As all of them
experienced significant muscle loss, cortisol excess does not explain
the consistent wasting. Another paradox is that, once back on the
ground, the astronauts regained lean body mass while cortisol level
was at its peak.
This means that you can waste away while having a normal cortisol
level, and you can put on lean mass despite a high cortisol level. It
should be a major eye-opener for bodybuilders.
Next on the list of candidates were the catecholamines (epinephrine
and norepinephrine). Depending on whom you listen to, catecholamines
are either anti-catabolic or catabolic. Whatever their effect, every
scientist would agree that it is at best mild. The expected drops and
rebounds of catecholamines were detected during the flight and the
post flight periods, respectively. To explain the lean mass
fluctuations, it would mean that catecholamines are very potent
anabolic or anti-catabolic substances -- information that no research
has ever demonstrated even at high doses in humans. So they are not
the mediator the scientists were looking for.
The next substances to be measured were the anabolic hormones and
growth factors such as GH, IGF-1 or insulin. Stein did not find any
significant alteration of their levels taking place during the phase
of wasting or regrowth. He did notice that T3 (an active thyroid
hormone) level dropped during the flight, to rebound after landing. T3
fluctuations concur with the mass loss and regain, so Stein suggests
that T3 could be one of the mediators of the lean mass fluctuation. As
T3 drops during the flight, so would the rate of muscle protein
synthesis. After landing, the increased T3 would boost anabolism and
therefore muscle growth.
I disagree with Stein on this point. I consider the space-induced drop
in T3 as a protective mechanism against excessive muscle wasting
rather than a mediator of the growth inhibition. T3 is both an
anabolic and catabolic hormone. A minimal amount of T3 is required for
muscle to grow at an optimal rate, but as the T3 level increases, its
catabolic actions start to predominate and overwhelm its anabolic
properties.
This is why you'll never meet a bodybuilder claiming to have gained
muscles by taking only T3. In fact, bodybuilders using T3 start to
lose both lean and adipose mass. Studies performed in bed-rested
people which attempt to duplicate weightlessness showed that in this
situation, exogenous T3 promoted protein degradation and not
anabolism. Therefore, T3 is unlikely to be the mass modulator we are
looking for.
Stein's genuine breakthrough came from the fact that he measured the
levels of prostaglandins in both the blood and urine and compared them
with the degree of muscle wasting.
Both measures were used for better accuracy as the levels of
prostaglandins are very hard to evaluate, prostaglandins being mainly
a local and not systemic growth modulator. Skeletal muscles and bones
are both net producers of prostaglandins with muscles being the major
site of manufacture. Those locally produced prostaglandins will
eventually pass into the blood before being quickly destroyed. So the
blood level of prostaglandins roughly reflects the rate of production
of prostaglandins inside the muscles. With urine prostaglandins,
results tend to be harder to interpret as prostaglandins produced in
the kidney tend to bias the figures. Nevertheless, Dr. Stein found out
that both measures agreed anyway.
To the surprise of the scientific community (but not to bodybuilders),
the levels of the prostaglandins measured dropped during the flight --
especially the PGE2.
After landing, there was a significant rebound of the prostaglandin
levels, especially of the PGF2. Those fluctuations closely reflected
the observed changes in lean muscle mass.
The major cause of this drop is the lack of resistance placed on both
the muscles and bones. As we flex our muscles, a local formation and
release of prostaglandins is taking place. The harder we flex, the
more the local level of prostaglandins is elevated. Weightlessness
prevents the astronauts from flexing their muscles against a
resistance. Therefore, a significant drop in muscle prostaglandins can
be expected. As less prostaglandins are produced in our muscles, the
drop will quickly be reflected by the blood measurements.
This may explain the well known development of insulin resistance
occuring during space flight as prostaglandins mediate many of the
actions of insulin on muscles. This resistance also contributes to the
muscle protein loss and again we find prostaglandins as key mediators
of this phenomenon.
Stein's interpretations of these new findings are somewhat less
convincing. Scientists are expected to accurately measure the results
they obtained during an experiment, but also they are also expected to
interpret their results. Sometimes, their discussion is well
researched and documented which provides a worthwhile reading.
Unfortunately, many times it is not so well researched and the
discussion is a big step backward. This is the case in the above
mentioned study. The basic ideas are bright and the results original
but the comments made by the team of scientists is at the very least
poor. Paradoxally, they reached a good conclusion with a biased
reasoning.
The discussion part of this study is based on a very selective reading
of the scientific literature while the bottom line conclusion is very
good. It concludes that "the inflight data support a major role for
decreased prostaglandin production in the protein loss by muscles."
This is very refreshing as the average scientist considers
prostaglandins as mediators of wasting and certainly not of muscle
growth. Stein's conclusion fits very well with his findings. The fall
in muscle prostaglandins induced by the lack of resistance during the
spaceflight results in a sharp fall in protein synthesis.
For a quick recap:
Our muscles are subjected to a constant protein turnover. This means
that the old proteins composing the contractile tissue of each cell
are constantly destroyed (catabolism) and replaced by new proteins
(anabolism).
If you are a sedentary person between 20 to 40 year old, this constant
basal turnover is neutral. The rate of catabolism is roughly equal to
the rate of anabolism.
Young growing adolescents acquire their muscle mass as anabolic rate
exceeds catabolism.
Elderly people slowly waste away as anabolism is slower than
degradation.
During spaceflight, anabolism is reduced, causing the rebuilding
mechanisms to be overwhelmed by the catabolic pathways. A loss of lean
mass ensues.
The big issue is to understand which hormones or factors are involved
in the drop of anabolism.
Stein based his reasoning on the common belief concerning
prostaglandins, i.e., that PGF2 is anabolic and PGE2 is catabolic.
From there, he tries to explain how PGE2, a catabolic factor according
to him, could make our muscle grow. Good luck! Also, if PGE2 is a key
mediator of muscle wasting as many believe, how to explain its drop
while catabolism is intense? This belief concerning the so-called
wasting effect of PGE2 is due to some old, badly conducted, and flawed
studies which other laboratories have been unable to reproduce. Other
newer and more comprehensive studies have shown that PGE2 has an
overall positive influence on the protein turnover [2]. In other
words, PGE2 is an anabolic mediator rather than a catabolic one.
This fits better into the NASA findings. During the flight, muscle
prostaglandins fall, which depresses anabolism. After the flight,
muscle prostaglandin production bounces back as astronaut muscles are
once against submitted to the resistance of gravity. The extra
prostaglandins strongly stimulate anabolism which explains the fast
muscle rebuilding.
--------------------------------------------------------------------------------
Let's speculate a little!
With this major role of prostaglandins in mind, let's try to go a bit
further. Scientists specializing in Aeronautics have spent years
trying to combat space-induced wasting. In fact, the main research on
bodybuilding hormones has mostly been conducted by those scientists.
They have tried to administer hormones such as GH or IGF-1 during
spaceflights in order to combat the muscle loss. They have had little
success -- hardly surprising in light of recent findings. As the
levels of these peptide hormones hardly fluctuate, administering some
more does not appear to be the optimal solution. Usage of anabolic
steroids during weightlessness has achieved some but not exceptional
results. The next step is now to administer prostaglandins during a
flight and see what will happen.
The lack of effects of the tested anabolic hormones on muscles
suggests that their receptors failed to function normally. In other
words, the lack of muscle contractions rapidly produce a receptor
insensitivity. What if it was the level of muscle prostaglandins that
was one of the major controllers of the sensitivity of the main
anabolic hormones? I've mentioned that the potency of steroids was
enhanced by exogenous PGF2. By the same token, PGF2 sensitivity is
enhanced by androgens.
So:
Prostaglandins control androgen and IGF-1 receptor activities.
Androgens control prostaglandin receptor expression.
IGF-1 and anabolics are major controllers of the level of muscle
prostaglandins.
This looks like a righteous anabolic cycle. Therefore, the major issue
for the scientists of the third millennium is to figure out how, at
which part of the cycle and where to enter this anabolic cycle for
maximal effectiveness of our muscle building tools.
--------------------------------------------------------------------------------
References:
Stein TP. 1999 Jan. Endocrine relationships during human spaceflight.
Am J Physiol. 276:E155-62.
Fagan JM, Goldberg AL. 1986 Apr. Inhibitors of protein and RNA
synthesis cause a rapid block in prostaglandin production at the
prostaglandin synthase step. Proc Natl Acad Sci U S A. 83(8):2771-5.
SOURCE:
http://www.mesomorphosis.com/articles/dharkam/anabolic-properties-of-prostaglandins.htm
AND SOME RELATED READING (just to see how prostaglandins are also mis/
used):
http://www.mesomorphosis.com/articles/dharkam/prostaglandins.htm
http://www.mesomorphosis.com/articles/dharkam/how-dharkam-uses-pgf2.htm
the links are not working
cheers,
Ira
--------------------------------------------------------
Random Link:
http://engleskirjecnik.com/praznina
--------------------------------------------------------
cheers,
Ira
--------------------------------------------------------
Random Link:
http://engleskirjecnik.com/praznina
--------------------------------------------------------
On May 10, 7:39 pm, Ira.Ko...@gmail.com wrote:
> the links are not working
>
> cheers,
>
> Ira
>
> --------------------------------------------------------
> Random Link:http://engleskirjecnik.com/praznina
> --------------------------------------------------------
They are working for me but sometimes slow. I will post some
interesting articles from the site here. Human experiments cannot be
normally done but bodybuilders are in fact conducting great
experiments on themselves which can tell us lot about the human
physiology, hormones and nutrition. I just wish they try to challenge
the arachidonic acid (AA) dogma someday ... But as can be seen on the
current California governor, AA doesn't significantly impair the
normal lifespan nor leads to the development of degenerative chronic
diseases in physically active people. There was a lot of corn oil in
America in the 70ties when Arnie was the top performer but I don't
think he ever supplemented with fish oil or any of the "modern"
Omega-3 hits.
Taka
> the links are not working
>
> cheers,
>
> Ira
>
> --------------------------------------------------------
> Random Link:http://engleskirjecnik.com/praznina
> --------------------------------------------------------
They are working for me but sometimes slow. I will post some
interesting articles from the site here. Human experiments cannot be
normally done but bodybuilders are in fact conducting great
experiments on themselves which can tell us lot about the human
physiology, hormones and nutrition. I just wish they try to challenge
the arachidonic acid (AA) dogma someday ... But as can be seen on the
current California governor, AA doesn't significantly impair the
normal lifespan nor leads to the development of degenerative chronic
diseases in physically active people. There was a lot of corn oil in
America in the 70ties when Arnie was the top performer but I don't
think he ever supplemented with fish oil or any of the "modern"
Omega-3 hits.
Taka
Deeper Into Prostaglandin Use
by Dharkam
Many readers enjoyed my previous article about prostaglandins as
muscle builders. This short introduction to prostaglandins produced
critics, controversies and queries. Prostaglandins, especially PGF2
are no wonder drugs. They will not make you a Mr. Olympia in a matter
of days. They do not represent a substitute for training. Neither are
they free of side-effects. Some are benign while others are more
worrying. Besides, PGF2 is tricky to manipulate. So by no means do I
pretend to have uncovered the ultimate anabolics. There is one fact
though that cannot be denied: prostaglandins are very potent anabolic
substances. It is true that thousands of champions were able to build
their muscle mass without it, but we are living in a society in which
the extra edge is always needed to more quickly achieve or exceed your
goals. This is why I am going to discuss the pros and cons as well as
the how-to of prostaglandins.
Prostaglandins: a very important modulator of growth
Each of our muscle cells produces prostaglandins naturally and
continuously. Each of our muscle cells contains prostaglandin
receptors. A muscle failing to manufacture enough prostaglandins will
rapidly waste away. Animal studies have shown that immunization
against PGF2 impairs the muscle growth even though scientists were
expecting it would boost anabolism. In humans, a reduction of muscle
prostaglandin production is associated with wasting. The potent
inhibitors of prostaglandin synthesis such as cortisol produce their
wasting effects in great part by reducing the muscle production of
prostaglandins, thus slowing protein synthesis rate.
From a physiological point of view, prostaglandins are very important
if not one of the ultimate growth mediators. All the problems arise
from their mode of actions. The cells which need more prostaglandins
manufacture them for their own consumption or for the nearby cells.
Prostaglandins do not have to circulate like testosterone which is
mostly an endocrine hormone. Once in the blood, prostaglandins are
rapidly destroyed. Those major discrepancies mean that prostaglandins
cannot be used in the same way as anabolic steroids.
Once injected, steroids slowly pass into the blood. They will
eventually find their ways to the muscles among other tissues. Steroid
usage is therefore pretty simple: inject and wait. Because of both
their very short life cycle and their very localized actions,
prostaglandins are far harder to manipulate.
Fighting the side effects
PGF2 analogues
Just as testosterone has analogues such as nandrolone, so do
prostaglandins. The analogues are an attempt to solve the problems
caused by the original hormone or substance. Steroid molecules such as
nandrolone or trenbolone were developed in the hope they would induce
more favorable actions (anabolism) while producing less side effects
(virilization) compared to testosterone. Researchers designed PGF2
analogues in order to address the three main problems inherent to
PGF2. First: to increase its very short life cycle, second: to lessen
the incidence of the numerous side effects associated with PGF2 usage,
third: to ease prostaglandin usage by developing oral versions.
As with testosterone some analogues proved useless while others do
have some interesting properties, at least in the test tube. I am not
going to tell you which analogue is the best. The truth is that I
don't know. I only have experience with the real thing. This may be
disappointing but I am not going to lie just to look better.
Aspirin as an anti-prostaglandin
Aspirin or aspirin-like substances have the potential to reduce some
of the side effects such as pain associated with PGF2 administration.
However I tend to consider that the use of aspirin along with PGF2
weakens the overall anabolic effects without effectively fighting the
side effects. This is true for the aspirin you can find in medication
as well as the aspirin hidden in some ephedrine-caffeine stacks. I
suggest that you avoid both of them. Several hypotheses could be
advanced about the inhibiting effects of aspirin. Some research has
shown that aspirin could block prostaglandin receptors. It may also
impair the conversion of PGF2 to PGE2 which seems important for a
maximal muscle building effect. I know that PGE2 is considered as a
muscle enemy in the bodybuilding magazines, but the fact is that
several studies have pointed out its usefulness in the bodybuilding
process as a growth agent for the muscles. One last hypothesis is that
PGF2 stimulates the subsequent natural release of muscle PGF2 or PGE2
which could further enhance the anabolic process. Aspirin would
prevent this secondary anabolic secretion.
Preventing the local growth by rotating the sites of injections
I consider the local growth induced by PGF2 as a side effect. As I
said last month, it is due to a weakness of PGF2 (a very rapid
degradation) rather than a magical effect. Unless you want to bring up
a specific weak point, you should constantly rotate the sites of
injections. One more restriction is that it is easy, for example, to
inject PGF2 in some body part like the front shoulders but far harder
in the inner side of the biceps. You should also make sure to avoid
hitting too close to the intestine which exacerbates the gastro-
intestinal discomfort caused by PGF2. Though close to the intestine,
the front legs are a rather interesting and "easy" site of injections.
You just may feel your quads "better" as you walk. I would suggest you
mark all the possible injection sites you have in order to structure
your injection pattern. If you have weak points, they should be hit
more often than your strong bodyparts.
No injecting your right calf will make your left calve grow to the
same extent. Same thing with the gastronemius and the soleus. Hitting
one will mostly make the injected muscle grow with a lesser
stimulation for the nearby muscles. So for the calves only, we have at
least 15 possible sites of injections. One on the upper, outer soleus,
one for the lower, outer soleus and one for the lower inner part of
the soleus. One or two for the front calves depending on your degree
of development. For the gastronemius, you have both the upper and
lower part of the outer side as well as the upper and lower parts of
the inner/rear part. Of course, you can multiply that by two as you
hopefully have 2 calves. I consider that you have the same number of
sites on the upper legs. Avoid the abs, the lower back and maybe the
forearms. Your triceps hold at least 6 sites and at least 4 for your
biceps. Your shoulders have at least 12. If you are not too sensitive,
you can manage 12 more on your chest. It is a total of at least 64
sites (excluding the back) to choose from every day.
If you are not sure about the muscle locations, check with an anatomy
chart to avoid hitting a tendon or a bone. Note carefully which side
of the body you last hit so that you can shift from the right to the
left and from the left to the right with each injection. If a friend
of yours is willing to help you with the injections, it will increase
the potential number of injection sites by adding your whole upper
back and helping the right handed persons with their right side of
their upper body (and the opposite for the left handed persons). You
will always find a helping hand in the gym.
The main problem with the rotation is to inject into muscles that you
are not about to train or muscles that you trained recently. This is
why training each bodypart seriously only once a week will ease our
use of PGF2. Light pumping sessions should not interfere with the PGF2
rotation schedule as the mild pain should be bearable. In fact, during
a light workout, having a soreness-like mild pain should help you feel
the muscle contraction better and should enhance your focus on the
trained muscles.
As I said last month, you should wait for at least two to three days
after training to inject PGF2 because of its pain promoting effect.
This length of time depends upon the degree of trauma inflicted to the
trained muscles. If your training was really traumatic (by including
plenty of heavy negative reps), you may have to wait longer. But PGF2
users do not have to traumatize their muscles to get results. In fact,
thanks to the muscle pump you will obtain with the light weights, you
will not have to go too heavy. Your workouts are more likely to be non-
traumatic, allowing you to inject after only two days after the
workout.
I also advised to stop injecting into a muscle 24 hours before
retraining it. This means that you have a three day window of
opportunity for a single muscle per week to soak it up with PGF2.
Here is a one week schedule example. It assumes that your upper body
is lagging a bit compared to your legs and is therefore trained a bit
more. The first muscle is the bodypart of the day and should be
trained hard (but avoid overly traumatic techniques such as pure
negative reps and super heavy weights). The second and sometimes third
muscles are meant to be trained in a light high rep fashion for around
5 sets each. In the least column, the muscles receiving PGF2 are
mentioned. You will note that even though there are days off training,
it is best to administer PGF2 everyday. Again, this is due to the
short life cycle of PGF2 which makes it necessary to repeat injections
frequently.
Day Muscle of the day Pumping muscles of the day Muscles in which PGF2
can be administered for the day
Monday Back Chest Chest*, Arms
Tuesday Legs Shoulders Shoulders*, Arms
Wesnesday Chest Back Shoulders, Arms
Thursday Rest Rest Shoulders, Back.
Friday Arms Legs Back, legs*.
Saturday Shoulders Back, Chest Back*, legs, chest*
Sunday Rest Rest Legs, Chest
* Inject after training rather than before.
The dosage issue
Most readers are interested in an ideal dosage schedule.
Unfortunately, such a miraculous schedule does not exist. Steroids
have been used for decades, yet no one is able to come up with a one
fits all, fail-safe schedule. Though some claim to know exactly how to
use steroids and how to stack them, this is a lie. The same applies to
PGF2. The ideal schedule does not exist. It is up to you to figure out
which one suits you best. I can give you some guidelines but I am more
able to tell you how not to use it than to prescribe its use.
As mentioned last month, I suggest to start with half a milligram. At
that dosage, not much should occur. Better to be safe than sorry. If
everything goes well, go up to a milligram the next time. See what is
happening. If you are fine, try 2 milligrams. I think you understand
how to build up your dosage during the first days of your very first
cycle. There is normally 25 mg of PGF2 per 5 milliliters. At 1 ml.
(therefore 5 mg.), you should start to be able to tell the drug is
working. I suggest not to go above 2 ml. per injection. If you are
using 1 ml. five times a day, it means one vial a day (two if you use
2 ml.s). 5 ml. is the most I have ever heard with a single injection,
but I consider it as a huge dosage. Maybe in 5 to 10 years, it will
sound like a sissy dosage, but only time will help us determine an
upper limit.
Lowering the required dosage
One easy way to reduce the PGF2 dosage (and therefore the side
effects) while optimizing the anabolic response is to administer PGF2
while insulin secretion is high. This means at meal time -- or more
precisely after a meal. Insulin can trigger the muscle secretion of
PGF2. This is probably how it produces anabolism. But insulin does not
stop here: it increases the muscle sensitivity to the anabolic effects
of PGF2. This is why you can reduce your PGF2 dosage if it is used at
meal time or administered with insulin or an insulin booster. The
dosages mentioned above already take into account the beneficial
synergetic action of insulin on PGF2.
How often?
Due to its short life cycle, PGF2 has to be administered as often as
possible for optimal effect. This makes it very uncomfortable to use
but as I mentioned in the introduction, it is a potent yet not ideal
drug to use. As most bodybuilders eat at least five times, it means
that there are five opportunities per day for PGF2 administration. Of
course this assumes that you have plenty of free time. Not everybody
is a pro bodybuilder and you may not need (or want) to reach their
degree of muscularity or to act like them. Administered only twice or
three times a day along with your major meals, PGF2 will still perform
its magic. I would not recommend less than twice a day. During week
ends, you may have more time and so you may be able to increase the
injection frequency. You can resume your twice a day schedule as you
go back to work on Monday.
Just understand that the more often you inject PGF2, the longer time
your muscles will be exposed to this anabolic substance. Let's assume
the anabolic stimulation of a single PGF2 administration lasts for two
hours. Of course, this figure depends upon the dosage: the higher the
dose, the longer it lasts, as it will take more time for our body to
degrade the prostaglandins. If you inject only twice a day, you will
generate a total of four hours of intense anabolism per 24 hours. It
means that 20 hours during the day are wasted. If you inject 5 times a
day, you create 10 hours of intense anabolism per 24 hours.
Is this a strength or a weakness of PGF2 over steroids? You are
exposed to steroids 24 hours per day (assuming you use injectables
over orals). So, again steroids are more comfortable to use. But you
may have noticed that the levels of most of our endogenous hormones
fluctuate throughout the day. It prevents our muscles from
downregulating their anabolic responses to the growth stimulating
hormones. This is one of main the problem associated with the constant
delivery of steroids. The time off PGF2 inherent in its short life
cycle helps fight the tendency toward reduced anabolic response as
time goes by. It is therefore a source of discomfort but also an
advantage as far as results are concerned.
I am going to propose two schedules as examples. One will be for
beginners who want to build up some lean muscles. The other is for
more advanced bodybuilders who want to fill the gap between two
steroid cycles.
The beginner schedule
Inject PGF2 (half a ml.) 30 minutes after the noon lunch. Inject the
whole half a ml. at only one place. Your lunch should be high in
proteins and carbs while low in fats. Make sure you have a serving of
weight gainers at hand during the next two hours. This has two
purposes. First, some people report a hypoglycemia-like feeling after
PGF2. Of course this side effect should be countered. Eating a liquid
meal generally makes them feel better. Second, whenever anabolism is
elevated, so should be protein feeding frequency. Repeat a similar
procedure after the evening meal. Change the side of injection.
For the most daring, adding an insulin booster before the meals may be
a good idea. I like Glipizide (2.5 mg) but Glibenclamide (the insulin
booster of reference) has been shown to lessen the incidence of side
effects of PGF2 especially on the intestine. For Glibenclamide, start
with the 1.25 mg pills and build up to the 2.5 mg. This makes it a
smart stack to enhance anabolism while reducing side effects. Of
course, you should be extra careful about the potential hypoglycemia
so make sure you ingest some carbs every 30 minutes for the next two
hours when it is time for the weight gainers. I suggest that you
increase your creatine intake according to your PGF2 dosage as
prostaglandins like most other anabolic substances accelerate the
wasting of creatine. Go with at leas
by Dharkam
Many readers enjoyed my previous article about prostaglandins as
muscle builders. This short introduction to prostaglandins produced
critics, controversies and queries. Prostaglandins, especially PGF2
are no wonder drugs. They will not make you a Mr. Olympia in a matter
of days. They do not represent a substitute for training. Neither are
they free of side-effects. Some are benign while others are more
worrying. Besides, PGF2 is tricky to manipulate. So by no means do I
pretend to have uncovered the ultimate anabolics. There is one fact
though that cannot be denied: prostaglandins are very potent anabolic
substances. It is true that thousands of champions were able to build
their muscle mass without it, but we are living in a society in which
the extra edge is always needed to more quickly achieve or exceed your
goals. This is why I am going to discuss the pros and cons as well as
the how-to of prostaglandins.
Prostaglandins: a very important modulator of growth
Each of our muscle cells produces prostaglandins naturally and
continuously. Each of our muscle cells contains prostaglandin
receptors. A muscle failing to manufacture enough prostaglandins will
rapidly waste away. Animal studies have shown that immunization
against PGF2 impairs the muscle growth even though scientists were
expecting it would boost anabolism. In humans, a reduction of muscle
prostaglandin production is associated with wasting. The potent
inhibitors of prostaglandin synthesis such as cortisol produce their
wasting effects in great part by reducing the muscle production of
prostaglandins, thus slowing protein synthesis rate.
From a physiological point of view, prostaglandins are very important
if not one of the ultimate growth mediators. All the problems arise
from their mode of actions. The cells which need more prostaglandins
manufacture them for their own consumption or for the nearby cells.
Prostaglandins do not have to circulate like testosterone which is
mostly an endocrine hormone. Once in the blood, prostaglandins are
rapidly destroyed. Those major discrepancies mean that prostaglandins
cannot be used in the same way as anabolic steroids.
Once injected, steroids slowly pass into the blood. They will
eventually find their ways to the muscles among other tissues. Steroid
usage is therefore pretty simple: inject and wait. Because of both
their very short life cycle and their very localized actions,
prostaglandins are far harder to manipulate.
Fighting the side effects
PGF2 analogues
Just as testosterone has analogues such as nandrolone, so do
prostaglandins. The analogues are an attempt to solve the problems
caused by the original hormone or substance. Steroid molecules such as
nandrolone or trenbolone were developed in the hope they would induce
more favorable actions (anabolism) while producing less side effects
(virilization) compared to testosterone. Researchers designed PGF2
analogues in order to address the three main problems inherent to
PGF2. First: to increase its very short life cycle, second: to lessen
the incidence of the numerous side effects associated with PGF2 usage,
third: to ease prostaglandin usage by developing oral versions.
As with testosterone some analogues proved useless while others do
have some interesting properties, at least in the test tube. I am not
going to tell you which analogue is the best. The truth is that I
don't know. I only have experience with the real thing. This may be
disappointing but I am not going to lie just to look better.
Aspirin as an anti-prostaglandin
Aspirin or aspirin-like substances have the potential to reduce some
of the side effects such as pain associated with PGF2 administration.
However I tend to consider that the use of aspirin along with PGF2
weakens the overall anabolic effects without effectively fighting the
side effects. This is true for the aspirin you can find in medication
as well as the aspirin hidden in some ephedrine-caffeine stacks. I
suggest that you avoid both of them. Several hypotheses could be
advanced about the inhibiting effects of aspirin. Some research has
shown that aspirin could block prostaglandin receptors. It may also
impair the conversion of PGF2 to PGE2 which seems important for a
maximal muscle building effect. I know that PGE2 is considered as a
muscle enemy in the bodybuilding magazines, but the fact is that
several studies have pointed out its usefulness in the bodybuilding
process as a growth agent for the muscles. One last hypothesis is that
PGF2 stimulates the subsequent natural release of muscle PGF2 or PGE2
which could further enhance the anabolic process. Aspirin would
prevent this secondary anabolic secretion.
Preventing the local growth by rotating the sites of injections
I consider the local growth induced by PGF2 as a side effect. As I
said last month, it is due to a weakness of PGF2 (a very rapid
degradation) rather than a magical effect. Unless you want to bring up
a specific weak point, you should constantly rotate the sites of
injections. One more restriction is that it is easy, for example, to
inject PGF2 in some body part like the front shoulders but far harder
in the inner side of the biceps. You should also make sure to avoid
hitting too close to the intestine which exacerbates the gastro-
intestinal discomfort caused by PGF2. Though close to the intestine,
the front legs are a rather interesting and "easy" site of injections.
You just may feel your quads "better" as you walk. I would suggest you
mark all the possible injection sites you have in order to structure
your injection pattern. If you have weak points, they should be hit
more often than your strong bodyparts.
No injecting your right calf will make your left calve grow to the
same extent. Same thing with the gastronemius and the soleus. Hitting
one will mostly make the injected muscle grow with a lesser
stimulation for the nearby muscles. So for the calves only, we have at
least 15 possible sites of injections. One on the upper, outer soleus,
one for the lower, outer soleus and one for the lower inner part of
the soleus. One or two for the front calves depending on your degree
of development. For the gastronemius, you have both the upper and
lower part of the outer side as well as the upper and lower parts of
the inner/rear part. Of course, you can multiply that by two as you
hopefully have 2 calves. I consider that you have the same number of
sites on the upper legs. Avoid the abs, the lower back and maybe the
forearms. Your triceps hold at least 6 sites and at least 4 for your
biceps. Your shoulders have at least 12. If you are not too sensitive,
you can manage 12 more on your chest. It is a total of at least 64
sites (excluding the back) to choose from every day.
If you are not sure about the muscle locations, check with an anatomy
chart to avoid hitting a tendon or a bone. Note carefully which side
of the body you last hit so that you can shift from the right to the
left and from the left to the right with each injection. If a friend
of yours is willing to help you with the injections, it will increase
the potential number of injection sites by adding your whole upper
back and helping the right handed persons with their right side of
their upper body (and the opposite for the left handed persons). You
will always find a helping hand in the gym.
The main problem with the rotation is to inject into muscles that you
are not about to train or muscles that you trained recently. This is
why training each bodypart seriously only once a week will ease our
use of PGF2. Light pumping sessions should not interfere with the PGF2
rotation schedule as the mild pain should be bearable. In fact, during
a light workout, having a soreness-like mild pain should help you feel
the muscle contraction better and should enhance your focus on the
trained muscles.
As I said last month, you should wait for at least two to three days
after training to inject PGF2 because of its pain promoting effect.
This length of time depends upon the degree of trauma inflicted to the
trained muscles. If your training was really traumatic (by including
plenty of heavy negative reps), you may have to wait longer. But PGF2
users do not have to traumatize their muscles to get results. In fact,
thanks to the muscle pump you will obtain with the light weights, you
will not have to go too heavy. Your workouts are more likely to be non-
traumatic, allowing you to inject after only two days after the
workout.
I also advised to stop injecting into a muscle 24 hours before
retraining it. This means that you have a three day window of
opportunity for a single muscle per week to soak it up with PGF2.
Here is a one week schedule example. It assumes that your upper body
is lagging a bit compared to your legs and is therefore trained a bit
more. The first muscle is the bodypart of the day and should be
trained hard (but avoid overly traumatic techniques such as pure
negative reps and super heavy weights). The second and sometimes third
muscles are meant to be trained in a light high rep fashion for around
5 sets each. In the least column, the muscles receiving PGF2 are
mentioned. You will note that even though there are days off training,
it is best to administer PGF2 everyday. Again, this is due to the
short life cycle of PGF2 which makes it necessary to repeat injections
frequently.
Day Muscle of the day Pumping muscles of the day Muscles in which PGF2
can be administered for the day
Monday Back Chest Chest*, Arms
Tuesday Legs Shoulders Shoulders*, Arms
Wesnesday Chest Back Shoulders, Arms
Thursday Rest Rest Shoulders, Back.
Friday Arms Legs Back, legs*.
Saturday Shoulders Back, Chest Back*, legs, chest*
Sunday Rest Rest Legs, Chest
* Inject after training rather than before.
The dosage issue
Most readers are interested in an ideal dosage schedule.
Unfortunately, such a miraculous schedule does not exist. Steroids
have been used for decades, yet no one is able to come up with a one
fits all, fail-safe schedule. Though some claim to know exactly how to
use steroids and how to stack them, this is a lie. The same applies to
PGF2. The ideal schedule does not exist. It is up to you to figure out
which one suits you best. I can give you some guidelines but I am more
able to tell you how not to use it than to prescribe its use.
As mentioned last month, I suggest to start with half a milligram. At
that dosage, not much should occur. Better to be safe than sorry. If
everything goes well, go up to a milligram the next time. See what is
happening. If you are fine, try 2 milligrams. I think you understand
how to build up your dosage during the first days of your very first
cycle. There is normally 25 mg of PGF2 per 5 milliliters. At 1 ml.
(therefore 5 mg.), you should start to be able to tell the drug is
working. I suggest not to go above 2 ml. per injection. If you are
using 1 ml. five times a day, it means one vial a day (two if you use
2 ml.s). 5 ml. is the most I have ever heard with a single injection,
but I consider it as a huge dosage. Maybe in 5 to 10 years, it will
sound like a sissy dosage, but only time will help us determine an
upper limit.
Lowering the required dosage
One easy way to reduce the PGF2 dosage (and therefore the side
effects) while optimizing the anabolic response is to administer PGF2
while insulin secretion is high. This means at meal time -- or more
precisely after a meal. Insulin can trigger the muscle secretion of
PGF2. This is probably how it produces anabolism. But insulin does not
stop here: it increases the muscle sensitivity to the anabolic effects
of PGF2. This is why you can reduce your PGF2 dosage if it is used at
meal time or administered with insulin or an insulin booster. The
dosages mentioned above already take into account the beneficial
synergetic action of insulin on PGF2.
How often?
Due to its short life cycle, PGF2 has to be administered as often as
possible for optimal effect. This makes it very uncomfortable to use
but as I mentioned in the introduction, it is a potent yet not ideal
drug to use. As most bodybuilders eat at least five times, it means
that there are five opportunities per day for PGF2 administration. Of
course this assumes that you have plenty of free time. Not everybody
is a pro bodybuilder and you may not need (or want) to reach their
degree of muscularity or to act like them. Administered only twice or
three times a day along with your major meals, PGF2 will still perform
its magic. I would not recommend less than twice a day. During week
ends, you may have more time and so you may be able to increase the
injection frequency. You can resume your twice a day schedule as you
go back to work on Monday.
Just understand that the more often you inject PGF2, the longer time
your muscles will be exposed to this anabolic substance. Let's assume
the anabolic stimulation of a single PGF2 administration lasts for two
hours. Of course, this figure depends upon the dosage: the higher the
dose, the longer it lasts, as it will take more time for our body to
degrade the prostaglandins. If you inject only twice a day, you will
generate a total of four hours of intense anabolism per 24 hours. It
means that 20 hours during the day are wasted. If you inject 5 times a
day, you create 10 hours of intense anabolism per 24 hours.
Is this a strength or a weakness of PGF2 over steroids? You are
exposed to steroids 24 hours per day (assuming you use injectables
over orals). So, again steroids are more comfortable to use. But you
may have noticed that the levels of most of our endogenous hormones
fluctuate throughout the day. It prevents our muscles from
downregulating their anabolic responses to the growth stimulating
hormones. This is one of main the problem associated with the constant
delivery of steroids. The time off PGF2 inherent in its short life
cycle helps fight the tendency toward reduced anabolic response as
time goes by. It is therefore a source of discomfort but also an
advantage as far as results are concerned.
I am going to propose two schedules as examples. One will be for
beginners who want to build up some lean muscles. The other is for
more advanced bodybuilders who want to fill the gap between two
steroid cycles.
The beginner schedule
Inject PGF2 (half a ml.) 30 minutes after the noon lunch. Inject the
whole half a ml. at only one place. Your lunch should be high in
proteins and carbs while low in fats. Make sure you have a serving of
weight gainers at hand during the next two hours. This has two
purposes. First, some people report a hypoglycemia-like feeling after
PGF2. Of course this side effect should be countered. Eating a liquid
meal generally makes them feel better. Second, whenever anabolism is
elevated, so should be protein feeding frequency. Repeat a similar
procedure after the evening meal. Change the side of injection.
For the most daring, adding an insulin booster before the meals may be
a good idea. I like Glipizide (2.5 mg) but Glibenclamide (the insulin
booster of reference) has been shown to lessen the incidence of side
effects of PGF2 especially on the intestine. For Glibenclamide, start
with the 1.25 mg pills and build up to the 2.5 mg. This makes it a
smart stack to enhance anabolism while reducing side effects. Of
course, you should be extra careful about the potential hypoglycemia
so make sure you ingest some carbs every 30 minutes for the next two
hours when it is time for the weight gainers. I suggest that you
increase your creatine intake according to your PGF2 dosage as
prostaglandins like most other anabolic substances accelerate the
wasting of creatine. Go with at leas
Dharkam's Way - The 'How-To" of PGF2
Let me begin by saying that I do not have the answers to many of the
questions that you, readers, are asking me. I will try my best to
address all of them even if I do not have the exact answer, by using
common sense.
The how-to of PGF2
Q: How long should you use PGF2, do you cycle it or is there no need
to come off it?
A: Bodybuilders are so used to steroid cycling that it is legitimate
to wonder about the necessity of cycling PGF2. After more than 50
years of both continuous usage and scientific research, no one has
been able to come up with a universal steroid cycling pattern that
could suit everyone. Do not expect that after such a limited
experience with PGF2, anyone could come up with an optimal cycling
pattern. So let's look at a rational way of cycling. If you are off
steroids for 2 months at a time, your PGF2 cycle should last 2 months
in order to turn this potential wasting period into an opportunity to
pack on lean muscle.
Another way of looking at PGF2 cycling is to use it for as long as you
can stand it. PGF2 usage is not as comfortable as steroid use. Most
bodybuilders are not motivated enough to inject several times a day
for more than 60-90 days at a time. So, here is your cycle length. It
is counterproductive for bodybuilders to use drugs reluctantly.
As far as the need to come off is concerned, there is as much need to
come off prostaglandins as need to come off steroids. Although
everyone should discontinue anabolics from time to time, most pros
never do. If you use PGF2 just to look good on the beach, yes, you
should come off. If you have to make a living from body, you may not
have much choice.
--------------------------------------------------------------------------------
Q: How long does it take to see the first results?
A: Cosmetically speaking, less than a week. Most of the early gains
are due to the diuretic properties of prostaglandins. Then you realize
that your muscles get very hard even when relaxed. To get a similar
hardening effect, you would have needed quite a bit of steroids. You
will also remark quickly that the overall shape of your muscles is
much more pleasing. To understand what I mean, take a picture of
yourself and compare it to the picture of a pro. You will notice that
the pro's muscles are fuller and rounder. Again, you could duplicate
this with long and heavy cycles of steroids. PGF2 simply speeds up
this process. In one or two weeks of PGF2, you can achieve what could
have taken one to two years of continuous steroids to obtain as far as
muscle roundness is concerned.
--------------------------------------------------------------------------------
Q: What sort of gains can I expect from the use of PGF2, and how much
fat can I lose e.g. average man 200 pounds, bodybuilder, with a normal
fat layer?
A: Please understand that PGF2 is not a weight gainer. The first use
of steroids is usually associated with a tremendous weight gain. Most
of it is due to water retention and often fat gains too. You can see
this because steroids tend to blow up your face. Most bodybuilders'
faces, offseason, look like a fish tank. They are usually very pleased
with such impressive gains, but as they try to get rid of the water
and the fat to regain a leaner appearance they realize that the net
pure muscle gains while on steroids are more modest. This is why you
cannot transform yourself into a new Yates with only a few cycles
under your belt even if you gain 30 pounds each time.
With PGF2, you may gain 5 pounds of bodyweight. This certainly does
not sound like a lot. But you have to add the two or three pounds of
extra water you got rid of plus the fat you are shedding. In terms of
pure bodyweight gain, this is not very impressive. On the other hand,
packing on lean muscles and getting rid of the fat is a better and
faster way to get to the top.
As far as fat loss is concerned, it depends of course of your diet and
the other drugs you are using (i.e: insulin). It is hard to make any
estimate as it is impossible to differentiate the water and the fat
losses. Let's say that you can get rid of in between 5 to 10 pounds of
water and fat in a matter of 8 - 10 weeks with a moderate cycle.
--------------------------------------------------------------------------------
Q: For how long has PGF2 has been used? How was it discovered?
A: As far as I know, bodybuilders have been using prostaglandins on a
regular basis for more than 5 years. Perhaps it was used before that,
but I'm not aware of it. Its use has not been reported in the
bodybuilding magazines. In fact, I am sure you will keep reading
articles claiming prostaglandins are very bad.
About its discovery, I would say that it comes from farmers who have
used this substance to grow their animals in a way that was
undetectable at any drug test used by various governmental agencies.
It may have leaked out from there. If it makes a steer more muscular
why not a bodybuilder? But this was the easiest part -- when it was
first speculated that PGF2 could be a muscle builder, no one knew
whether it would work. There are many potential anabolic substances
out there. Very few really work in the real world. Whenever a new
substance is tried, the odds are very against it in that its chances
of truly working are remote. If it does not work, is it because not
enough was used, is it because it was used the wrong way or simply as
it does nothing at all? The next issue is how much should be used?
What are the side effects? Most of the steroid users may have been a
bit scared about their first time even though millions of people have
used them before. Imagine what it could be with an obscure veterinary
substance that almost no one you are aware of has ever used!
Fortunately, PGF2 has already been employed in women so the side
effects were more or less known. A very few women did die, but it was
not directly because of prostaglandins (not even PGF2) but a
concomitant administration with RU 486 for abortion.
Even though the administration modes in women are very strange, PGF2
administration did not result in sudden death. Next, the type of
administration had to be decided. All this is not easy, so the science
of PGF2 usage is not very advanced. Ten years from now, bodybuilders
will probably laugh at the way PGF2 is presently used.
--------------------------------------------------------------------------------
Q: Is there a pro using prostaglandins? If PGF2 is not able to build
up a pro rapidly, isn't that a proof of its ineffectiveness?
A: I do not know if any pro is using PGF2 though I would not be
surprised if it were so. The early use of PGF2 had to be done on drug
free bodybuilders which meant beginners. If someone is already using a
tremendous amount of various drugs, how can you tell PGF2 is actually
working? You may feel that it is bringing an extra edge but you are
not sure, nor do you know how much is due to PGF2 or the synergy
between steroids and the prostaglandins. In order to really discover
what PGF2 would do, only one variable (one drug) had to be used at a
time. A beginner with six months to a year of consistent drug free
training under his belt has no reason to experience any sudden and
dramatic change on his body.
A speed-up of the muscle building process was the testimony that the
prostaglandins were working. Only then, steroid users could experiment
with PGF2. First it was used, while off cycle without steroids. This
is again certainly not a good way to become a pro fast. But one had to
figure out whether PGF2 anabolic actions were strong enough not only
to prevent the muscle wasting but rather to continue to gain lean mass
while off steroids. Then only, the steroid plus prostaglandin stack
could be studied. The amounts of both drugs were varied to see what
would happen. To sum up, the discovery of a new drug has nothing to do
with building up a pro physique. Once a minimal amount of research is
done, only then can pros benefit optimally from it.
--------------------------------------------------------------------------------
What about PGE2?
Q: Isn't PGE2 catabolic? You seem to think otherwise.
Whenever prostaglandins are mentioned, it is usually PGE2 rather than
PGF2 that is discussed. The consensus is that PGE2 is bad. The main
reason for this is because the early major prostaglandin study
performed on muscles did suggest PGE2 was catabolic. In fact, this is
what you would probably conclude after a 5 minute search on Medline.
In a lesser known study, the very same scientific team admitted that
they kind of messed up during their first study. It is very rare to
see this study mentioned, including in scientific papers. Later,
another team of scientists did indeed prove that they were in error.
As most of the information in the bodybuilding world is based on
hearsay and repetition, it suffices that one writer suggests PGE2 is
bad, for another to repeat. You then have two different writers making
the same claim, therefore the readers considered it as gospel. What
I've not figured out yet is why only the wrong assumptions get
repeated in the muscle magazines while the right information is
generally omitted.
To answer your question in a more direct way: I do not consider that
PGE2 is catabolic. Newer research shows that it accelerates the muscle
protein turnover just like androgens. Understand that it increases
both catabolism and anabolism at the same time except that it
accelerates synthesis rate more than degradation. An overall gain
results.
--------------------------------------------------------------------------------
Drug testing
Q: Will PGF2 show up at drug test?
A: So far, PGF2 is not tested for. I doubt that it will ever be
tested. It is a pure muscle builder, not a performance enhancer. In
fact, it tends to reduce strength and performance. Furthermore, it may
be very hard to test as we naturally produce some and it might be
tough to differentiate between natural and exogenous prostaglandins.
On the other hand, PGF2 does alter steroid hormones in many ways. For
example, it might alter the testosterone/epitestosterone ratio.
--------------------------------------------------------------------------------
Side effects
Q: After some of my own research on PGF2 I have found a few ways of
overcoming a few of the side effects. As you said in your paper, the
side effects were bronchoconstriction and violent spasms of the
intestines and bowel. Could you take salbutamol (Ventolin Inhaler for
asthmatics) for relief of the tightening of the chest? And could you
also take an anti-spasmodic drug such as Mebeverine Hydrochloride,
which is used in irritable bowel syndrome complaints, to relief the
spasms of the bowels and intestines?
A: Beta agonists can help reduce the bronchoconstriction (which does
not occur in all users) but it is not an ideal solution. First,
because it does not completely prevent it. Second, it will increase
the tightening of the muscles. This is going to truly impress your
fellow bodybuilders as they touch your "relaxed" muscles but it makes
it very hard to train.
As far as the intestines are concerned, this is disturbing at first,
then you realize there is a rapid reduction of the impact of PGF2 so
that it is not so disturbing. You also get used to it. It may be wiser
not to mess around with additional drugs.
--------------------------------------------------------------------------------
Q: Are there any drugs or supplements that will prolong the half life
of PGF2 in the body?
A: Sure there are. I just do not know which ones.
--------------------------------------------------------------------------------
Aspirin and prostaglandins
Q: I have read that aspirin can effect prostaglandins in the body, is
this true or does it not apply to PGF2, and should I avoid any other
substance which can effect PGF2?
A: It is true that aspirin is a prostaglandin inhibitor. At normal
dosage, it only weakly affects the muscle prostaglandins. But whenever
you use aspirin, your muscle insulin sensitivity is reduced because of
a lesser secretion of muscle prostaglandins. Several people did report
a significant muscle growth after discontinuing aspirin.
Prostaglandins will also affect your adipose tissue both directly and
indirectly. Because of the aspirin-induced insulin resistance, your
insulin secretion will increase in order to make up for the weaker
effects in muscles, resulting in an excess of insulin effect within
the adipose tissue. Insulin promotes fat aggregation if unopposed.
Therefore, I do not recommend continual use of aspirin for
bodybuilders unless you want to get smaller and fatter. Of course, the
dose also matters. A little bit of aspirin may not hurt much while
high doses will.
Paradoxically, for someone who has no adipose tissue problem, it may
be interesting to "play" with aspirin. As I said, a muscle gain
usually results from aspirin discontinuance. Chances are it is because
muscles try to overcome the inhibitory action of aspirin on
prostaglandin secretion. Once you stop aspirin, there is a rebound in
the muscle production of prostaglandins (i.e: there is an excess of
prostaglandins) leading to muscle growth. It may be possible to do
small but repeated cycles of aspirin in order to boost growth this
way. This is a worthwhile way to pursue. For those who desires to try
this more "natural" approach, do not forget to use small doses oral
PGE1 in order to minimize the side effects of aspirin on the
gastrointestinal tract plus high doses of a prostaglandin precursor
such as primrose oil.
--------------------------------------------------------------------------------
DNP and prostaglandins
The following is not a question but rather a remark that I would like
to address in a prostaglandin way:
"I feel that DNP, in doses of 2mg/kg can be an effective anabolic
agent. I just can't tell all the mechanisms why it works so well."
Whenever one studies prostaglandins, one hears about DNP a lot. DNP
causes cellular damages which results in prostaglandin leaks. PGE2
release in particular is severely increased as a result of the
addition of DNP. At first, scientists speculated that it was because
of the PGE2 elevation that cell damages appeared (the catabolic theory
of PGE2). The mere addition of aspirin proved this theory wrong.
Whenever aspirin is administered along with DNP, PGE2 release was
inhibited yet, cellular damage remained. Therefore, PGE2 release is
the consequence and not the cause of the cellular damage. All this to
say that DNP will cause muscle damage a bit like training does. But
unlike a workout-induced damage, it is not localized to a single
muscle group but is rather spread all over. Of course, the body will
try to stop or minimize the wasting process that DNP is trying to
trigger. Your body will try to calm down the main catabolic pathways
DNP puts into play. Once DNP is discontinued, the rate of protein
degradation in the muscle will be restricted a a bare minimum while
the long-lasting prostaglandin leaks will keep on going. The end
result is that the rate of synthesis is boosted while the catabolic
pathways are slowed. We are then placed in the most favorable
situation possible to build muscles fast.
--------------------------------------------------------------------------------
Q: Can I stack DNP with PGF2 for better thermogenic response?
A: I would say no as I speculate that DNP thermogenic actions require
the release of prostaglandins or at least employ similar pathways. To
determine this for sure, scientists (do not try this at home) could
use very high doses of aspirin a bit before DNP t
Let me begin by saying that I do not have the answers to many of the
questions that you, readers, are asking me. I will try my best to
address all of them even if I do not have the exact answer, by using
common sense.
The how-to of PGF2
Q: How long should you use PGF2, do you cycle it or is there no need
to come off it?
A: Bodybuilders are so used to steroid cycling that it is legitimate
to wonder about the necessity of cycling PGF2. After more than 50
years of both continuous usage and scientific research, no one has
been able to come up with a universal steroid cycling pattern that
could suit everyone. Do not expect that after such a limited
experience with PGF2, anyone could come up with an optimal cycling
pattern. So let's look at a rational way of cycling. If you are off
steroids for 2 months at a time, your PGF2 cycle should last 2 months
in order to turn this potential wasting period into an opportunity to
pack on lean muscle.
Another way of looking at PGF2 cycling is to use it for as long as you
can stand it. PGF2 usage is not as comfortable as steroid use. Most
bodybuilders are not motivated enough to inject several times a day
for more than 60-90 days at a time. So, here is your cycle length. It
is counterproductive for bodybuilders to use drugs reluctantly.
As far as the need to come off is concerned, there is as much need to
come off prostaglandins as need to come off steroids. Although
everyone should discontinue anabolics from time to time, most pros
never do. If you use PGF2 just to look good on the beach, yes, you
should come off. If you have to make a living from body, you may not
have much choice.
--------------------------------------------------------------------------------
Q: How long does it take to see the first results?
A: Cosmetically speaking, less than a week. Most of the early gains
are due to the diuretic properties of prostaglandins. Then you realize
that your muscles get very hard even when relaxed. To get a similar
hardening effect, you would have needed quite a bit of steroids. You
will also remark quickly that the overall shape of your muscles is
much more pleasing. To understand what I mean, take a picture of
yourself and compare it to the picture of a pro. You will notice that
the pro's muscles are fuller and rounder. Again, you could duplicate
this with long and heavy cycles of steroids. PGF2 simply speeds up
this process. In one or two weeks of PGF2, you can achieve what could
have taken one to two years of continuous steroids to obtain as far as
muscle roundness is concerned.
--------------------------------------------------------------------------------
Q: What sort of gains can I expect from the use of PGF2, and how much
fat can I lose e.g. average man 200 pounds, bodybuilder, with a normal
fat layer?
A: Please understand that PGF2 is not a weight gainer. The first use
of steroids is usually associated with a tremendous weight gain. Most
of it is due to water retention and often fat gains too. You can see
this because steroids tend to blow up your face. Most bodybuilders'
faces, offseason, look like a fish tank. They are usually very pleased
with such impressive gains, but as they try to get rid of the water
and the fat to regain a leaner appearance they realize that the net
pure muscle gains while on steroids are more modest. This is why you
cannot transform yourself into a new Yates with only a few cycles
under your belt even if you gain 30 pounds each time.
With PGF2, you may gain 5 pounds of bodyweight. This certainly does
not sound like a lot. But you have to add the two or three pounds of
extra water you got rid of plus the fat you are shedding. In terms of
pure bodyweight gain, this is not very impressive. On the other hand,
packing on lean muscles and getting rid of the fat is a better and
faster way to get to the top.
As far as fat loss is concerned, it depends of course of your diet and
the other drugs you are using (i.e: insulin). It is hard to make any
estimate as it is impossible to differentiate the water and the fat
losses. Let's say that you can get rid of in between 5 to 10 pounds of
water and fat in a matter of 8 - 10 weeks with a moderate cycle.
--------------------------------------------------------------------------------
Q: For how long has PGF2 has been used? How was it discovered?
A: As far as I know, bodybuilders have been using prostaglandins on a
regular basis for more than 5 years. Perhaps it was used before that,
but I'm not aware of it. Its use has not been reported in the
bodybuilding magazines. In fact, I am sure you will keep reading
articles claiming prostaglandins are very bad.
About its discovery, I would say that it comes from farmers who have
used this substance to grow their animals in a way that was
undetectable at any drug test used by various governmental agencies.
It may have leaked out from there. If it makes a steer more muscular
why not a bodybuilder? But this was the easiest part -- when it was
first speculated that PGF2 could be a muscle builder, no one knew
whether it would work. There are many potential anabolic substances
out there. Very few really work in the real world. Whenever a new
substance is tried, the odds are very against it in that its chances
of truly working are remote. If it does not work, is it because not
enough was used, is it because it was used the wrong way or simply as
it does nothing at all? The next issue is how much should be used?
What are the side effects? Most of the steroid users may have been a
bit scared about their first time even though millions of people have
used them before. Imagine what it could be with an obscure veterinary
substance that almost no one you are aware of has ever used!
Fortunately, PGF2 has already been employed in women so the side
effects were more or less known. A very few women did die, but it was
not directly because of prostaglandins (not even PGF2) but a
concomitant administration with RU 486 for abortion.
Even though the administration modes in women are very strange, PGF2
administration did not result in sudden death. Next, the type of
administration had to be decided. All this is not easy, so the science
of PGF2 usage is not very advanced. Ten years from now, bodybuilders
will probably laugh at the way PGF2 is presently used.
--------------------------------------------------------------------------------
Q: Is there a pro using prostaglandins? If PGF2 is not able to build
up a pro rapidly, isn't that a proof of its ineffectiveness?
A: I do not know if any pro is using PGF2 though I would not be
surprised if it were so. The early use of PGF2 had to be done on drug
free bodybuilders which meant beginners. If someone is already using a
tremendous amount of various drugs, how can you tell PGF2 is actually
working? You may feel that it is bringing an extra edge but you are
not sure, nor do you know how much is due to PGF2 or the synergy
between steroids and the prostaglandins. In order to really discover
what PGF2 would do, only one variable (one drug) had to be used at a
time. A beginner with six months to a year of consistent drug free
training under his belt has no reason to experience any sudden and
dramatic change on his body.
A speed-up of the muscle building process was the testimony that the
prostaglandins were working. Only then, steroid users could experiment
with PGF2. First it was used, while off cycle without steroids. This
is again certainly not a good way to become a pro fast. But one had to
figure out whether PGF2 anabolic actions were strong enough not only
to prevent the muscle wasting but rather to continue to gain lean mass
while off steroids. Then only, the steroid plus prostaglandin stack
could be studied. The amounts of both drugs were varied to see what
would happen. To sum up, the discovery of a new drug has nothing to do
with building up a pro physique. Once a minimal amount of research is
done, only then can pros benefit optimally from it.
--------------------------------------------------------------------------------
What about PGE2?
Q: Isn't PGE2 catabolic? You seem to think otherwise.
Whenever prostaglandins are mentioned, it is usually PGE2 rather than
PGF2 that is discussed. The consensus is that PGE2 is bad. The main
reason for this is because the early major prostaglandin study
performed on muscles did suggest PGE2 was catabolic. In fact, this is
what you would probably conclude after a 5 minute search on Medline.
In a lesser known study, the very same scientific team admitted that
they kind of messed up during their first study. It is very rare to
see this study mentioned, including in scientific papers. Later,
another team of scientists did indeed prove that they were in error.
As most of the information in the bodybuilding world is based on
hearsay and repetition, it suffices that one writer suggests PGE2 is
bad, for another to repeat. You then have two different writers making
the same claim, therefore the readers considered it as gospel. What
I've not figured out yet is why only the wrong assumptions get
repeated in the muscle magazines while the right information is
generally omitted.
To answer your question in a more direct way: I do not consider that
PGE2 is catabolic. Newer research shows that it accelerates the muscle
protein turnover just like androgens. Understand that it increases
both catabolism and anabolism at the same time except that it
accelerates synthesis rate more than degradation. An overall gain
results.
--------------------------------------------------------------------------------
Drug testing
Q: Will PGF2 show up at drug test?
A: So far, PGF2 is not tested for. I doubt that it will ever be
tested. It is a pure muscle builder, not a performance enhancer. In
fact, it tends to reduce strength and performance. Furthermore, it may
be very hard to test as we naturally produce some and it might be
tough to differentiate between natural and exogenous prostaglandins.
On the other hand, PGF2 does alter steroid hormones in many ways. For
example, it might alter the testosterone/epitestosterone ratio.
--------------------------------------------------------------------------------
Side effects
Q: After some of my own research on PGF2 I have found a few ways of
overcoming a few of the side effects. As you said in your paper, the
side effects were bronchoconstriction and violent spasms of the
intestines and bowel. Could you take salbutamol (Ventolin Inhaler for
asthmatics) for relief of the tightening of the chest? And could you
also take an anti-spasmodic drug such as Mebeverine Hydrochloride,
which is used in irritable bowel syndrome complaints, to relief the
spasms of the bowels and intestines?
A: Beta agonists can help reduce the bronchoconstriction (which does
not occur in all users) but it is not an ideal solution. First,
because it does not completely prevent it. Second, it will increase
the tightening of the muscles. This is going to truly impress your
fellow bodybuilders as they touch your "relaxed" muscles but it makes
it very hard to train.
As far as the intestines are concerned, this is disturbing at first,
then you realize there is a rapid reduction of the impact of PGF2 so
that it is not so disturbing. You also get used to it. It may be wiser
not to mess around with additional drugs.
--------------------------------------------------------------------------------
Q: Are there any drugs or supplements that will prolong the half life
of PGF2 in the body?
A: Sure there are. I just do not know which ones.
--------------------------------------------------------------------------------
Aspirin and prostaglandins
Q: I have read that aspirin can effect prostaglandins in the body, is
this true or does it not apply to PGF2, and should I avoid any other
substance which can effect PGF2?
A: It is true that aspirin is a prostaglandin inhibitor. At normal
dosage, it only weakly affects the muscle prostaglandins. But whenever
you use aspirin, your muscle insulin sensitivity is reduced because of
a lesser secretion of muscle prostaglandins. Several people did report
a significant muscle growth after discontinuing aspirin.
Prostaglandins will also affect your adipose tissue both directly and
indirectly. Because of the aspirin-induced insulin resistance, your
insulin secretion will increase in order to make up for the weaker
effects in muscles, resulting in an excess of insulin effect within
the adipose tissue. Insulin promotes fat aggregation if unopposed.
Therefore, I do not recommend continual use of aspirin for
bodybuilders unless you want to get smaller and fatter. Of course, the
dose also matters. A little bit of aspirin may not hurt much while
high doses will.
Paradoxically, for someone who has no adipose tissue problem, it may
be interesting to "play" with aspirin. As I said, a muscle gain
usually results from aspirin discontinuance. Chances are it is because
muscles try to overcome the inhibitory action of aspirin on
prostaglandin secretion. Once you stop aspirin, there is a rebound in
the muscle production of prostaglandins (i.e: there is an excess of
prostaglandins) leading to muscle growth. It may be possible to do
small but repeated cycles of aspirin in order to boost growth this
way. This is a worthwhile way to pursue. For those who desires to try
this more "natural" approach, do not forget to use small doses oral
PGE1 in order to minimize the side effects of aspirin on the
gastrointestinal tract plus high doses of a prostaglandin precursor
such as primrose oil.
--------------------------------------------------------------------------------
DNP and prostaglandins
The following is not a question but rather a remark that I would like
to address in a prostaglandin way:
"I feel that DNP, in doses of 2mg/kg can be an effective anabolic
agent. I just can't tell all the mechanisms why it works so well."
Whenever one studies prostaglandins, one hears about DNP a lot. DNP
causes cellular damages which results in prostaglandin leaks. PGE2
release in particular is severely increased as a result of the
addition of DNP. At first, scientists speculated that it was because
of the PGE2 elevation that cell damages appeared (the catabolic theory
of PGE2). The mere addition of aspirin proved this theory wrong.
Whenever aspirin is administered along with DNP, PGE2 release was
inhibited yet, cellular damage remained. Therefore, PGE2 release is
the consequence and not the cause of the cellular damage. All this to
say that DNP will cause muscle damage a bit like training does. But
unlike a workout-induced damage, it is not localized to a single
muscle group but is rather spread all over. Of course, the body will
try to stop or minimize the wasting process that DNP is trying to
trigger. Your body will try to calm down the main catabolic pathways
DNP puts into play. Once DNP is discontinued, the rate of protein
degradation in the muscle will be restricted a a bare minimum while
the long-lasting prostaglandin leaks will keep on going. The end
result is that the rate of synthesis is boosted while the catabolic
pathways are slowed. We are then placed in the most favorable
situation possible to build muscles fast.
--------------------------------------------------------------------------------
Q: Can I stack DNP with PGF2 for better thermogenic response?
A: I would say no as I speculate that DNP thermogenic actions require
the release of prostaglandins or at least employ similar pathways. To
determine this for sure, scientists (do not try this at home) could
use very high doses of aspirin a bit before DNP t
Prostaglandin PGF2a
by Bryan Haycock
Where does it come from? How does it work? Taking a closer look at
this up and coming weapon in the bodybuilders arsenal
In January 1999, Mesomorphosis revealed a little known strategy being
used by several elite European athletes to boost size and strength.
What was this secret weapon? The prostaglandin PGF2 of course. It is
purported to increase muscle mass wherever you inject it, as well as
reduce body fat by increasing body temperature. This has caused quite
a stir within the bodybuilding community. Gym rats all over the globe
are already scampering to get their hands on this unique bodybuilding
tool. No doubt you will soon see other magazines jumping on the
bandwagon in order not to miss out on what Mesomorphosis has started.
Mesomorphosis believes that the day of bodybuilders blindly following
the advice of others based on hearsay is gone. For this reason,
bodybuilders must not only be abreast of what tools are available to
them in there quest for muscle growth, but also be educated about the
science behind these sometimes exotic compounds. Hereafter we will
take a closer look at prostaglandins and their role in muscle growth.
It is only after we gain knowledge that we can effectively put to use
those tools available to us.
Prostaglandins and their Discovery
Prostaglandins are part of a class of substances called eicosanoids.
Eicosanoids are a group of substances derived from fatty acids and
include prostaglandins, thromboxanes, and leukotrienes, all of which
are formed from precursor fatty acids by the incorporation of oxygen
atoms into the fatty acid chains. This reaction is called oxygenation
and is carried out by cyclo-oxygenase enzymes. Prostaglandins and
their metabolites have been found in virtually every tissue in the
body.
The discovery of prostaglandins and determination of their structure
began in 1930, when Raphael Kurzrok and Charles Lieb, both new York
gynecologists, observed that human seminal fluid stimulates
contraction of isolated uterine muscle. A few years later in Sweden,
Ulf von Euler confirmed this report and noted that human seminal fluid
also produces contraction in intestinal smooth muscle and lowers blood
pressure when injected into the blood stream. It was Von Euler who
came up with the name prostaglandin for this mysterious substance. The
name prostaglandin seemed appropriate because he thought it originated
in the prostate gland. Today, we know that prostaglandin production is
not limited to the prostate, in fact, there is virtually no soft
tissue in the body that doesn=92t produce them. The name, however, has
stuck with us through the years. If Von Euler had known his name for
prostaglandins would still be with us into the next millennia, I=92m
sure he would have chosen to name them "Von Eulers" or "UVEs" instead
of prostaglandins. By 1960, several specific prostaglandins had been
isolated in pure crystalline form and their structures determined.
Because our concern with prostaglandins involves primarily PGF2a, and
perhaps PGE2, we will not go into detail about the myriad of other
prostaglandins. Just know that prostaglandins are abbreviated "PG".
The additional letter and numerical script indicate the type and
series. The various types differ in the functional group present in
the five-membered ring.
While scientists were studying the structure of these new compounds,
other research was being done to determine their role in human
physiology and their potential as drugs. Initially these compounds
were extremely expensive to synthesize and/or isolate in sufficient
quantities for research. In 1969, the price of prostaglandins dropped
dramatically with the discovery that the gorgonian sea whip, or sea
fan, is a rich source of prostaglandin-like materials. Now however,
there is no need to rely on natural sources because chemists have
developed highly effective laboratory methods for the synthesis of
almost any prostaglandin or prostaglandin analog.
----------------------------------------------------------------------------=
----
Endogenous production from Arachidonic Acid
Prostaglandins (PGs) are not stored in the tissues of your body. PGs
are produced in response to some physiological trigger. The starting
material for PG synthesis are unsaturated fatty acids that have 20
carbon structures. The fatty acid that is used to make PGF2a is
arachidonic acid.
----------------------------------------------------------------------------=
----
Functions of prostaglandins in the body
Prostaglandins are classified as autocrine (effecting the same cell
that produced it), as well as paracrine (effecting adjacent cells),
regulators. They do not really fit into the category of hormones, nor
are they neurotransmitters, instead they are simply considered as a
corollary of the endocrine system.
The following are some of the regulatory functions of prostaglandins
in various organs and systems of the body:
Inflammation & Pain. PGs promote many aspects of the inflammatory
response. They are involved in the sensation of pain associated with
inflammation and vasoconstriction and/or dilation, and the development
of fever. PGs, when injected directly into the hypothalamus, induce
fever. Anecdotally, the use of PGF2a also induces a rise in body
temperature presumably by interacting with the hypothalamus as well.
Reproductive systems. PGs may play a role in ovulation and corpus
luteum function in the ovaries and in contraction of the uterus.
Excessive PG production may be involved in premature labor,
endometriosis, dysmenorrhea (menstrual cramps), and other
gynecological disorders. PGs are often given to induce labor.
Gastrointestinal tract. The stomach and intestine produce PGs. PGs are
believed to inhibit gastric secretions and influence gastric motility
as well as fluid absorption. Drugs such as aspirin that inhibit
prostaglandin production can lead to overproduction of gastric
secretion. This predisposes the person to gastric ulcers.
Respiratory System. PGs can cause vasoconstriction as well as
vasodilation of blood vessels within the lungs, depending on which PGs
are being produced. PGs also cause both dilation and constriction of
bronchial smooth muscle. PGs as well as other eicosanoids may play a
role in asthma.
Blood vessels. Some PGs are vasoconstrictors, others are vasodilators.
The overall effect is determined by which PG is present in greater
concentration.
Blood clotting. Thromboxanes, also a product of cyclo-oxygenase, are
produced by blood platelets. These eicosanoids promote platelet
aggregation and vasoconstriction. Prostacyclin, produced by vascular
endothelial cells, inhibits platelet aggregation and causes
vasodilation.
Kidneys. PGs are produced in the medulla of the kidneys and cause
vasodilation, resulting in increased renal blood flow and increased
excretion of water and electrolytes in the urine. In particular, high
potassium intake has been shown to selectively increase PGF2a
excretion in animals.
Protein synthesis. PGs are known to be regulators of protein synthesis
in skeletal muscle. PGE2 and PGF2a being involved in protein breakdown
and protein synthesis rates respectively. Stretch induced hypertrophy
of skeletal muscle is in part regulated by prostaglandins. More on the
role of PGs in protein synthesis in later sections.
Adipogenesis. PGF2a directly inhibits adipogenesis. You should not be
surprised to hear that yet another prostaglandin serves to induce
adipogenesis, namely PGJ2. PGJ2 derivatives function as activating
ligands for peroxisome proliferator-activated receptor (PPAR), a
nuclear hormone receptor that is central to fat cell proliferation.
PGF2 blocks adipogenesis through activation of mitogen-activated
protein kinase (the same kinase involved in insulin action), resulting
in inhibitory phosphorylation of PPAR. Both mitogen-activated protein
kinase activation and PPAR phosphorylation are required for the anti-
adipogenic effects of PGF2. So you have PGs within the cell telling
the fat cell to divide while at the same time you have other PGs, such
as PGF2a, at the outside preventing it from taking place.
----------------------------------------------------------------------------=
----
Current uses of PGF2a
Humans PGF2a is not currently FDA approved for use in humans. Products
containing PGF2a should be considered hazardous to women and must be
handled with extreme care. PGF2a is readily absorbed through the skin
and may result in birth defects and/or instantaneous abortion.
Prostaglandins of use today in humans are of the "E" class and are
administered to women for abortion or to induce labor. Prostaglandins
are also used for impotence in men. In such case it (PGE1) is injected
directly into the penis.
Animals PGF2a has been tested in a wide range of animals from monkeys
to horses. In most cases the side effects are increased body
temperature, vomiting and diarrhea, bronchial constriction, confusion,
loss of coordination, tachycardia, and low blood pressure just to name
a few. PGF2a is nontoxic with a serum half life of only minutes.
PGF2a is currently used in animal husbandry to manage breeding. It is
used commonly as dinoprost in the form of a tromethamine salt. Upjohn
makes a version called Lutalyse=AE as a sterile solution for
subcutaneous and intramuscular injection. It=92s purpose is to
synchronizing ovulation in cattle by sequential injection of several
hormones along with PGF2a. A hormone selected from the group
consisting of gonadotropin releasing hormone (GnRH), luteinizing
hormone (LH), or human chorionic gonadotropin (hCG) is administered to
an open cow during an estrous cycle in order to stimulate follicle
development. PGF2a is then administered to initiate corpus luteum
regression about five to eight days after administration of the GnRH,
LH or hCG. A second dose of GnRH, LH or hCG is then administered
concomitantly with the PGF2a injection or up to about three days after
the PGF2a injection. This second dose of hormone functions to
stimulate the ovulation of a dominant follicle and the cow is then
breed within one day of the administration of the second dose of
hormone.
----------------------------------------------------------------------------=
----
The Role of PGF2a in Muscle Growth
After that brief introduction into prostaglandins, we can now begin to
discuss more specifically the role of prostaglandins in muscle growth.
In a nutshell, mechanical stimulation (i.e. intermittent stretch)
results in the production and efflux of two prostaglandins, PGE2 and
PGF2a. PGE2 increases protein degradation where as PGF2a increases
protein synthesis. Muscle hypertrophy is usually achieved by an
increase in protein synthesis as well as a proportionately smaller
increase in degradation. The simultaneous release of both PGE2 and
PGF2a creates this condition.
It is well known that mechanical stretch, without any electrical
activity, is sufficient to induce muscle hypertrophy. Recent studies
have shown that the mechanism by which mechanical stretch leads to
prostaglandin production and ultimately muscle growth, involves G
proteins embedded in the cell membrane. These G proteins increase the
amount of cyclo-oxygenase, the enzyme responsible for making
prostaglandins from arachidonic acid. Skeletal muscle cyclooxygenase
generates PGE2 and PGF2 alpha at a ratio approximately equal to one.
The exact mechanism by which PGF2a increases protein synthesis is not
entirely clear. That=92s just a spineless way of saying, "I don=92t know
the exact answer to that!" We are free to speculate though. It may
involve short phase protein synthesis and/or long phase protein
synthesis.
2 phases of protein synthesis Modulation
Modulation of protein synthesis rates occurs at two levels, the short
phase and the long phase. The short phase alteration in protein
synthesis rates occurs by altering the activity of existing ribosomes
and/or eukaryotic initiation factors (eIFs). This happens within
minutes of the appropriate physiological trigger. The long phase
modulation of protein synthesis happens by way of increasing the
number of myonuclei. This mechanism involves hormones and growth
factors such as HGH and IGF-1 bringing about the activation of
myogenic stem cells. This can take several days to effect protein
synthesis rates. This is a simplified view but for our purposes it is
sufficient.
The role of PGF2a in short phase protein synthesis in muscle tissue is
speculative at best. In non-muscle tissue, prostaglandins effect
calcium fluxes, plasma membrane ionic channel activities, and cyclic
nucleotide levels. All of which are important regulators of protein
synthesis rates in muscle. PGF2a has been shown to interact with the
S6 small ribosomal subunit, increasing its potential to form the
ribosomal initiation complex with the large subunits. It is also
plausible that PGF2a may effect the activity of eIFs.
Initiation of translation (the binding of mRNA to the ribosomal pre-
initiation complex) requires group 4 eukaryotic initiation factors
(eIFs). These initiation factors interact with the mRNA in such a way
that makes translation (the construction of new proteins from the mRNA
strand) possible. Two eIFs, called eIF4A and eIF4B, act in concert to
unwind the mRNA strand. Another one called eIF4E binds to what is
called the "cap region" and is important for controlling which mRNA
strands are translated and also for stabilization of the mRNA strand.
Finally, eIF4G is a large polypeptide that acts as a scaffold or
framework around which all of these initiation factors and the mRNA
and ribosome can be kept in place and proper orientation for
translation. There is yet no direct evidence to confirm that PGF2a
works through this mechanism however.
Long term modulation of protein synthesis involves the activation of
myogenic stem cells or satellite cells. If you recall, when a muscle
is stretched it not only produces PGF2a, but also PGE2. PGE2 is a
potent inducer of satellite cell proliferation and fusion. This is how
existing muscle cells increase the number of nuclei they contain. This
is important because in order for a muscle to grow rapidly, it must
produce more mRNA. This is done in the nucleus of the muscle cell. The
more nuclei you have, the more mRNA you can produce. Within the cell,
prostaglandins may also be involved in regulating the number of
ribosomes. This could have long term implications on growth and
development as well as stretch induced hypertrophy.
----------------------------------------------------------------------------=
----
The role of other hormones, drugs and diet in the action of PGs.
Because prostaglandins are signaling molecules that get their message
across through multi step signal transduction pathways, they are
susceptible to modulation by several chemical, hormonal, and dietary
factors. I will do my best to shed some light on the subject without
bogging you down with meaningless terms and jargon. It is well to
remember that the action and interaction of prostaglandins in the
human body is complex.
Cortisol
Cortisol effects the production of prostaglandins in muscle tissue by
at least two mechanisms. First, cortisol by way of lipocortins,
inhibits the action of phospholipase A2. Phospholipase is necessary in
order to make arachidonic acid available for PGF2a production.
Cortisol also inhibits the production of cyclo-oxygenase mRNA content
within cells. As mentioned earlier, cyclo-oxygenase is the enzyme that
converts arachidonic acid into prostaglandins. So cortisol inhibits
muscle growth by preventing the production of PGF2a in response to
training (mechanica
by Bryan Haycock
Where does it come from? How does it work? Taking a closer look at
this up and coming weapon in the bodybuilders arsenal
In January 1999, Mesomorphosis revealed a little known strategy being
used by several elite European athletes to boost size and strength.
What was this secret weapon? The prostaglandin PGF2 of course. It is
purported to increase muscle mass wherever you inject it, as well as
reduce body fat by increasing body temperature. This has caused quite
a stir within the bodybuilding community. Gym rats all over the globe
are already scampering to get their hands on this unique bodybuilding
tool. No doubt you will soon see other magazines jumping on the
bandwagon in order not to miss out on what Mesomorphosis has started.
Mesomorphosis believes that the day of bodybuilders blindly following
the advice of others based on hearsay is gone. For this reason,
bodybuilders must not only be abreast of what tools are available to
them in there quest for muscle growth, but also be educated about the
science behind these sometimes exotic compounds. Hereafter we will
take a closer look at prostaglandins and their role in muscle growth.
It is only after we gain knowledge that we can effectively put to use
those tools available to us.
Prostaglandins and their Discovery
Prostaglandins are part of a class of substances called eicosanoids.
Eicosanoids are a group of substances derived from fatty acids and
include prostaglandins, thromboxanes, and leukotrienes, all of which
are formed from precursor fatty acids by the incorporation of oxygen
atoms into the fatty acid chains. This reaction is called oxygenation
and is carried out by cyclo-oxygenase enzymes. Prostaglandins and
their metabolites have been found in virtually every tissue in the
body.
The discovery of prostaglandins and determination of their structure
began in 1930, when Raphael Kurzrok and Charles Lieb, both new York
gynecologists, observed that human seminal fluid stimulates
contraction of isolated uterine muscle. A few years later in Sweden,
Ulf von Euler confirmed this report and noted that human seminal fluid
also produces contraction in intestinal smooth muscle and lowers blood
pressure when injected into the blood stream. It was Von Euler who
came up with the name prostaglandin for this mysterious substance. The
name prostaglandin seemed appropriate because he thought it originated
in the prostate gland. Today, we know that prostaglandin production is
not limited to the prostate, in fact, there is virtually no soft
tissue in the body that doesn=92t produce them. The name, however, has
stuck with us through the years. If Von Euler had known his name for
prostaglandins would still be with us into the next millennia, I=92m
sure he would have chosen to name them "Von Eulers" or "UVEs" instead
of prostaglandins. By 1960, several specific prostaglandins had been
isolated in pure crystalline form and their structures determined.
Because our concern with prostaglandins involves primarily PGF2a, and
perhaps PGE2, we will not go into detail about the myriad of other
prostaglandins. Just know that prostaglandins are abbreviated "PG".
The additional letter and numerical script indicate the type and
series. The various types differ in the functional group present in
the five-membered ring.
While scientists were studying the structure of these new compounds,
other research was being done to determine their role in human
physiology and their potential as drugs. Initially these compounds
were extremely expensive to synthesize and/or isolate in sufficient
quantities for research. In 1969, the price of prostaglandins dropped
dramatically with the discovery that the gorgonian sea whip, or sea
fan, is a rich source of prostaglandin-like materials. Now however,
there is no need to rely on natural sources because chemists have
developed highly effective laboratory methods for the synthesis of
almost any prostaglandin or prostaglandin analog.
----------------------------------------------------------------------------=
----
Endogenous production from Arachidonic Acid
Prostaglandins (PGs) are not stored in the tissues of your body. PGs
are produced in response to some physiological trigger. The starting
material for PG synthesis are unsaturated fatty acids that have 20
carbon structures. The fatty acid that is used to make PGF2a is
arachidonic acid.
----------------------------------------------------------------------------=
----
Functions of prostaglandins in the body
Prostaglandins are classified as autocrine (effecting the same cell
that produced it), as well as paracrine (effecting adjacent cells),
regulators. They do not really fit into the category of hormones, nor
are they neurotransmitters, instead they are simply considered as a
corollary of the endocrine system.
The following are some of the regulatory functions of prostaglandins
in various organs and systems of the body:
Inflammation & Pain. PGs promote many aspects of the inflammatory
response. They are involved in the sensation of pain associated with
inflammation and vasoconstriction and/or dilation, and the development
of fever. PGs, when injected directly into the hypothalamus, induce
fever. Anecdotally, the use of PGF2a also induces a rise in body
temperature presumably by interacting with the hypothalamus as well.
Reproductive systems. PGs may play a role in ovulation and corpus
luteum function in the ovaries and in contraction of the uterus.
Excessive PG production may be involved in premature labor,
endometriosis, dysmenorrhea (menstrual cramps), and other
gynecological disorders. PGs are often given to induce labor.
Gastrointestinal tract. The stomach and intestine produce PGs. PGs are
believed to inhibit gastric secretions and influence gastric motility
as well as fluid absorption. Drugs such as aspirin that inhibit
prostaglandin production can lead to overproduction of gastric
secretion. This predisposes the person to gastric ulcers.
Respiratory System. PGs can cause vasoconstriction as well as
vasodilation of blood vessels within the lungs, depending on which PGs
are being produced. PGs also cause both dilation and constriction of
bronchial smooth muscle. PGs as well as other eicosanoids may play a
role in asthma.
Blood vessels. Some PGs are vasoconstrictors, others are vasodilators.
The overall effect is determined by which PG is present in greater
concentration.
Blood clotting. Thromboxanes, also a product of cyclo-oxygenase, are
produced by blood platelets. These eicosanoids promote platelet
aggregation and vasoconstriction. Prostacyclin, produced by vascular
endothelial cells, inhibits platelet aggregation and causes
vasodilation.
Kidneys. PGs are produced in the medulla of the kidneys and cause
vasodilation, resulting in increased renal blood flow and increased
excretion of water and electrolytes in the urine. In particular, high
potassium intake has been shown to selectively increase PGF2a
excretion in animals.
Protein synthesis. PGs are known to be regulators of protein synthesis
in skeletal muscle. PGE2 and PGF2a being involved in protein breakdown
and protein synthesis rates respectively. Stretch induced hypertrophy
of skeletal muscle is in part regulated by prostaglandins. More on the
role of PGs in protein synthesis in later sections.
Adipogenesis. PGF2a directly inhibits adipogenesis. You should not be
surprised to hear that yet another prostaglandin serves to induce
adipogenesis, namely PGJ2. PGJ2 derivatives function as activating
ligands for peroxisome proliferator-activated receptor (PPAR), a
nuclear hormone receptor that is central to fat cell proliferation.
PGF2 blocks adipogenesis through activation of mitogen-activated
protein kinase (the same kinase involved in insulin action), resulting
in inhibitory phosphorylation of PPAR. Both mitogen-activated protein
kinase activation and PPAR phosphorylation are required for the anti-
adipogenic effects of PGF2. So you have PGs within the cell telling
the fat cell to divide while at the same time you have other PGs, such
as PGF2a, at the outside preventing it from taking place.
----------------------------------------------------------------------------=
----
Current uses of PGF2a
Humans PGF2a is not currently FDA approved for use in humans. Products
containing PGF2a should be considered hazardous to women and must be
handled with extreme care. PGF2a is readily absorbed through the skin
and may result in birth defects and/or instantaneous abortion.
Prostaglandins of use today in humans are of the "E" class and are
administered to women for abortion or to induce labor. Prostaglandins
are also used for impotence in men. In such case it (PGE1) is injected
directly into the penis.
Animals PGF2a has been tested in a wide range of animals from monkeys
to horses. In most cases the side effects are increased body
temperature, vomiting and diarrhea, bronchial constriction, confusion,
loss of coordination, tachycardia, and low blood pressure just to name
a few. PGF2a is nontoxic with a serum half life of only minutes.
PGF2a is currently used in animal husbandry to manage breeding. It is
used commonly as dinoprost in the form of a tromethamine salt. Upjohn
makes a version called Lutalyse=AE as a sterile solution for
subcutaneous and intramuscular injection. It=92s purpose is to
synchronizing ovulation in cattle by sequential injection of several
hormones along with PGF2a. A hormone selected from the group
consisting of gonadotropin releasing hormone (GnRH), luteinizing
hormone (LH), or human chorionic gonadotropin (hCG) is administered to
an open cow during an estrous cycle in order to stimulate follicle
development. PGF2a is then administered to initiate corpus luteum
regression about five to eight days after administration of the GnRH,
LH or hCG. A second dose of GnRH, LH or hCG is then administered
concomitantly with the PGF2a injection or up to about three days after
the PGF2a injection. This second dose of hormone functions to
stimulate the ovulation of a dominant follicle and the cow is then
breed within one day of the administration of the second dose of
hormone.
----------------------------------------------------------------------------=
----
The Role of PGF2a in Muscle Growth
After that brief introduction into prostaglandins, we can now begin to
discuss more specifically the role of prostaglandins in muscle growth.
In a nutshell, mechanical stimulation (i.e. intermittent stretch)
results in the production and efflux of two prostaglandins, PGE2 and
PGF2a. PGE2 increases protein degradation where as PGF2a increases
protein synthesis. Muscle hypertrophy is usually achieved by an
increase in protein synthesis as well as a proportionately smaller
increase in degradation. The simultaneous release of both PGE2 and
PGF2a creates this condition.
It is well known that mechanical stretch, without any electrical
activity, is sufficient to induce muscle hypertrophy. Recent studies
have shown that the mechanism by which mechanical stretch leads to
prostaglandin production and ultimately muscle growth, involves G
proteins embedded in the cell membrane. These G proteins increase the
amount of cyclo-oxygenase, the enzyme responsible for making
prostaglandins from arachidonic acid. Skeletal muscle cyclooxygenase
generates PGE2 and PGF2 alpha at a ratio approximately equal to one.
The exact mechanism by which PGF2a increases protein synthesis is not
entirely clear. That=92s just a spineless way of saying, "I don=92t know
the exact answer to that!" We are free to speculate though. It may
involve short phase protein synthesis and/or long phase protein
synthesis.
2 phases of protein synthesis Modulation
Modulation of protein synthesis rates occurs at two levels, the short
phase and the long phase. The short phase alteration in protein
synthesis rates occurs by altering the activity of existing ribosomes
and/or eukaryotic initiation factors (eIFs). This happens within
minutes of the appropriate physiological trigger. The long phase
modulation of protein synthesis happens by way of increasing the
number of myonuclei. This mechanism involves hormones and growth
factors such as HGH and IGF-1 bringing about the activation of
myogenic stem cells. This can take several days to effect protein
synthesis rates. This is a simplified view but for our purposes it is
sufficient.
The role of PGF2a in short phase protein synthesis in muscle tissue is
speculative at best. In non-muscle tissue, prostaglandins effect
calcium fluxes, plasma membrane ionic channel activities, and cyclic
nucleotide levels. All of which are important regulators of protein
synthesis rates in muscle. PGF2a has been shown to interact with the
S6 small ribosomal subunit, increasing its potential to form the
ribosomal initiation complex with the large subunits. It is also
plausible that PGF2a may effect the activity of eIFs.
Initiation of translation (the binding of mRNA to the ribosomal pre-
initiation complex) requires group 4 eukaryotic initiation factors
(eIFs). These initiation factors interact with the mRNA in such a way
that makes translation (the construction of new proteins from the mRNA
strand) possible. Two eIFs, called eIF4A and eIF4B, act in concert to
unwind the mRNA strand. Another one called eIF4E binds to what is
called the "cap region" and is important for controlling which mRNA
strands are translated and also for stabilization of the mRNA strand.
Finally, eIF4G is a large polypeptide that acts as a scaffold or
framework around which all of these initiation factors and the mRNA
and ribosome can be kept in place and proper orientation for
translation. There is yet no direct evidence to confirm that PGF2a
works through this mechanism however.
Long term modulation of protein synthesis involves the activation of
myogenic stem cells or satellite cells. If you recall, when a muscle
is stretched it not only produces PGF2a, but also PGE2. PGE2 is a
potent inducer of satellite cell proliferation and fusion. This is how
existing muscle cells increase the number of nuclei they contain. This
is important because in order for a muscle to grow rapidly, it must
produce more mRNA. This is done in the nucleus of the muscle cell. The
more nuclei you have, the more mRNA you can produce. Within the cell,
prostaglandins may also be involved in regulating the number of
ribosomes. This could have long term implications on growth and
development as well as stretch induced hypertrophy.
----------------------------------------------------------------------------=
----
The role of other hormones, drugs and diet in the action of PGs.
Because prostaglandins are signaling molecules that get their message
across through multi step signal transduction pathways, they are
susceptible to modulation by several chemical, hormonal, and dietary
factors. I will do my best to shed some light on the subject without
bogging you down with meaningless terms and jargon. It is well to
remember that the action and interaction of prostaglandins in the
human body is complex.
Cortisol
Cortisol effects the production of prostaglandins in muscle tissue by
at least two mechanisms. First, cortisol by way of lipocortins,
inhibits the action of phospholipase A2. Phospholipase is necessary in
order to make arachidonic acid available for PGF2a production.
Cortisol also inhibits the production of cyclo-oxygenase mRNA content
within cells. As mentioned earlier, cyclo-oxygenase is the enzyme that
converts arachidonic acid into prostaglandins. So cortisol inhibits
muscle growth by preventing the production of PGF2a in response to
training (mechanica
And last but not least something about cholesterol - 3 eggs per day
for serious weight training is a must ...
Taka
Manipulating Dietary Cholesterol for Optimum Muscle Growth
by Dharkam
Vince Gironda, the Iron Guru, used to recommend eating up to three
dozen eggs a day in order to pack on mass fast. His rational was that
the high cholesterol content would trigger a natural anabolic effect.
Ronnie Coleman, in his last video, Relentless, is taking a cholesterol
lowering drug. Yet, such drugs are said to be detrimental to muscles.
Both behaviors seem contradictory!
Is high or low cholesterol better for muscle growth?
Why would anyone use a muscle wasting drug?
New research reconciles this paradox revealing that proper cholesterol
manipulations can optimize muscle growth.
Acute training impact on cholesterol level
If moderate weight training does not seem to affect cholesterol
levels, a traumatic workout will most definitely induce an acute
reduction of blood cholesterol level within 2 hours (1). This shortage
of cholesterol can last up to several days during the recovery phase.
This lowering effect is due to an accelerated uptake of cholesterol by
skeletal muscle. It reveals our fibers need this extra cholesterol in
order to recover and grow.
Considering the positive impact of cholesterol on muscle growth (see
below), it might be a good idea to include cholesterol-rich foods such
as whole eggs in you first real post-workout meal. This strategy would
make sure your muscles obtain all the cholesterol they need,
preventing any potential shortage which would postpone recovery.
Dietary cholesterol intake on muscle growth
Riechman has studied the impact of cholesterol on (resistance)
training-induced hypertrophy (2). This research has been conducted on
elderly men and women, yet its findings seem relevant to younger
subjects:
For 12 week, those people weight trained. When their daily cholesterol
intake was inferior to 3.5 mg per kg of lean mass, no hypertrophy was
detected. Strength only increased 36%. When their cholesterol
consumption was above 5.7 mg/kg, muscle mass increased an average of
2.1 kg. Heavy cholesterol consumers experienced a strength increase of
86%.
Muscle growth and strength gains are closely related to dietary
cholesterol intake. Considering a large egg contains around 200 mg of
cholesterol, a 220 lbs bodybuilder would need at least 3 whole eggs a
day.
Blood cholesterol level on muscle growth
Subjects with serum cholesterol lower than 178 mg/dl did not
experienced much growth (+300 g of lean mass). When serum cholesterol
was above 238 mg/dl, lean mass increased an average of 2.3 kg. The
correlation between serum cholesterol and strength gains is
statistically weaker. Subjects with low cholesterol level experienced
an increase of 37% Vs 70% for subjects with high levels.
Muscle growth is positively correlated with blood cholesterol level.
Cholesterol lowering drugs on muscle growth
Statins are a class of drugs prescribed to lower the level of
cholesterol in the blood. This class of drugs includes lovastatin
(Mevacor), simvastatin, (Zocor), fluvastatin (Lescol), pravastatin
(Pravachol), rosuvastatin (Crestor) and atorvastatin (Lipitor). The
mechanism by which statins lower cholesterol is by blocking the enzyme
in the liver, hydroxy-methylglutaryl-coenzyme A (HMCoA) reductase,
responsible for producing cholesterol. Statin drugs lower total serum
cholesterol levels, including HDL, as well as LDL levels.
Cholesterol intake and blood level represent two independent variables
affecting hypertrophy. Subjects who responded the best to weight
training were those consuming a cholesterol rich diet AND having a
high blood cholesterol level AND using anti-cholesterol statin drugs.
It is very surprising to discover that such drugs improved muscle
gains as they are associated with myalgia, muscle weakness and muscle
wasting in sedentary subjects.
Statin drugs accelerate muscle hypertrophy. The more we train, the
more resistant our fibers get. It is increasingly difficult to damage
them sufficiently to force them to grow. By rendering our fibers more
fragile, statin drugs allow each rep to be more damaging to our
muscles. As our muscles cannot seem to strengthen its fibers enough to
counteract this fragilizing effect, they have no choice but to keep on
growing.
Will cholesterol-related muscle catabolism favor growth?
I am not surprised that catabolic drugs facilitate muscle gains in
trained subjects. I have already explained this paradox in a
previously published clenbuterol article. Even cholesterol seems to
enhance catabolism. Following an acute eccentric workout, soreness as
well as strength loss are higher in young men consuming a whole egg
diet rather than a low cholesterol diet (1). In response to this
exacerbated catabolism, muscle strengthening is much more robust with
the whole egg than with the white egg diet (1). This greater anabolic
response explains the results observed on elderly. It also suggests
that conclusions reached in older subjects apply to young men as
well.
It may be important to note that if training-induced catabolism is
enhanced by cholesterol lowering drugs, they also protect muscle cells
from apoptosis (death) (3). This protective effect may facilitate an
additional growth response.
Anabolic steroids and cholesterol
Anabolic steroids can either increase or decrease cholesterol levels
depending on the choice of the drug as well as the individual response
of the user. For example, orally active 17-alkylated anabolic-
androgenic steroid are known to cause and undesirable reduction in HDL
cholesterol levels. A severe reduction (which can go as low as having
almost no cholesterol) is really bad for 2 reasons:
Cholesterol is needed for muscle growth (as well as for general
health). It is very hard to bring cholesterol production back up to
normal even with discontinuation of the steroids.
An increase in serum cholesterol levels would be a much better
scenario as more cholesterol would be available for growth. It would
also provide a good reason to get a prescription for the anti-
cholesterol drug class of statins.
In conclusion:
With regards to muscle hypertrophy, It is a good idea to follow a high
cholesterol diet (at least 3 whole eggs a day).
This is especially true if your training is both intense and
traumatic.
Be careful during a low calorie diet as cholesterol intake usually is
reduced during this period.
Cholesterol level tends to decline in summer, so be careful at that
time, too.
Whole eggs are very appropriate and recommended following a workout.
Steroid users should closely monitor their blood cholesterol level as
a decrease may reduce muscle growth.
Steroid users with high cholesterol levels should consult a physician
and may consider the use of statin drugs in order to grow even more
rapidly.
References
Riechman SE. Dietary Cholesterol Alters Recovery from Eccentric Muscle
Damage in Humans. Medicine & Science in Sports & Exercise: Volume
38(5) Supplement May 2006 p S386
Riechman SE. Dietary and blood cholesterol and statins increase
hypertrophy with resistance training. FASEB J. 2005 19 A1571
Urso ML. Changes in ubiquitin proteasome pathway gene expression in
skeletal muscle with exercise and statins. Arterioscler Thromb Vasc
Biol. 2005 Dec;25(12):2441-4.
for serious weight training is a must ...
Taka
Manipulating Dietary Cholesterol for Optimum Muscle Growth
by Dharkam
Vince Gironda, the Iron Guru, used to recommend eating up to three
dozen eggs a day in order to pack on mass fast. His rational was that
the high cholesterol content would trigger a natural anabolic effect.
Ronnie Coleman, in his last video, Relentless, is taking a cholesterol
lowering drug. Yet, such drugs are said to be detrimental to muscles.
Both behaviors seem contradictory!
Is high or low cholesterol better for muscle growth?
Why would anyone use a muscle wasting drug?
New research reconciles this paradox revealing that proper cholesterol
manipulations can optimize muscle growth.
Acute training impact on cholesterol level
If moderate weight training does not seem to affect cholesterol
levels, a traumatic workout will most definitely induce an acute
reduction of blood cholesterol level within 2 hours (1). This shortage
of cholesterol can last up to several days during the recovery phase.
This lowering effect is due to an accelerated uptake of cholesterol by
skeletal muscle. It reveals our fibers need this extra cholesterol in
order to recover and grow.
Considering the positive impact of cholesterol on muscle growth (see
below), it might be a good idea to include cholesterol-rich foods such
as whole eggs in you first real post-workout meal. This strategy would
make sure your muscles obtain all the cholesterol they need,
preventing any potential shortage which would postpone recovery.
Dietary cholesterol intake on muscle growth
Riechman has studied the impact of cholesterol on (resistance)
training-induced hypertrophy (2). This research has been conducted on
elderly men and women, yet its findings seem relevant to younger
subjects:
For 12 week, those people weight trained. When their daily cholesterol
intake was inferior to 3.5 mg per kg of lean mass, no hypertrophy was
detected. Strength only increased 36%. When their cholesterol
consumption was above 5.7 mg/kg, muscle mass increased an average of
2.1 kg. Heavy cholesterol consumers experienced a strength increase of
86%.
Muscle growth and strength gains are closely related to dietary
cholesterol intake. Considering a large egg contains around 200 mg of
cholesterol, a 220 lbs bodybuilder would need at least 3 whole eggs a
day.
Blood cholesterol level on muscle growth
Subjects with serum cholesterol lower than 178 mg/dl did not
experienced much growth (+300 g of lean mass). When serum cholesterol
was above 238 mg/dl, lean mass increased an average of 2.3 kg. The
correlation between serum cholesterol and strength gains is
statistically weaker. Subjects with low cholesterol level experienced
an increase of 37% Vs 70% for subjects with high levels.
Muscle growth is positively correlated with blood cholesterol level.
Cholesterol lowering drugs on muscle growth
Statins are a class of drugs prescribed to lower the level of
cholesterol in the blood. This class of drugs includes lovastatin
(Mevacor), simvastatin, (Zocor), fluvastatin (Lescol), pravastatin
(Pravachol), rosuvastatin (Crestor) and atorvastatin (Lipitor). The
mechanism by which statins lower cholesterol is by blocking the enzyme
in the liver, hydroxy-methylglutaryl-coenzyme A (HMCoA) reductase,
responsible for producing cholesterol. Statin drugs lower total serum
cholesterol levels, including HDL, as well as LDL levels.
Cholesterol intake and blood level represent two independent variables
affecting hypertrophy. Subjects who responded the best to weight
training were those consuming a cholesterol rich diet AND having a
high blood cholesterol level AND using anti-cholesterol statin drugs.
It is very surprising to discover that such drugs improved muscle
gains as they are associated with myalgia, muscle weakness and muscle
wasting in sedentary subjects.
Statin drugs accelerate muscle hypertrophy. The more we train, the
more resistant our fibers get. It is increasingly difficult to damage
them sufficiently to force them to grow. By rendering our fibers more
fragile, statin drugs allow each rep to be more damaging to our
muscles. As our muscles cannot seem to strengthen its fibers enough to
counteract this fragilizing effect, they have no choice but to keep on
growing.
Will cholesterol-related muscle catabolism favor growth?
I am not surprised that catabolic drugs facilitate muscle gains in
trained subjects. I have already explained this paradox in a
previously published clenbuterol article. Even cholesterol seems to
enhance catabolism. Following an acute eccentric workout, soreness as
well as strength loss are higher in young men consuming a whole egg
diet rather than a low cholesterol diet (1). In response to this
exacerbated catabolism, muscle strengthening is much more robust with
the whole egg than with the white egg diet (1). This greater anabolic
response explains the results observed on elderly. It also suggests
that conclusions reached in older subjects apply to young men as
well.
It may be important to note that if training-induced catabolism is
enhanced by cholesterol lowering drugs, they also protect muscle cells
from apoptosis (death) (3). This protective effect may facilitate an
additional growth response.
Anabolic steroids and cholesterol
Anabolic steroids can either increase or decrease cholesterol levels
depending on the choice of the drug as well as the individual response
of the user. For example, orally active 17-alkylated anabolic-
androgenic steroid are known to cause and undesirable reduction in HDL
cholesterol levels. A severe reduction (which can go as low as having
almost no cholesterol) is really bad for 2 reasons:
Cholesterol is needed for muscle growth (as well as for general
health). It is very hard to bring cholesterol production back up to
normal even with discontinuation of the steroids.
An increase in serum cholesterol levels would be a much better
scenario as more cholesterol would be available for growth. It would
also provide a good reason to get a prescription for the anti-
cholesterol drug class of statins.
In conclusion:
With regards to muscle hypertrophy, It is a good idea to follow a high
cholesterol diet (at least 3 whole eggs a day).
This is especially true if your training is both intense and
traumatic.
Be careful during a low calorie diet as cholesterol intake usually is
reduced during this period.
Cholesterol level tends to decline in summer, so be careful at that
time, too.
Whole eggs are very appropriate and recommended following a workout.
Steroid users should closely monitor their blood cholesterol level as
a decrease may reduce muscle growth.
Steroid users with high cholesterol levels should consult a physician
and may consider the use of statin drugs in order to grow even more
rapidly.
References
Riechman SE. Dietary Cholesterol Alters Recovery from Eccentric Muscle
Damage in Humans. Medicine & Science in Sports & Exercise: Volume
38(5) Supplement May 2006 p S386
Riechman SE. Dietary and blood cholesterol and statins increase
hypertrophy with resistance training. FASEB J. 2005 19 A1571
Urso ML. Changes in ubiquitin proteasome pathway gene expression in
skeletal muscle with exercise and statins. Arterioscler Thromb Vasc
Biol. 2005 Dec;25(12):2441-4.
One implication of this is that in physically active people who are
moving in the Earth gravity field or even put weights on their moving
bodies the arachidonic acid (AA) is constantly being "depleted" by
conversion into the "good" prostaglandins (another way of depletion
may be sex, because the PROSTAte gland also produces
PROSTAglandins ...). But once one gets sedentary, the AA has chance
to accumulate to higher amounts in tissues. If the tissues are
overloaded with AA it gets released spontaneously or in a response to
minor stressors and in the absence of the prostaglandin-making
machinery it gets converted by oxidation to the dangerous leukotrienes
such as LTB4 which stimulate destructive inflammation/allergic
responses. Ever noticed you catch cold easier when inactive?
Fortunately, one can reduce AA not only by exercise but also by
appropriate diet :-) BTW I am wondering which fats they are putting
into the astronaut's food ?
Taka
> NASA Discovers the Anabolic Properties of Prostaglandins
>
> In the January 1999 issue of the American Journal of Physiology, a new
> study performed on astronauts during spaceflight demonstrates the key
> role played by prostaglandins in maintaining the strength of muscles.
> A major problem during spaceflight is the rapid loss of lean muscle
> mass in both animals and humans. This prevents the space agencies from
> sending men into space for extended periods without threatening their
> health. It is, of course, the lack of resistance and weight due to the
> weightlessness that is the cause of muscle atrophy. The million dollar
> question is: how does this lack of resistance alter the intracellular
> environment so that muscle wasting is free to take place?
>
> Why are these experiments relevant to bodybuilders? Simply because the
> pathways triggering the muscle wasting in space flight are the same
> that make our muscle grow when we train. They just work in opposite
> directions in each case.
>
>
> --------------------------------------------------------------------------------
>
> Hormone fluctuations during spaceflight
> Hormones are obvious candidates as possible mediators of this wasting
> process. The favored hypothesis is that spaceflight induces some major
> alterations in our hormone levels. Two main pathways could be
> involved. First, the levels of catabolic hormones could rise and so be
> the cause of this wasting. Second, the level of the anabolic hormones
> could drop so that the constant basal renewal of muscle protein could
> not take place at a sufficient rate, resulting in a net negative
> balance.
>
> The study by Dr. Peter Stein [1] of the University of Medicine and
> Dentistry of New Jersey consisted of measuring the key hormones in
> astronauts during a space shuttle mission. Cortisol, a known wasting
> hormone, was one of the favorite candidates. Unfortunately, a
> consistent pattern of fluctuations in cortisol level was not apparent.
> Cortisol increased in some but not all subjects. As all of them
> experienced significant muscle loss, cortisol excess does not explain
> the consistent wasting. Another paradox is that, once back on the
> ground, the astronauts regained lean body mass while cortisol level
> was at its peak.
>
> This means that you can waste away while having a normal cortisol
> level, and you can put on lean mass despite a high cortisol level. It
> should be a major eye-opener for bodybuilders.
>
> Next on the list of candidates were the catecholamines (epinephrine
> and norepinephrine). Depending on whom you listen to, catecholamines
> are either anti-catabolic or catabolic. Whatever their effect, every
> scientist would agree that it is at best mild. The expected drops and
> rebounds of catecholamines were detected during the flight and the
> post flight periods, respectively. To explain the lean mass
> fluctuations, it would mean that catecholamines are very potent
> anabolic or anti-catabolic substances -- information that no research
> has ever demonstrated even at high doses in humans. So they are not
> the mediator the scientists were looking for.
>
> The next substances to be measured were the anabolic hormones and
> growth factors such as GH, IGF-1 or insulin. Stein did not find any
> significant alteration of their levels taking place during the phase
> of wasting or regrowth. He did notice that T3 (an active thyroid
> hormone) level dropped during the flight, to rebound after landing. T3
> fluctuations concur with the mass loss and regain, so Stein suggests
> that T3 could be one of the mediators of the lean mass fluctuation. As
> T3 drops during the flight, so would the rate of muscle protein
> synthesis. After landing, the increased T3 would boost anabolism and
> therefore muscle growth.
>
> I disagree with Stein on this point. I consider the space-induced drop
> in T3 as a protective mechanism against excessive muscle wasting
> rather than a mediator of the growth inhibition. T3 is both an
> anabolic and catabolic hormone. A minimal amount of T3 is required for
> muscle to grow at an optimal rate, but as the T3 level increases, its
> catabolic actions start to predominate and overwhelm its anabolic
> properties.
>
> This is why you'll never meet a bodybuilder claiming to have gained
> muscles by taking only T3. In fact, bodybuilders using T3 start to
> lose both lean and adipose mass. Studies performed in bed-rested
> people which attempt to duplicate weightlessness showed that in this
> situation, exogenous T3 promoted protein degradation and not
> anabolism. Therefore, T3 is unlikely to be the mass modulator we are
> looking for.
>
> Stein's genuine breakthrough came from the fact that he measured the
> levels of prostaglandins in both the blood and urine and compared them
> with the degree of muscle wasting.
>
> Both measures were used for better accuracy as the levels of
> prostaglandins are very hard to evaluate, prostaglandins being mainly
> a local and not systemic growth modulator. Skeletal muscles and bones
> are both net producers of prostaglandins with muscles being the major
> site of manufacture. Those locally produced prostaglandins will
> eventually pass into the blood before being quickly destroyed. So the
> blood level of prostaglandins roughly reflects the rate of production
> of prostaglandins inside the muscles. With urine prostaglandins,
> results tend to be harder to interpret as prostaglandins produced in
> the kidney tend to bias the figures. Nevertheless, Dr. Stein found out
> that both measures agreed anyway.
>
> To the surprise of the scientific community (but not to bodybuilders),
> the levels of the prostaglandins measured dropped during the flight --
> especially the PGE2.
>
> After landing, there was a significant rebound of the prostaglandin
> levels, especially of the PGF2. Those fluctuations closely reflected
> the observed changes in lean muscle mass.
>
> The major cause of this drop is the lack of resistance placed on both
> the muscles and bones. As we flex our muscles, a local formation and
> release of prostaglandins is taking place. The harder we flex, the
> more the local level of prostaglandins is elevated. Weightlessness
> prevents the astronauts from flexing their muscles against a
> resistance. Therefore, a significant drop in muscle prostaglandins can
> be expected. As less prostaglandins are produced in our muscles, the
> drop will quickly be reflected by the blood measurements.
>
> This may explain the well known development of insulin resistance
> occuring during space flight as prostaglandins mediate many of the
> actions of insulin on muscles. This resistance also contributes to the
> muscle protein loss and again we find prostaglandins as key mediators
> of this phenomenon.
>
> Stein's interpretations of these new findings are somewhat less
> convincing. Scientists are expected to accurately measure the results
> they obtained during an experiment, but also they are also expected to
> interpret their results. Sometimes, their discussion is well
> researched and documented which provides a worthwhile reading.
> Unfortunately, many times it is not so well researched and the
> discussion is a big step backward. This is the case in the above
> mentioned study. The basic ideas are bright and the results original
> but the comments made by the team of scientists is at the very least
> poor. Paradoxally, they reached a good conclusion with a biased
> reasoning.
>
> The discussion part of this study is based on a very selective reading
> of the scientific literature while the bottom line conclusion is very
> good. It concludes that "the inflight data support a major role for
> decreased prostaglandin production in the protein loss by muscles."
> This is very refreshing as the average scientist considers
> prostaglandins as mediators of wasting and certainly not of muscle
> growth. Stein's conclusion fits very well with his findings. The fall
> in muscle prostaglandins induced by the lack of resistance during the
> spaceflight results in a sharp fall in protein synthesis.
>
> For a quick recap:
>
> Our muscles are subjected to a constant protein turnover. This means
> that the old proteins composing the contractile tissue of each cell
> are constantly destroyed (catabolism) and replaced by new proteins
> (anabolism).
> If you are a sedentary person between 20 to 40 year old, this constant
> basal turnover is neutral. The rate of catabolism is roughly equal to
> the rate of anabolism.
> Young growing adolescents acquire their muscle mass as anabolic rate
> exceeds catabolism.
> Elderly people slowly waste away as anabolism is slower than
> degradation.
> During spaceflight, anabolism is reduced, causing the rebuilding
> mechanisms to be overwhelmed by the catabolic pathways. A loss of lean
> mass ensues.
> The big issue is to understand which hormones or factors are involved
> in the drop of anabolism.
>
> Stein based his reasoning on the common belief concerning
> prostaglandins, i.e., that PGF2 is anabolic and PGE2 is catabolic.
> From there, he tries to explain how PGE2, a catabolic factor according
> to him, could make our muscle grow. Good luck! Also, if PGE2 is a key
> mediator of muscle wasting as many believe, how to explain its drop
> while catabolism is intense? This belief concerning the so-called
> wasting effect of PGE2 is due to some old, badly conducted, and flawed
> studies which other laboratories have been unable to reproduce. Other
> newer and more comprehensive studies have shown that PGE2 has an
> overall positive influence on the protein turnover [2]. In other
> words, PGE2 is an anabolic mediator rather than a catabolic one.
>
> This fits better into the NASA findings. During the flight, muscle
> prostaglandins fall, which depresses anabolism. After the flight,
> muscle prostaglandin production bounces back as astronaut muscles are
> once against submitted to the resistance of gravity. The extra
> prostaglandins strongly stimulate anabolism which explains the fast
> muscle rebuilding.
>
>
> --------------------------------------------------------------------------------
>
> Let's speculate a little!
> With this major role of prostaglandins in mind, let's try to go a bit
> further. Scientists specializing in Aeronautics have spent years
> trying to combat space-induced wasting. In fact, the main research on
> bodybuilding hormones has mostly been conducted by those scientists.
> They have tried to administer hormones such as GH or IGF-1 during
> spaceflights in order to combat the muscle loss. They have had little
> success -- hardly surprising in light of recent findings. As the
> levels of these peptide hormones hardly fluctuate, administering some
> more does not appear to be the optimal solution. Usage of anabolic
> steroids during weightlessness has achieved some but not exceptional
> results. The next step is now to administer prostaglandins during a
> flight and see what will happen.
>
> The lack of effects of the tested anabolic hormones on muscles
> suggests that their receptors failed to function normally. In other
> words, the lack of muscle contractions rapidly produce a receptor
> insensitivity. What if it was the level of muscle prostaglandins that
> was one of the major controllers of the sensitivity of the main
> anabolic hormones? I've mentioned that the potency of steroids was
> enhanced by exogenous PGF2. By the same token, PGF2 sensitivity is
> enhanced by androgens.
>
> So:
>
> Prostaglandins control androgen and IGF-1 receptor activities.
> Androgens control prostaglandin receptor expression.
> IGF-1 and anabolics are major controllers of the level of muscle
> prostaglandins.
> This looks like a righteous anabolic cycle. Therefore, the major issue
> for the scientists of the third millennium is to figure out how, at
> which part of the cycle and where to enter this anabolic cycle for
> maximal effectiveness of our muscle building tools.
>
>
> --------------------------------------------------------------------------------
>
> References:
> Stein TP. 1999 Jan. Endocrine relationships during human spaceflight.
> Am J Physiol. 276:E155-62.
> Fagan JM, Goldberg AL. 1986 Apr. Inhibitors of protein and RNA
> synthesis cause a rapid block in prostaglandin production at the
> prostaglandin synthase step. Proc Natl Acad Sci U S A. 83(8):2771-5.
>
> SOURCE:
> http://www.mesomorphosis.com/articles/dharkam/anabolic-properties-of-prostaglandins.htm
>
> AND SOME RELATED READING (just to see how prostaglandins are also mis/
> used):
> http://www.mesomorphosis.com/articles/dharkam/prostaglandins.htm
> http://www.mesomorphosis.com/articles/dharkam/how-dharkam-uses-pgf2.htm
moving in the Earth gravity field or even put weights on their moving
bodies the arachidonic acid (AA) is constantly being "depleted" by
conversion into the "good" prostaglandins (another way of depletion
may be sex, because the PROSTAte gland also produces
PROSTAglandins ...). But once one gets sedentary, the AA has chance
to accumulate to higher amounts in tissues. If the tissues are
overloaded with AA it gets released spontaneously or in a response to
minor stressors and in the absence of the prostaglandin-making
machinery it gets converted by oxidation to the dangerous leukotrienes
such as LTB4 which stimulate destructive inflammation/allergic
responses. Ever noticed you catch cold easier when inactive?
Fortunately, one can reduce AA not only by exercise but also by
appropriate diet :-) BTW I am wondering which fats they are putting
into the astronaut's food ?
Taka
> NASA Discovers the Anabolic Properties of Prostaglandins
>
> In the January 1999 issue of the American Journal of Physiology, a new
> study performed on astronauts during spaceflight demonstrates the key
> role played by prostaglandins in maintaining the strength of muscles.
> A major problem during spaceflight is the rapid loss of lean muscle
> mass in both animals and humans. This prevents the space agencies from
> sending men into space for extended periods without threatening their
> health. It is, of course, the lack of resistance and weight due to the
> weightlessness that is the cause of muscle atrophy. The million dollar
> question is: how does this lack of resistance alter the intracellular
> environment so that muscle wasting is free to take place?
>
> Why are these experiments relevant to bodybuilders? Simply because the
> pathways triggering the muscle wasting in space flight are the same
> that make our muscle grow when we train. They just work in opposite
> directions in each case.
>
>
> --------------------------------------------------------------------------------
>
> Hormone fluctuations during spaceflight
> Hormones are obvious candidates as possible mediators of this wasting
> process. The favored hypothesis is that spaceflight induces some major
> alterations in our hormone levels. Two main pathways could be
> involved. First, the levels of catabolic hormones could rise and so be
> the cause of this wasting. Second, the level of the anabolic hormones
> could drop so that the constant basal renewal of muscle protein could
> not take place at a sufficient rate, resulting in a net negative
> balance.
>
> The study by Dr. Peter Stein [1] of the University of Medicine and
> Dentistry of New Jersey consisted of measuring the key hormones in
> astronauts during a space shuttle mission. Cortisol, a known wasting
> hormone, was one of the favorite candidates. Unfortunately, a
> consistent pattern of fluctuations in cortisol level was not apparent.
> Cortisol increased in some but not all subjects. As all of them
> experienced significant muscle loss, cortisol excess does not explain
> the consistent wasting. Another paradox is that, once back on the
> ground, the astronauts regained lean body mass while cortisol level
> was at its peak.
>
> This means that you can waste away while having a normal cortisol
> level, and you can put on lean mass despite a high cortisol level. It
> should be a major eye-opener for bodybuilders.
>
> Next on the list of candidates were the catecholamines (epinephrine
> and norepinephrine). Depending on whom you listen to, catecholamines
> are either anti-catabolic or catabolic. Whatever their effect, every
> scientist would agree that it is at best mild. The expected drops and
> rebounds of catecholamines were detected during the flight and the
> post flight periods, respectively. To explain the lean mass
> fluctuations, it would mean that catecholamines are very potent
> anabolic or anti-catabolic substances -- information that no research
> has ever demonstrated even at high doses in humans. So they are not
> the mediator the scientists were looking for.
>
> The next substances to be measured were the anabolic hormones and
> growth factors such as GH, IGF-1 or insulin. Stein did not find any
> significant alteration of their levels taking place during the phase
> of wasting or regrowth. He did notice that T3 (an active thyroid
> hormone) level dropped during the flight, to rebound after landing. T3
> fluctuations concur with the mass loss and regain, so Stein suggests
> that T3 could be one of the mediators of the lean mass fluctuation. As
> T3 drops during the flight, so would the rate of muscle protein
> synthesis. After landing, the increased T3 would boost anabolism and
> therefore muscle growth.
>
> I disagree with Stein on this point. I consider the space-induced drop
> in T3 as a protective mechanism against excessive muscle wasting
> rather than a mediator of the growth inhibition. T3 is both an
> anabolic and catabolic hormone. A minimal amount of T3 is required for
> muscle to grow at an optimal rate, but as the T3 level increases, its
> catabolic actions start to predominate and overwhelm its anabolic
> properties.
>
> This is why you'll never meet a bodybuilder claiming to have gained
> muscles by taking only T3. In fact, bodybuilders using T3 start to
> lose both lean and adipose mass. Studies performed in bed-rested
> people which attempt to duplicate weightlessness showed that in this
> situation, exogenous T3 promoted protein degradation and not
> anabolism. Therefore, T3 is unlikely to be the mass modulator we are
> looking for.
>
> Stein's genuine breakthrough came from the fact that he measured the
> levels of prostaglandins in both the blood and urine and compared them
> with the degree of muscle wasting.
>
> Both measures were used for better accuracy as the levels of
> prostaglandins are very hard to evaluate, prostaglandins being mainly
> a local and not systemic growth modulator. Skeletal muscles and bones
> are both net producers of prostaglandins with muscles being the major
> site of manufacture. Those locally produced prostaglandins will
> eventually pass into the blood before being quickly destroyed. So the
> blood level of prostaglandins roughly reflects the rate of production
> of prostaglandins inside the muscles. With urine prostaglandins,
> results tend to be harder to interpret as prostaglandins produced in
> the kidney tend to bias the figures. Nevertheless, Dr. Stein found out
> that both measures agreed anyway.
>
> To the surprise of the scientific community (but not to bodybuilders),
> the levels of the prostaglandins measured dropped during the flight --
> especially the PGE2.
>
> After landing, there was a significant rebound of the prostaglandin
> levels, especially of the PGF2. Those fluctuations closely reflected
> the observed changes in lean muscle mass.
>
> The major cause of this drop is the lack of resistance placed on both
> the muscles and bones. As we flex our muscles, a local formation and
> release of prostaglandins is taking place. The harder we flex, the
> more the local level of prostaglandins is elevated. Weightlessness
> prevents the astronauts from flexing their muscles against a
> resistance. Therefore, a significant drop in muscle prostaglandins can
> be expected. As less prostaglandins are produced in our muscles, the
> drop will quickly be reflected by the blood measurements.
>
> This may explain the well known development of insulin resistance
> occuring during space flight as prostaglandins mediate many of the
> actions of insulin on muscles. This resistance also contributes to the
> muscle protein loss and again we find prostaglandins as key mediators
> of this phenomenon.
>
> Stein's interpretations of these new findings are somewhat less
> convincing. Scientists are expected to accurately measure the results
> they obtained during an experiment, but also they are also expected to
> interpret their results. Sometimes, their discussion is well
> researched and documented which provides a worthwhile reading.
> Unfortunately, many times it is not so well researched and the
> discussion is a big step backward. This is the case in the above
> mentioned study. The basic ideas are bright and the results original
> but the comments made by the team of scientists is at the very least
> poor. Paradoxally, they reached a good conclusion with a biased
> reasoning.
>
> The discussion part of this study is based on a very selective reading
> of the scientific literature while the bottom line conclusion is very
> good. It concludes that "the inflight data support a major role for
> decreased prostaglandin production in the protein loss by muscles."
> This is very refreshing as the average scientist considers
> prostaglandins as mediators of wasting and certainly not of muscle
> growth. Stein's conclusion fits very well with his findings. The fall
> in muscle prostaglandins induced by the lack of resistance during the
> spaceflight results in a sharp fall in protein synthesis.
>
> For a quick recap:
>
> Our muscles are subjected to a constant protein turnover. This means
> that the old proteins composing the contractile tissue of each cell
> are constantly destroyed (catabolism) and replaced by new proteins
> (anabolism).
> If you are a sedentary person between 20 to 40 year old, this constant
> basal turnover is neutral. The rate of catabolism is roughly equal to
> the rate of anabolism.
> Young growing adolescents acquire their muscle mass as anabolic rate
> exceeds catabolism.
> Elderly people slowly waste away as anabolism is slower than
> degradation.
> During spaceflight, anabolism is reduced, causing the rebuilding
> mechanisms to be overwhelmed by the catabolic pathways. A loss of lean
> mass ensues.
> The big issue is to understand which hormones or factors are involved
> in the drop of anabolism.
>
> Stein based his reasoning on the common belief concerning
> prostaglandins, i.e., that PGF2 is anabolic and PGE2 is catabolic.
> From there, he tries to explain how PGE2, a catabolic factor according
> to him, could make our muscle grow. Good luck! Also, if PGE2 is a key
> mediator of muscle wasting as many believe, how to explain its drop
> while catabolism is intense? This belief concerning the so-called
> wasting effect of PGE2 is due to some old, badly conducted, and flawed
> studies which other laboratories have been unable to reproduce. Other
> newer and more comprehensive studies have shown that PGE2 has an
> overall positive influence on the protein turnover [2]. In other
> words, PGE2 is an anabolic mediator rather than a catabolic one.
>
> This fits better into the NASA findings. During the flight, muscle
> prostaglandins fall, which depresses anabolism. After the flight,
> muscle prostaglandin production bounces back as astronaut muscles are
> once against submitted to the resistance of gravity. The extra
> prostaglandins strongly stimulate anabolism which explains the fast
> muscle rebuilding.
>
>
> --------------------------------------------------------------------------------
>
> Let's speculate a little!
> With this major role of prostaglandins in mind, let's try to go a bit
> further. Scientists specializing in Aeronautics have spent years
> trying to combat space-induced wasting. In fact, the main research on
> bodybuilding hormones has mostly been conducted by those scientists.
> They have tried to administer hormones such as GH or IGF-1 during
> spaceflights in order to combat the muscle loss. They have had little
> success -- hardly surprising in light of recent findings. As the
> levels of these peptide hormones hardly fluctuate, administering some
> more does not appear to be the optimal solution. Usage of anabolic
> steroids during weightlessness has achieved some but not exceptional
> results. The next step is now to administer prostaglandins during a
> flight and see what will happen.
>
> The lack of effects of the tested anabolic hormones on muscles
> suggests that their receptors failed to function normally. In other
> words, the lack of muscle contractions rapidly produce a receptor
> insensitivity. What if it was the level of muscle prostaglandins that
> was one of the major controllers of the sensitivity of the main
> anabolic hormones? I've mentioned that the potency of steroids was
> enhanced by exogenous PGF2. By the same token, PGF2 sensitivity is
> enhanced by androgens.
>
> So:
>
> Prostaglandins control androgen and IGF-1 receptor activities.
> Androgens control prostaglandin receptor expression.
> IGF-1 and anabolics are major controllers of the level of muscle
> prostaglandins.
> This looks like a righteous anabolic cycle. Therefore, the major issue
> for the scientists of the third millennium is to figure out how, at
> which part of the cycle and where to enter this anabolic cycle for
> maximal effectiveness of our muscle building tools.
>
>
> --------------------------------------------------------------------------------
>
> References:
> Stein TP. 1999 Jan. Endocrine relationships during human spaceflight.
> Am J Physiol. 276:E155-62.
> Fagan JM, Goldberg AL. 1986 Apr. Inhibitors of protein and RNA
> synthesis cause a rapid block in prostaglandin production at the
> prostaglandin synthase step. Proc Natl Acad Sci U S A. 83(8):2771-5.
>
> SOURCE:
> http://www.mesomorphosis.com/articles/dharkam/anabolic-properties-of-prostaglandins.htm
>
> AND SOME RELATED READING (just to see how prostaglandins are also mis/
> used):
> http://www.mesomorphosis.com/articles/dharkam/prostaglandins.htm
> http://www.mesomorphosis.com/articles/dharkam/how-dharkam-uses-pgf2.htm
On May 14, 10:30 am, Taka <taka0...@gmail.com> wrote:
> One implication of this is that in physically active people who are
> moving in the Earth gravity field or even put weights on their moving
> bodies the arachidonic acid (AA) is constantly being "depleted" by
> conversion into the "good" prostaglandins (another way of depletion
> may be sex, because the PROSTAte gland also produces
> PROSTAglandins ...). But once one gets sedentary, the AA has chance
> to accumulate to higher amounts in tissues. If the tissues are
> overloaded with AA it gets released spontaneously or in a response to
> minor stressors and in the absence of the prostaglandin-making
> machinery it gets converted by oxidation to the dangerous leukotrienes
> such as LTB4 which stimulate destructive inflammation/allergic
> responses. Ever noticed you catch cold easier when inactive?
> Fortunately, one can reduce AA not only by exercise but also by
> appropriate diet :-) BTW I am wondering which fats they are putting
> into the astronaut's food ?Taka
>
> > NASA Discovers the Anabolic Properties of Prostaglandins
Just for record here are the references:
Am J Physiol. 1999 Jan;276(1 Pt 1):E155-62.
Endocrine relationships during human spaceflight.
Stein TP, Schluter MD, Moldawer LL.
Collaborators (1)
Department of Surgery, University of Medicine and Dentistry of New
Jersey, School of Osteopathic Medicine, Stratford, New Jersey 08084,
USA.
Human spaceflight is associated with a chronic loss of protein from
muscle. The objective of this study was to determine whether changes
in urinary hormone excretion could identify a hormonal role for this
loss. Urine samples were collected from the crews of two Life Sciences
Space Shuttle missions before and during spaceflight. Data are means
+/- SE with the number of subjects in parentheses. The first value is
the mean preflight measurement, and the second value is the mean
inflight measurement. Adrenocorticotropic hormone (ACTH) [27.7 +/- 4.4
(9) vs. 25.1 +/- 3.4 (9) ng/day], growth hormone [724 +/- 251 (9) vs.
710 +/- 206 (9) ng/day], insulin-like growth factor I [6.81 +/- 0.62
vs. 6.04 +/- 0.51 (8) nM/day], and C-peptide [44.9 +/- 8.3 (9) vs.
50.7 +/- 10.3 (9) micrograms/day] were unchanged with spaceflight. In
contrast, free 3,5,3'-triiodothyronine [791 +/- 159 (9) vs. 371 +/- 41
(9) pg/day, P < 0.05], prostaglandin E2 (PGE2) [1, 064 +/- 391 (8) vs.
465 +/- 146 (8) ng/day, P < 0.05], and its metabolite PGE-M [1,015 +/-
98 (9) vs. 678 +/- 105 (9) ng/day, P < 0. 05] were decreased inflight.
The urinary excretion of most hormones returned to their preflight
levels during the postflight period, with the exception of ACTH [47.5
+/- 10.3 (9) ng/day], PGE2 [1,433 +/- 327 (8) ng/day], PGF2alpha,
[2,786 +/- 313 (8) ng/day], and its metabolite PGF-M [4,814 +/- 402
(9) ng/day], which were all increased compared with the preflight
measurement (P < 0.05). There was a trend for urinary cortisol to be
elevated inflight [55.3 +/- 5. 9 (9) vs. 72.5 +/- 11.1 micrograms/day,
P = 0.27] and postflight [82.7 +/- 8.6 (8) micrograms/day, P = 0.13].
The inflight human data support ground-based in vitro work showing
that prostaglandins have a major role in modulating the changes in
muscle protein content in response to tension or the lack thereof.
PMID: 9886962
Proc Natl Acad Sci U S A. 1986 Apr;83(8):2771-5.
Inhibitors of protein and RNA synthesis cause a rapid block in
prostaglandin production at the prostaglandin synthase step.
Fagan JM, Goldberg AL.
Inhibitors of protein or RNA synthesis prevented prostaglandin (PG)
production in isolated skeletal muscles, brain, and spleen. Incubation
of rat muscles with cycloheximide prevented the stimulation of PGE2
production induced in vitro by the Ca2+ ionophore A23187 and in vivo
by injection of endotoxin. Cycloheximide also inhibited the
stimulation by arachidonic acid of PGE2, PGF2 alpha, and prostacyclin.
These observations suggest that the block in prostanoid production
results from a loss of PG synthase activity (EC 1.14.99.1). These
effects were detectable within 10 min after exposure of the muscle to
cycloheximide. The degree of inhibition of PG production correlated
with the degree of inhibition of protein synthesis. Other inhibitors
of protein synthesis, puromycin and emetine, also prevented conversion
of arachidonate into PGE2 in these tissues, but they did not inhibit
purified PG synthase. Exposure of muscles to actinomycin D for 20 min
also reduced PGE2 production from arachidonate by 90%. Thus, both the
PG synthase and its mRNA appear to be inactivated rapidly (t1/2 less
than 10 min) in muscle and other mammalian tissues. The block in PG
production induced by inhibitors of protein and RNA synthesis may
account for their antipyrogenic actions and certain of their other
physiological effects.
PMID: 3085105
> One implication of this is that in physically active people who are
> moving in the Earth gravity field or even put weights on their moving
> bodies the arachidonic acid (AA) is constantly being "depleted" by
> conversion into the "good" prostaglandins (another way of depletion
> may be sex, because the PROSTAte gland also produces
> PROSTAglandins ...). But once one gets sedentary, the AA has chance
> to accumulate to higher amounts in tissues. If the tissues are
> overloaded with AA it gets released spontaneously or in a response to
> minor stressors and in the absence of the prostaglandin-making
> machinery it gets converted by oxidation to the dangerous leukotrienes
> such as LTB4 which stimulate destructive inflammation/allergic
> responses. Ever noticed you catch cold easier when inactive?
> Fortunately, one can reduce AA not only by exercise but also by
> appropriate diet :-) BTW I am wondering which fats they are putting
> into the astronaut's food ?Taka
>
> > NASA Discovers the Anabolic Properties of Prostaglandins
Just for record here are the references:
Am J Physiol. 1999 Jan;276(1 Pt 1):E155-62.
Endocrine relationships during human spaceflight.
Stein TP, Schluter MD, Moldawer LL.
Collaborators (1)
Department of Surgery, University of Medicine and Dentistry of New
Jersey, School of Osteopathic Medicine, Stratford, New Jersey 08084,
USA.
Human spaceflight is associated with a chronic loss of protein from
muscle. The objective of this study was to determine whether changes
in urinary hormone excretion could identify a hormonal role for this
loss. Urine samples were collected from the crews of two Life Sciences
Space Shuttle missions before and during spaceflight. Data are means
+/- SE with the number of subjects in parentheses. The first value is
the mean preflight measurement, and the second value is the mean
inflight measurement. Adrenocorticotropic hormone (ACTH) [27.7 +/- 4.4
(9) vs. 25.1 +/- 3.4 (9) ng/day], growth hormone [724 +/- 251 (9) vs.
710 +/- 206 (9) ng/day], insulin-like growth factor I [6.81 +/- 0.62
vs. 6.04 +/- 0.51 (8) nM/day], and C-peptide [44.9 +/- 8.3 (9) vs.
50.7 +/- 10.3 (9) micrograms/day] were unchanged with spaceflight. In
contrast, free 3,5,3'-triiodothyronine [791 +/- 159 (9) vs. 371 +/- 41
(9) pg/day, P < 0.05], prostaglandin E2 (PGE2) [1, 064 +/- 391 (8) vs.
465 +/- 146 (8) ng/day, P < 0.05], and its metabolite PGE-M [1,015 +/-
98 (9) vs. 678 +/- 105 (9) ng/day, P < 0. 05] were decreased inflight.
The urinary excretion of most hormones returned to their preflight
levels during the postflight period, with the exception of ACTH [47.5
+/- 10.3 (9) ng/day], PGE2 [1,433 +/- 327 (8) ng/day], PGF2alpha,
[2,786 +/- 313 (8) ng/day], and its metabolite PGF-M [4,814 +/- 402
(9) ng/day], which were all increased compared with the preflight
measurement (P < 0.05). There was a trend for urinary cortisol to be
elevated inflight [55.3 +/- 5. 9 (9) vs. 72.5 +/- 11.1 micrograms/day,
P = 0.27] and postflight [82.7 +/- 8.6 (8) micrograms/day, P = 0.13].
The inflight human data support ground-based in vitro work showing
that prostaglandins have a major role in modulating the changes in
muscle protein content in response to tension or the lack thereof.
PMID: 9886962
Proc Natl Acad Sci U S A. 1986 Apr;83(8):2771-5.
Inhibitors of protein and RNA synthesis cause a rapid block in
prostaglandin production at the prostaglandin synthase step.
Fagan JM, Goldberg AL.
Inhibitors of protein or RNA synthesis prevented prostaglandin (PG)
production in isolated skeletal muscles, brain, and spleen. Incubation
of rat muscles with cycloheximide prevented the stimulation of PGE2
production induced in vitro by the Ca2+ ionophore A23187 and in vivo
by injection of endotoxin. Cycloheximide also inhibited the
stimulation by arachidonic acid of PGE2, PGF2 alpha, and prostacyclin.
These observations suggest that the block in prostanoid production
results from a loss of PG synthase activity (EC 1.14.99.1). These
effects were detectable within 10 min after exposure of the muscle to
cycloheximide. The degree of inhibition of PG production correlated
with the degree of inhibition of protein synthesis. Other inhibitors
of protein synthesis, puromycin and emetine, also prevented conversion
of arachidonate into PGE2 in these tissues, but they did not inhibit
purified PG synthase. Exposure of muscles to actinomycin D for 20 min
also reduced PGE2 production from arachidonate by 90%. Thus, both the
PG synthase and its mRNA appear to be inactivated rapidly (t1/2 less
than 10 min) in muscle and other mammalian tissues. The block in PG
production induced by inhibitors of protein and RNA synthesis may
account for their antipyrogenic actions and certain of their other
physiological effects.
PMID: 3085105
Taka wrote:
> One implication of this is that in physically active people who are
> moving in the Earth gravity field or even put weights on their moving
> bodies the arachidonic acid (AA) is constantly being "depleted" by
> conversion into the "good" prostaglandins (another way of depletion
> may be sex, because the PROSTAte gland also produces
> PROSTAglandins ...).
Aren't you jumping to conclusions here? Are you aware of any studies
showing connections between sexual activities and prostaglandins? It
occurs to me that male orgasm, by lowering libido, might have the
opposite effect.
> But once one gets sedentary, the AA has chance
> to accumulate to higher amounts in tissues. If the tissues are
> overloaded with AA it gets released spontaneously or in a response to
> minor stressors and in the absence of the prostaglandin-making
> machinery it gets converted by oxidation to the dangerous leukotrienes
> such as LTB4 which stimulate destructive inflammation/allergic
> responses. Ever noticed you catch cold easier when inactive?
> Fortunately, one can reduce AA not only by exercise but also by
> appropriate diet :-) BTW I am wondering which fats they are putting
> into the astronaut's food ?
> Taka
>
>> NASA Discovers the Anabolic Properties of Prostaglandins
>>
>> In the January 1999 issue of the American Journal of Physiology, a new
>> study performed on astronauts during spaceflight demonstrates the key
>> role played by prostaglandins in maintaining the strength of muscles.
>> A major problem during spaceflight is the rapid loss of lean muscle
>> mass in both animals and humans. This prevents the space agencies from
>> sending men into space for extended periods without threatening their
>> health. It is, of course, the lack of resistance and weight due to the
>> weightlessness that is the cause of muscle atrophy. The million dollar
>> question is: how does this lack of resistance alter the intracellular
>> environment so that muscle wasting is free to take place?
>>
>> Why are these experiments relevant to bodybuilders? Simply because the
>> pathways triggering the muscle wasting in space flight are the same
>> that make our muscle grow when we train. They just work in opposite
>> directions in each case.
>>
>>
>> --------------------------------------------------------------------------------
>>
>> Hormone fluctuations during spaceflight
>> Hormones are obvious candidates as possible mediators of this wasting
>> process. The favored hypothesis is that spaceflight induces some major
>> alterations in our hormone levels. Two main pathways could be
>> involved. First, the levels of catabolic hormones could rise and so be
>> the cause of this wasting. Second, the level of the anabolic hormones
>> could drop so that the constant basal renewal of muscle protein could
>> not take place at a sufficient rate, resulting in a net negative
>> balance.
>>
>> The study by Dr. Peter Stein [1] of the University of Medicine and
>> Dentistry of New Jersey consisted of measuring the key hormones in
>> astronauts during a space shuttle mission. Cortisol, a known wasting
>> hormone, was one of the favorite candidates. Unfortunately, a
>> consistent pattern of fluctuations in cortisol level was not apparent.
>> Cortisol increased in some but not all subjects. As all of them
>> experienced significant muscle loss, cortisol excess does not explain
>> the consistent wasting. Another paradox is that, once back on the
>> ground, the astronauts regained lean body mass while cortisol level
>> was at its peak.
>>
>> This means that you can waste away while having a normal cortisol
>> level, and you can put on lean mass despite a high cortisol level. It
>> should be a major eye-opener for bodybuilders.
>>
>> Next on the list of candidates were the catecholamines (epinephrine
>> and norepinephrine). Depending on whom you listen to, catecholamines
>> are either anti-catabolic or catabolic. Whatever their effect, every
>> scientist would agree that it is at best mild. The expected drops and
>> rebounds of catecholamines were detected during the flight and the
>> post flight periods, respectively. To explain the lean mass
>> fluctuations, it would mean that catecholamines are very potent
>> anabolic or anti-catabolic substances -- information that no research
>> has ever demonstrated even at high doses in humans. So they are not
>> the mediator the scientists were looking for.
>>
>> The next substances to be measured were the anabolic hormones and
>> growth factors such as GH, IGF-1 or insulin. Stein did not find any
>> significant alteration of their levels taking place during the phase
>> of wasting or regrowth. He did notice that T3 (an active thyroid
>> hormone) level dropped during the flight, to rebound after landing. T3
>> fluctuations concur with the mass loss and regain, so Stein suggests
>> that T3 could be one of the mediators of the lean mass fluctuation. As
>> T3 drops during the flight, so would the rate of muscle protein
>> synthesis. After landing, the increased T3 would boost anabolism and
>> therefore muscle growth.
>>
>> I disagree with Stein on this point. I consider the space-induced drop
>> in T3 as a protective mechanism against excessive muscle wasting
>> rather than a mediator of the growth inhibition. T3 is both an
>> anabolic and catabolic hormone. A minimal amount of T3 is required for
>> muscle to grow at an optimal rate, but as the T3 level increases, its
>> catabolic actions start to predominate and overwhelm its anabolic
>> properties.
>>
>> This is why you'll never meet a bodybuilder claiming to have gained
>> muscles by taking only T3. In fact, bodybuilders using T3 start to
>> lose both lean and adipose mass. Studies performed in bed-rested
>> people which attempt to duplicate weightlessness showed that in this
>> situation, exogenous T3 promoted protein degradation and not
>> anabolism. Therefore, T3 is unlikely to be the mass modulator we are
>> looking for.
>>
>> Stein's genuine breakthrough came from the fact that he measured the
>> levels of prostaglandins in both the blood and urine and compared them
>> with the degree of muscle wasting.
>>
>> Both measures were used for better accuracy as the levels of
>> prostaglandins are very hard to evaluate, prostaglandins being mainly
>> a local and not systemic growth modulator. Skeletal muscles and bones
>> are both net producers of prostaglandins with muscles being the major
>> site of manufacture. Those locally produced prostaglandins will
>> eventually pass into the blood before being quickly destroyed. So the
>> blood level of prostaglandins roughly reflects the rate of production
>> of prostaglandins inside the muscles. With urine prostaglandins,
>> results tend to be harder to interpret as prostaglandins produced in
>> the kidney tend to bias the figures. Nevertheless, Dr. Stein found out
>> that both measures agreed anyway.
>>
>> To the surprise of the scientific community (but not to bodybuilders),
>> the levels of the prostaglandins measured dropped during the flight --
>> especially the PGE2.
>>
>> After landing, there was a significant rebound of the prostaglandin
>> levels, especially of the PGF2. Those fluctuations closely reflected
>> the observed changes in lean muscle mass.
>>
>> The major cause of this drop is the lack of resistance placed on both
>> the muscles and bones. As we flex our muscles, a local formation and
>> release of prostaglandins is taking place. The harder we flex, the
>> more the local level of prostaglandins is elevated. Weightlessness
>> prevents the astronauts from flexing their muscles against a
>> resistance. Therefore, a significant drop in muscle prostaglandins can
>> be expected. As less prostaglandins are produced in our muscles, the
>> drop will quickly be reflected by the blood measurements.
>>
>> This may explain the well known development of insulin resistance
>> occuring during space flight as prostaglandins mediate many of the
>> actions of insulin on muscles. This resistance also contributes to the
>> muscle protein loss and again we find prostaglandins as key mediators
>> of this phenomenon.
>>
>> Stein's interpretations of these new findings are somewhat less
>> convincing. Scientists are expected to accurately measure the results
>> they obtained during an experiment, but also they are also expected to
>> interpret their results. Sometimes, their discussion is well
>> researched and documented which provides a worthwhile reading.
>> Unfortunately, many times it is not so well researched and the
>> discussion is a big step backward. This is the case in the above
>> mentioned study. The basic ideas are bright and the results original
>> but the comments made by the team of scientists is at the very least
>> poor. Paradoxally, they reached a good conclusion with a biased
>> reasoning.
>>
>> The discussion part of this study is based on a very selective reading
>> of the scientific literature while the bottom line conclusion is very
>> good. It concludes that "the inflight data support a major role for
>> decreased prostaglandin production in the protein loss by muscles."
>> This is very refreshing as the average scientist considers
>> prostaglandins as mediators of wasting and certainly not of muscle
>> growth. Stein's conclusion fits very well with his findings. The fall
>> in muscle prostaglandins induced by the lack of resistance during the
>> spaceflight results in a sharp fall in protein synthesis.
>>
>> For a quick recap:
>>
>> Our muscles are subjected to a constant protein turnover. This means
>> that the old proteins composing the contractile tissue of each cell
>> are constantly destroyed (catabolism) and replaced by new proteins
>> (anabolism).
>> If you are a sedentary person between 20 to 40 year old, this constant
>> basal turnover is neutral. The rate of catabolism is roughly equal to
>> the rate of anabolism.
>> Young growing adolescents acquire their muscle mass as anabolic rate
>> exceeds catabolism.
>> Elderly people slowly waste away as anabolism is slower than
>> degradation.
>> During spaceflight, anabolism is reduced, causing the rebuilding
>> mechanisms to be overwhelmed by the catabolic pathways. A loss of lean
>> mass ensues.
>> The big issue is to understand which hormones or factors are involved
>> in the drop of anabolism.
>>
>> Stein based his reasoning on the common belief concerning
>> prostaglandins, i.e., that PGF2 is anabolic and PGE2 is catabolic.
>> From there, he tries to explain how PGE2, a catabolic factor according
>> to him, could make our muscle grow. Good luck! Also, if PGE2 is a key
>> mediator of muscle wasting as many believe, how to explain its drop
>> while catabolism is intense? This belief concerning the so-called
>> wasting effect of PGE2 is due to some old, badly conducted, and flawed
>> studies which other laboratories have been unable to reproduce. Other
>> newer and more comprehensive studies have shown that PGE2 has an
>> overall positive influence on the protein turnover [2]. In other
>> words, PGE2 is an anabolic mediator rather than a catabolic one.
>>
>> This fits better into the NASA findings. During the flight, muscle
>> prostaglandins fall, which depresses anabolism. After the flight,
>> muscle prostaglandin production bounces back as astronaut muscles are
>> once against submitted to the resistance of gravity. The extra
>> prostaglandins strongly stimulate anabolism which explains the fast
>> muscle rebuilding.
>>
>>
>> --------------------------------------------------------------------------------
>>
>> Let's speculate a little!
>> With this major role of prostaglandins in mind, let's try to go a bit
>> further. Scientists specializing in Aeronautics have spent years
>> trying to combat space-induced wasting. In fact, the main research on
>> bodybuilding hormones has mostly been conducted by those scientists.
>> They have tried to administer hormones such as GH or IGF-1 during
>> spaceflights in order to combat the muscle loss. They have had little
>> success -- hardly surprising in light of recent findings. As the
>> levels of these peptide hormones hardly fluctuate, administering some
>> more does not appear to be the optimal solution. Usage of anabolic
>> steroids during weightlessness has achieved some but not exceptional
>> results. The next step is now to administer prostaglandins during a
>> flight and see what will happen.
>>
>> The lack of effects of the tested anabolic hormones on muscles
>> suggests that their receptors failed to function normally. In other
>> words, the lack of muscle contractions rapidly produce a receptor
>> insensitivity. What if it was the level of muscle prostaglandins that
>> was one of the major controllers of the sensitivity of the main
>> anabolic hormones? I've mentioned that the potency of steroids was
>> enhanced by exogenous PGF2. By the same token, PGF2 sensitivity is
>> enhanced by androgens.
>>
>> So:
>>
>> Prostaglandins control androgen and IGF-1 receptor activities.
>> Androgens control prostaglandin receptor expression.
>> IGF-1 and anabolics are major controllers of the level of muscle
>> prostaglandins.
>> This looks like a righteous anabolic cycle. Therefore, the major issue
>> for the scientists of the third millennium is to figure out how, at
>> which part of the cycle and where to enter this anabolic cycle for
>> maximal effectiveness of our muscle building tools.
>>
>>
>> --------------------------------------------------------------------------------
>>
>> References:
>> Stein TP. 1999 Jan. Endocrine relationships during human spaceflight.
>> Am J Physiol. 276:E155-62.
>> Fagan JM, Goldberg AL. 1986 Apr. Inhibitors of protein and RNA
>> synthesis cause a rapid block in prostaglandin production at the
>> prostaglandin synthase step. Proc Natl Acad Sci U S A. 83(8):2771-5.
>>
>> SOURCE:
>> http://www.mesomorphosis.com/articles/dharkam/anabolic-properties-of-prostaglandins.htm
>>
>> AND SOME RELATED READING (just to see how prostaglandins are also mis/
>> used):
>> http://www.mesomorphosis.com/articles/dharkam/prostaglandins.htm
>> http://www.mesomorphosis.com/articles/dharkam/how-dharkam-uses-pgf2.htm
--
Marshall Price of Miami
Known to Yahoo as d021317c
> One implication of this is that in physically active people who are
> moving in the Earth gravity field or even put weights on their moving
> bodies the arachidonic acid (AA) is constantly being "depleted" by
> conversion into the "good" prostaglandins (another way of depletion
> may be sex, because the PROSTAte gland also produces
> PROSTAglandins ...).
Aren't you jumping to conclusions here? Are you aware of any studies
showing connections between sexual activities and prostaglandins? It
occurs to me that male orgasm, by lowering libido, might have the
opposite effect.
> But once one gets sedentary, the AA has chance
> to accumulate to higher amounts in tissues. If the tissues are
> overloaded with AA it gets released spontaneously or in a response to
> minor stressors and in the absence of the prostaglandin-making
> machinery it gets converted by oxidation to the dangerous leukotrienes
> such as LTB4 which stimulate destructive inflammation/allergic
> responses. Ever noticed you catch cold easier when inactive?
> Fortunately, one can reduce AA not only by exercise but also by
> appropriate diet :-) BTW I am wondering which fats they are putting
> into the astronaut's food ?
> Taka
>
>> NASA Discovers the Anabolic Properties of Prostaglandins
>>
>> In the January 1999 issue of the American Journal of Physiology, a new
>> study performed on astronauts during spaceflight demonstrates the key
>> role played by prostaglandins in maintaining the strength of muscles.
>> A major problem during spaceflight is the rapid loss of lean muscle
>> mass in both animals and humans. This prevents the space agencies from
>> sending men into space for extended periods without threatening their
>> health. It is, of course, the lack of resistance and weight due to the
>> weightlessness that is the cause of muscle atrophy. The million dollar
>> question is: how does this lack of resistance alter the intracellular
>> environment so that muscle wasting is free to take place?
>>
>> Why are these experiments relevant to bodybuilders? Simply because the
>> pathways triggering the muscle wasting in space flight are the same
>> that make our muscle grow when we train. They just work in opposite
>> directions in each case.
>>
>>
>> --------------------------------------------------------------------------------
>>
>> Hormone fluctuations during spaceflight
>> Hormones are obvious candidates as possible mediators of this wasting
>> process. The favored hypothesis is that spaceflight induces some major
>> alterations in our hormone levels. Two main pathways could be
>> involved. First, the levels of catabolic hormones could rise and so be
>> the cause of this wasting. Second, the level of the anabolic hormones
>> could drop so that the constant basal renewal of muscle protein could
>> not take place at a sufficient rate, resulting in a net negative
>> balance.
>>
>> The study by Dr. Peter Stein [1] of the University of Medicine and
>> Dentistry of New Jersey consisted of measuring the key hormones in
>> astronauts during a space shuttle mission. Cortisol, a known wasting
>> hormone, was one of the favorite candidates. Unfortunately, a
>> consistent pattern of fluctuations in cortisol level was not apparent.
>> Cortisol increased in some but not all subjects. As all of them
>> experienced significant muscle loss, cortisol excess does not explain
>> the consistent wasting. Another paradox is that, once back on the
>> ground, the astronauts regained lean body mass while cortisol level
>> was at its peak.
>>
>> This means that you can waste away while having a normal cortisol
>> level, and you can put on lean mass despite a high cortisol level. It
>> should be a major eye-opener for bodybuilders.
>>
>> Next on the list of candidates were the catecholamines (epinephrine
>> and norepinephrine). Depending on whom you listen to, catecholamines
>> are either anti-catabolic or catabolic. Whatever their effect, every
>> scientist would agree that it is at best mild. The expected drops and
>> rebounds of catecholamines were detected during the flight and the
>> post flight periods, respectively. To explain the lean mass
>> fluctuations, it would mean that catecholamines are very potent
>> anabolic or anti-catabolic substances -- information that no research
>> has ever demonstrated even at high doses in humans. So they are not
>> the mediator the scientists were looking for.
>>
>> The next substances to be measured were the anabolic hormones and
>> growth factors such as GH, IGF-1 or insulin. Stein did not find any
>> significant alteration of their levels taking place during the phase
>> of wasting or regrowth. He did notice that T3 (an active thyroid
>> hormone) level dropped during the flight, to rebound after landing. T3
>> fluctuations concur with the mass loss and regain, so Stein suggests
>> that T3 could be one of the mediators of the lean mass fluctuation. As
>> T3 drops during the flight, so would the rate of muscle protein
>> synthesis. After landing, the increased T3 would boost anabolism and
>> therefore muscle growth.
>>
>> I disagree with Stein on this point. I consider the space-induced drop
>> in T3 as a protective mechanism against excessive muscle wasting
>> rather than a mediator of the growth inhibition. T3 is both an
>> anabolic and catabolic hormone. A minimal amount of T3 is required for
>> muscle to grow at an optimal rate, but as the T3 level increases, its
>> catabolic actions start to predominate and overwhelm its anabolic
>> properties.
>>
>> This is why you'll never meet a bodybuilder claiming to have gained
>> muscles by taking only T3. In fact, bodybuilders using T3 start to
>> lose both lean and adipose mass. Studies performed in bed-rested
>> people which attempt to duplicate weightlessness showed that in this
>> situation, exogenous T3 promoted protein degradation and not
>> anabolism. Therefore, T3 is unlikely to be the mass modulator we are
>> looking for.
>>
>> Stein's genuine breakthrough came from the fact that he measured the
>> levels of prostaglandins in both the blood and urine and compared them
>> with the degree of muscle wasting.
>>
>> Both measures were used for better accuracy as the levels of
>> prostaglandins are very hard to evaluate, prostaglandins being mainly
>> a local and not systemic growth modulator. Skeletal muscles and bones
>> are both net producers of prostaglandins with muscles being the major
>> site of manufacture. Those locally produced prostaglandins will
>> eventually pass into the blood before being quickly destroyed. So the
>> blood level of prostaglandins roughly reflects the rate of production
>> of prostaglandins inside the muscles. With urine prostaglandins,
>> results tend to be harder to interpret as prostaglandins produced in
>> the kidney tend to bias the figures. Nevertheless, Dr. Stein found out
>> that both measures agreed anyway.
>>
>> To the surprise of the scientific community (but not to bodybuilders),
>> the levels of the prostaglandins measured dropped during the flight --
>> especially the PGE2.
>>
>> After landing, there was a significant rebound of the prostaglandin
>> levels, especially of the PGF2. Those fluctuations closely reflected
>> the observed changes in lean muscle mass.
>>
>> The major cause of this drop is the lack of resistance placed on both
>> the muscles and bones. As we flex our muscles, a local formation and
>> release of prostaglandins is taking place. The harder we flex, the
>> more the local level of prostaglandins is elevated. Weightlessness
>> prevents the astronauts from flexing their muscles against a
>> resistance. Therefore, a significant drop in muscle prostaglandins can
>> be expected. As less prostaglandins are produced in our muscles, the
>> drop will quickly be reflected by the blood measurements.
>>
>> This may explain the well known development of insulin resistance
>> occuring during space flight as prostaglandins mediate many of the
>> actions of insulin on muscles. This resistance also contributes to the
>> muscle protein loss and again we find prostaglandins as key mediators
>> of this phenomenon.
>>
>> Stein's interpretations of these new findings are somewhat less
>> convincing. Scientists are expected to accurately measure the results
>> they obtained during an experiment, but also they are also expected to
>> interpret their results. Sometimes, their discussion is well
>> researched and documented which provides a worthwhile reading.
>> Unfortunately, many times it is not so well researched and the
>> discussion is a big step backward. This is the case in the above
>> mentioned study. The basic ideas are bright and the results original
>> but the comments made by the team of scientists is at the very least
>> poor. Paradoxally, they reached a good conclusion with a biased
>> reasoning.
>>
>> The discussion part of this study is based on a very selective reading
>> of the scientific literature while the bottom line conclusion is very
>> good. It concludes that "the inflight data support a major role for
>> decreased prostaglandin production in the protein loss by muscles."
>> This is very refreshing as the average scientist considers
>> prostaglandins as mediators of wasting and certainly not of muscle
>> growth. Stein's conclusion fits very well with his findings. The fall
>> in muscle prostaglandins induced by the lack of resistance during the
>> spaceflight results in a sharp fall in protein synthesis.
>>
>> For a quick recap:
>>
>> Our muscles are subjected to a constant protein turnover. This means
>> that the old proteins composing the contractile tissue of each cell
>> are constantly destroyed (catabolism) and replaced by new proteins
>> (anabolism).
>> If you are a sedentary person between 20 to 40 year old, this constant
>> basal turnover is neutral. The rate of catabolism is roughly equal to
>> the rate of anabolism.
>> Young growing adolescents acquire their muscle mass as anabolic rate
>> exceeds catabolism.
>> Elderly people slowly waste away as anabolism is slower than
>> degradation.
>> During spaceflight, anabolism is reduced, causing the rebuilding
>> mechanisms to be overwhelmed by the catabolic pathways. A loss of lean
>> mass ensues.
>> The big issue is to understand which hormones or factors are involved
>> in the drop of anabolism.
>>
>> Stein based his reasoning on the common belief concerning
>> prostaglandins, i.e., that PGF2 is anabolic and PGE2 is catabolic.
>> From there, he tries to explain how PGE2, a catabolic factor according
>> to him, could make our muscle grow. Good luck! Also, if PGE2 is a key
>> mediator of muscle wasting as many believe, how to explain its drop
>> while catabolism is intense? This belief concerning the so-called
>> wasting effect of PGE2 is due to some old, badly conducted, and flawed
>> studies which other laboratories have been unable to reproduce. Other
>> newer and more comprehensive studies have shown that PGE2 has an
>> overall positive influence on the protein turnover [2]. In other
>> words, PGE2 is an anabolic mediator rather than a catabolic one.
>>
>> This fits better into the NASA findings. During the flight, muscle
>> prostaglandins fall, which depresses anabolism. After the flight,
>> muscle prostaglandin production bounces back as astronaut muscles are
>> once against submitted to the resistance of gravity. The extra
>> prostaglandins strongly stimulate anabolism which explains the fast
>> muscle rebuilding.
>>
>>
>> --------------------------------------------------------------------------------
>>
>> Let's speculate a little!
>> With this major role of prostaglandins in mind, let's try to go a bit
>> further. Scientists specializing in Aeronautics have spent years
>> trying to combat space-induced wasting. In fact, the main research on
>> bodybuilding hormones has mostly been conducted by those scientists.
>> They have tried to administer hormones such as GH or IGF-1 during
>> spaceflights in order to combat the muscle loss. They have had little
>> success -- hardly surprising in light of recent findings. As the
>> levels of these peptide hormones hardly fluctuate, administering some
>> more does not appear to be the optimal solution. Usage of anabolic
>> steroids during weightlessness has achieved some but not exceptional
>> results. The next step is now to administer prostaglandins during a
>> flight and see what will happen.
>>
>> The lack of effects of the tested anabolic hormones on muscles
>> suggests that their receptors failed to function normally. In other
>> words, the lack of muscle contractions rapidly produce a receptor
>> insensitivity. What if it was the level of muscle prostaglandins that
>> was one of the major controllers of the sensitivity of the main
>> anabolic hormones? I've mentioned that the potency of steroids was
>> enhanced by exogenous PGF2. By the same token, PGF2 sensitivity is
>> enhanced by androgens.
>>
>> So:
>>
>> Prostaglandins control androgen and IGF-1 receptor activities.
>> Androgens control prostaglandin receptor expression.
>> IGF-1 and anabolics are major controllers of the level of muscle
>> prostaglandins.
>> This looks like a righteous anabolic cycle. Therefore, the major issue
>> for the scientists of the third millennium is to figure out how, at
>> which part of the cycle and where to enter this anabolic cycle for
>> maximal effectiveness of our muscle building tools.
>>
>>
>> --------------------------------------------------------------------------------
>>
>> References:
>> Stein TP. 1999 Jan. Endocrine relationships during human spaceflight.
>> Am J Physiol. 276:E155-62.
>> Fagan JM, Goldberg AL. 1986 Apr. Inhibitors of protein and RNA
>> synthesis cause a rapid block in prostaglandin production at the
>> prostaglandin synthase step. Proc Natl Acad Sci U S A. 83(8):2771-5.
>>
>> SOURCE:
>> http://www.mesomorphosis.com/articles/dharkam/anabolic-properties-of-prostaglandins.htm
>>
>> AND SOME RELATED READING (just to see how prostaglandins are also mis/
>> used):
>> http://www.mesomorphosis.com/articles/dharkam/prostaglandins.htm
>> http://www.mesomorphosis.com/articles/dharkam/how-dharkam-uses-pgf2.htm
--
Marshall Price of Miami
Known to Yahoo as d021317c
On May 17, 3:51 am, Marshall Price <d0213...@yahoo.com> wrote:
> Taka wrote:
> > One implication of this is that in physically active people who are
> > moving in the Earth gravity field or even put weights on their moving
> > bodies the arachidonic acid (AA) is constantly being "depleted" by
> > conversion into the "good" prostaglandins (another way of depletion
> > may be sex, because the PROSTAte gland also produces
> > PROSTAglandins ...).
>
> Aren't you jumping to conclusions here? Are you aware of any studies
> showing connections between sexual activities and prostaglandins? It
> occurs to me that male orgasm, by lowering libido, might have the
> opposite effect.
Perhaps, but the prostate produces prostaglandings and the ejacuate is
rich in them so it's a way of getting them out of the body. However,
the amount may be too small compared to the daily manufacture of AA
from the vegetable oil precursors ingested ...
Taka
> Taka wrote:
> > One implication of this is that in physically active people who are
> > moving in the Earth gravity field or even put weights on their moving
> > bodies the arachidonic acid (AA) is constantly being "depleted" by
> > conversion into the "good" prostaglandins (another way of depletion
> > may be sex, because the PROSTAte gland also produces
> > PROSTAglandins ...).
>
> Aren't you jumping to conclusions here? Are you aware of any studies
> showing connections between sexual activities and prostaglandins? It
> occurs to me that male orgasm, by lowering libido, might have the
> opposite effect.
Perhaps, but the prostate produces prostaglandings and the ejacuate is
rich in them so it's a way of getting them out of the body. However,
the amount may be too small compared to the daily manufacture of AA
from the vegetable oil precursors ingested ...
Taka
Taka wrote:
> On May 17, 3:51 am, Marshall Price <d0213...@yahoo.com> wrote:
>> Taka wrote:
>>> One implication of this is that in physically active people who are
>>> moving in the Earth gravity field or even put weights on their moving
>>> bodies the arachidonic acid (AA) is constantly being "depleted" by
>>> conversion into the "good" prostaglandins (another way of depletion
>>> may be sex, because the PROSTAte gland also produces
>>> PROSTAglandins ...).
>> Aren't you jumping to conclusions here? Are you aware of any studies
>> showing connections between sexual activities and prostaglandins? It
>> occurs to me that male orgasm, by lowering libido, might have the
>> opposite effect.
>
> Perhaps, but the prostate produces prostaglandins and the ejaculate is
> rich in them so it's a way of getting them out of the body.
That remains to be seen.
> However,
> the amount may be too small compared to the daily manufacture of AA
> from the vegetable oil precursors ingested ...
And so does that.
Besides, it's not as though the endogenous production of arachidonic
acid is out of control. As the chapter I quoted from /Metabolism at a
Glance/ points out, it's a pathway involving about eight steps
(including chain elongation), four of which are mediated by enzymes
embedded in the membrane of the smooth endoplasmic reticulum, and it
requires energy.
--
Marshall Price of Miami
Known to Yahoo as d021317c
> On May 17, 3:51 am, Marshall Price <d0213...@yahoo.com> wrote:
>> Taka wrote:
>>> One implication of this is that in physically active people who are
>>> moving in the Earth gravity field or even put weights on their moving
>>> bodies the arachidonic acid (AA) is constantly being "depleted" by
>>> conversion into the "good" prostaglandins (another way of depletion
>>> may be sex, because the PROSTAte gland also produces
>>> PROSTAglandins ...).
>> Aren't you jumping to conclusions here? Are you aware of any studies
>> showing connections between sexual activities and prostaglandins? It
>> occurs to me that male orgasm, by lowering libido, might have the
>> opposite effect.
>
> Perhaps, but the prostate produces prostaglandins and the ejaculate is
> rich in them so it's a way of getting them out of the body.
That remains to be seen.
> However,
> the amount may be too small compared to the daily manufacture of AA
> from the vegetable oil precursors ingested ...
And so does that.
Besides, it's not as though the endogenous production of arachidonic
acid is out of control. As the chapter I quoted from /Metabolism at a
Glance/ points out, it's a pathway involving about eight steps
(including chain elongation), four of which are mediated by enzymes
embedded in the membrane of the smooth endoplasmic reticulum, and it
requires energy.
--
Marshall Price of Miami
Known to Yahoo as d021317c
