# PGF2



## K1 (Jan 15, 2013)

– By geneticfreak



Disclaimer: Discussion of pharmaceutical agents below is presented for information only. Nothing here is meant to take the place of advice from a licensed health care practitioner. Consult a physician before taking any medication.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.

Among the most potent growth factors produced locally in the muscles are the prostaglandins. These quasi-hormones use fats as their raw materials. Several classes of prostaglandins exist. We will mainly focus on the most potent one, namely the prostaglandin F2 alpha or PGF2 for short. If you apply PGF2 to a muscle cell, you are going to trigger a very strong anabolic response. PGF2 has been used by veterinarians for years not only to get animals pregnant but also to make them grow. A few daredevils figured out that if it was making animals more muscular, it would make bodybuilders bigger too. This was a big leap of faith as many drugs produce wonderful effects in animals only to fail miserably in bodybuilders. Clenbuterol is a good example of this: ultra potent in animals, deceptive in humans. Amazingly enough, this time it worked wonders.

WARNING:

What I am going to reveal is true for men ONLY. Women will not get any “benefit” from what I will describe below. Further, no women should EVER touch this drug which will induce a very severe pain in their ovaries. As men do not have ovaries, this is something that will not happen to them. Ill side effect most probably will occour in males as well.

PGF2 and anabolism.

Many studies have demonstrated an anabolic effect of PGF2 in skeletal muscles of both humans and animals. Paradoxically, PGF2 usage is still reserved to a bodybuilding elite and no one is willing to
divulge the precious secret edge. One of the most remarkable effects of PGF2 is that it mediates the
major part of the anabolic effects of insulin. By using PGF2, you can use far less insulin and get a
far stronger muscle building effect.

PGF2 and weak bodyparts.

The cardinal rule of PGF2 is to inject as far away as possible from the intestine. You see, PGF2 induces a very strong contraction of the intestine and the bladder (both smooth muscles). The major candidate as a site of injection was the front shoulders. But by repeating injections in
the shoulders, bodybuilders soon ended up with grossly overdeveloped front delts. They looked like walking monkeys. The rest of their body was growing too, but not as fast as the muscles closest to the sites of
injections. What this means is that if one wants to develop a weak muscle, just inject PGF2 locally and watch
the muscle grow. We are talking about a real muscle growth and not an artificial swelling like Synthol or Esiclene would induce. Calves are a muscle of choice. In fact, even if your calves failed to grow no matter how much ******* and training you administered, PGF2 will solve your problem.
After a single cycle of PGF2, unresponsive calves start to respond to both training and *******s
even if they never did before.

The localized growth induced by PGF2 may appear magical, but there is a simple explanation. The
life cycle of the injected PGF2 is terribly short (minutes). Most of it will be destroyed in your lungs.
If you hit your right calf for example, this muscle will be exposed to a maximal concentration of
PGF2. As the prostaglandin rapidly leaks out of the calf and passes into the blood, it will quickly
reach the lungs where most of it will be destroyed. What is left of the PGF2 will be dispatched
evenly though your whole body. It means that the other muscles will be exposed to far less of the
anabolic effects of PGF2. So unless you want to make a weak point grow, you should rotate the
sites of injections frequently which as we will see is not a problem.

PGF2 is not to be confused with steroids.

You’ve probably realized by now that PGF2 produces growth in a radically different way from
*******s — although I do not exclude that part of the anabolic actions of androgens are mediated by a
local release of PGF2. The way PGF2 should be used is therefore radically different from that of
androgens. ******* use is comparitively comfortable. You inject or swallow them once in a while and wait
for the growth to occur. This is not the case with PGF2. Their main drawback is precisely their
difficulty of administration. *******s once injected survive several days in your body. PGF2 will last
only several minutes though their stimulatory actions on anabolism will be far longer lasting
(hours). It means that frequent injections are compulsory for significant effect. Ideally this would be five times per day,30 minutes after meals. You will also notice that once you have injected PGF2, the muscle which received it gets sore almost immediately. If the muscle was already sore from training, that painful sensation may
become very intense. You definitely do not want to repeat injections at the very same location,
hence the necessity for rotation. By the same token, you will notice that you cannot inject in a
muscle and then train this muscle. PGF2 is algesic (a pain mediator). Therefore, the timing of
injections is key. You should wait for at least 2 to 3 days after you have trained a muscle to inject
it. Then you will have to wait for 24 hours before training this muscle. If your muscle is already
sore, It is advised not to use it as a site of injection as long as it hurts if it is to be used at all.

You will also learn that it is more comfortable to hit the outer part of the muscle than the inner part.
For example, it is less painful to hit the outer head of the triceps than the inner head that touches
your lats. Some bodyparts such as the biceps, the back, etc. are especially sensitive to the pain
sensation PGF2 will induce.

What about fat: PGF2 vs DNP?

We are told that DNP is the strongest thermogenic (temperature elevating) drug available. I dispute
this statement. Inject PGF2, wait for ten minutes and you will sweat profusely. In fact, your body
temperature will rise so much that you may feel very cold while a witness will get scared as you
feel so hot. By elevating your body temperature, PGF2 will burn up your fat at an accelerated rate.
Furthermore, unlike muscle cells, fat cells do not like to be exposed to PGF2. As a result, they die.
Mark this well: unlike a classical diet which makes each fat cell shrink, PGF2 kills fat cells. With
PGF2, you can say goodbye to your excess adipose tissue.

What about stacking *******s with PGF2?

If PGF2 is so powerful, why not stack it along with *******s for maximal effect? It looks like a neat
idea until you try. PGF2 potentiates the effects of androgens on muscles most likely by increasing
androgen receptor level. *******s also increase the effects of PGF2 probably by increasing the
density of muscle PGF2 receptors. You will end up with a combination that is too powerful.

Within two or three days on PGF2, you will notice that your muscles get very tight. You cannot find
harder muscles than muscles from a PGF2 user. It looks and feels great until you try to train. Within
three to four reps even with an empty bar, your muscles will get so pumped that you will not be able
to move. In fact, your training poundage are likely to drop severely. I have witnessed someone going
from 3 reps at 500 pounds in the incline bench press, to failing at 6 reps at 130 after a week of
(serious) PGF2 administration plus *******s. Do not worry though, your muscles will grow and you
will be able to resume heavy training once PGF2 is stopped. This pumping effect is too exaggerated
if you take *******s along with PGF2. So it is best to use the prostaglandins to grow when you’re off
the *******s.

Is PGF2 safe?

The answer is clearly no, but neither is the use of *******s, insulin, clenbuterol, etc. By the way,
PGF2 is absolutely invisible at any drug test. What kind of side effects to expect? The first ones — if
we except the elevation of temperature — are that it will empty your guts of whatever they contain.
So make sure you have unrestricted use of a bathroom. This is going to last around 20 minutes.
What you do not want is to inject PGF2 into a vein! Learn to do the aspiration test. PGF2 is to be
injected intramuscularly with an insulin needle if you are lean enough. This is going to hurt like hell
and for a very long time (up to an hour) if you inject into a vein. You also may feel as if you had
some kind of cold in your throat. It is due to the vasoconstricting effect PGF2 has in your lungs.
Vomiting is a reported side effect but I have never heard of it in men.

Dosages.

You should start with a pretty low dosage (a half milligram) and see what happens. From there,
build up VERY slowly. Then, the sky is the limit. You can inject what is normally needed for several
cows and survive but believe me, you do not want to go through this. Do not forget to keep the vials
refrigerated. If you are new to PGF2, for simplicity choose the natural form and not an analog. PGF2
analogs have several advantages over straight PGF2 in that they have a longer half life and less
side effects, but some of them have no anabolic properties while others are more potent than
straight PGF2. Do not take a chance on that.

To sum up, I would like to paraphrase what Dan Duchaine has said about ******* users…

PGF2 users: Healthy, who knows? Big and lean, yes!

Re: PGF2A + Esiclene + Winstrol

Prostaglandins

Among the most potent growth factors produced locally in the muscles are the prostaglandins. These quasi-hormones use fats as their raw materials. Several classes of prostaglandins exist. We will mainly focus on the most potent one, namely the prostaglandin F2 alpha or PGF2 for short. If you apply PGF2 to a muscle cell, you are going to trigger a very strong anabolic response. PGF2 has been used by veterinarians for years not only to get animals pregnant but also to make them grow. A few daredevils figured out that if it was making animals more muscular, it would make bodybuilders bigger too. This was a big leap of faith as many drugs produce wonderful effects in animals only to fail miserably in bodybuilders. Clenbuterol is a good example of this: ultra potent in animals, deceptive in humans. Amazingly enough, this time it worked wonders.

WARNING:

What I am going to reveal is true for men ONLY. Women will not get any benefit from what I will describe below. Further, no women should EVER touch this drug which will induce a very severe pain in their ovaries. As men do not have ovaries, this is something that will not happen to them.

PGF2 and anabolism.

Many studies have demonstrated an anabolic effect of PGF2 in skeletal muscles of both humans and animals. Paradoxically, PGF2 usage is still reserved to a bodybuilding elite and no one is willing to divulge the precious secret edge. One of the most remarkable effects of PGF2 is that it mediates the major part of the anabolic effects of insulin. By using PGF2, you can use far less insulin and get a far stronger muscle building effect.
PGF2 and weak bodyparts. The cardinal rule of PGF2 is to inject as far away as possible from the intestine. You see, PGF2 induces a very strong contraction of the intestine and the bladder (both smooth muscles). The major candidate as a site of injection was the front shoulders. But by repeating injections in the shoulders, bodybuilders soon ended up with grossly overdeveloped front delts. They looked like walking monkeys. The rest of their body was growing too, but not as fast as the muscles closest to the sites of injections. What this means is that if you want to develop a weak muscle, just inject PGF2 locally and watch the muscle grow. We are talking about a real muscle growth and not an artificial swelling like Synthol or Esiclene would induce. Calves are a muscle of choice. In fact, even if your calves failed to grow no matter how much steroid and training you administered, PGF2 will solve your problem. After a single cycle of PGF2, unresponsive calves start to respond to both training and steroids even if they never did before.The localized growth induced by PGF2 may appear magical, but there is a simple explanation. The life cycle of the injected PGF2 is terribly short (minutes). Most of it will be destroyed in your lungs. If you hit your right calf for example, this muscle will be exposed to a maximal concentration of PGF2. As the prostaglandin rapidly leaks out of the calf and passes into the blood, it will quickly reach the lungs where most of it will be destroyed. What is left of the PGF2 will be dispatched evenly though your whole body. It means that the other muscles will be exposed to far less of the anabolic effects of PGF2. So unless you want to make a weak point grow, you should rotate the sites of injections frequently which as we will see is not a problem.

PGF2 is not to be confused with steroids. You’ve probably realized by now that PGF2 produces growth in a radically different way from steroids — although I do not exclude that part of the anabolic actions of androgens are mediated by a local release of PGF2. The way PGF2 should be used is therefore radically different from that of androgens. Steroid use is rather comfortable. You inject or swallow them once in a while and wait for the growth to occur. This is not the case with PGF2. Their main drawback is precisely their difficulty of administration. Steroids once injected survive several days in your body. PGF2 will last only several minutes though their stimulatory actions on anabolism will be far longer lasting (hours). It means that frequent injections are compulsory. Ideally this would be five times per day, 30 minutes after meals.
You will also notice that once you have injected PGF2, the muscle which received it gets sore almost immediately. If the muscle was already sore from training, that painful sensation may become very intense. You definitely do not want to repeat injections at the very same location, hence the necessity for rotation. By the same token, you will notice that you cannot inject in a muscle and then train this muscle. PGF2 is algesic (a pain mediator). Therefore, the timing of injections is key. You should wait for at least 2 to 3 days after you have trained a muscle to inject it. Then you will have to wait for 24 hours before training this muscle. If your muscle is already sore, I advise against using it as a site of injection as long as it hurts. You will also learn that it is more comfortable to hit the outer part of the muscle than the inner part. For example, it is less painful to hit the outer head of the triceps than the inner head that touches your lats. Some bodyparts such as the biceps, the back, etc. are especially sensitive to the pain sensation PGF2 will induce.

Is PGF2 safe?

The answer is clearly no, but neither is the use of steroids, insulin, clenbuterol, etc. By the way, PGF2 is absolutely invisible at any drug test. What kind of side effects to expect? The first ones — if we except the elevation of temperature — are that it will empty your guts of whatever they contain. So make sure you have unrestricted use of a bathroom. This is going to last around 20 minutes. What you do not want is to inject PGF2 into a vein! Learn to do the aspiration test. PGF2 is to be injected intramuscularly with an insulin needle if you are lean enough. This is going to hurt like hell and for a very long time (up to an hour) if you inject into a vein. You also may feel as if you had some kind of cold in your throat. It is due to the vasoconstricting effect PGF2 has in your lungs. Vomiting is a reported side effect but I have never heard of it in men.

Dosages.

The lowest possible “effective” dose should be used You should start with a low dosage no higher than (a half milligram) and see what happens. From there, build up VERY slowly. Then, the sky is the limit. You can inject what is normally needed for several cows and survive but believe me, you do not want to go through this and it is potentially deadly. Do not forget to keep the vials refrigerated. If you are new to PGF2, for simplicity choose the natural form and not an analog. PGF2 analogs have several advantages over straight PGF2 in that they have a longer half life and less side effects, but some of them have no anabolic properties while others are more potent than straight PGF2. Do not take a chance on that.

Disclaimer: Discussion of pharmaceutical agents below is presented for information only. Nothing here is meant to take the place of advice from a licensed health care practitioner. Consult a physician before taking any medication.
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 ex. (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. ex. 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 least 10 grams of creatine per day.

The advanced schedule

This is not a pro schedule. It should rather fit most of the readers’ needs for muscles. As you taper off your steroid intake, slowly build up your PGF2 intake first in terms of dosage, then in terms of frequency. The animal studies suggest that PGF2 tends to depress testosterone secretion. But the PGF2 users usually get very “horny”, which is a good sign, especially at the end of a steroid cycle. And do not discount the general hardening properties of PGF2 which amazingly is not restricted to skeletal muscles. Frequency of administration as well as dosage should be increased compared to beginners. You also have the choice between insulin injections and oral insulin boosters. Sticking with the oral booster may be wiser until you get more comfortable with the control of your glycemia. This is especially true as PGF2 will enhance the hypoglycemic effects of insulin. Wake up and have a liquid meal followed by a more solid meal within 30 minutes. Use that period for an insulin shot (start low with 5 UI and build up to no more than 15 UI per meal) or for oral Glipizide (2.5 to 5 mg). Prefer a long acting insulin to a short one. Wait for 15 minutes before your PGF2 (always start low and build up as you feel more comfortable). Repeat this procedure at lunch. Keep the liquid meal for after the lunch in case you feel hypoglycemia. Another reason to prefer Glipizide at that time is that you may get tired of the frequent injections. Repeat this procedure after training. You can use another PGF2 injection a bit before bedtime still with a meal but without the insulin or the booster. Some people who bad-mouth the prostaglandins argue that prostaglandins depress GH secretion. This is funny as the scientific literature points out the opposite. GH should be liberated overnight.
As you use more PGF2 than in the beginner cycle, go with at least 15 grams of creatine over 24 hours.

The science of cycling

The length of a PGF2 cycle is generally determined by default. The cycle usually lasts the whole time you want to be off steroids. It means it can go from between 24 hours to two months. Even though bodybuilders welcome a drug that allows them to grow while off steroids, most will get tired of using PGF2 after a while. They are usually happy to switch back to anabolics. A good rule of thumb is therefore to use PGF2 until you get tired of it. Again, there is no magic number here.
Yet many maintain a lighter intake of PGF2 centered around their weak bodypart. A lighter schedule includes one or two injections a day in a weak bodypart such as the calves to help bring them up but without having to go with all the trouble associated with normal PGF2 use.
To conclude, I again would like to quote Dan Duchaine about steroids in USH II:
“Rule #7: Most people who have taken massive amounts of steroids don’t get sick, don’t die, and don’t go crazy.
Rule #8: … Never assume that you are like ‘most people’ until you prove it.”
This exact same rule apply to PGF2 users. Do not assume that PGF2 use is benign. PGF2 will affect every one of the cells composing your body. You are not immune from a rare, unexpected reaction. Please do not consider PGF2 usage lightly. We would not like to hear from you in the horror story section of a bodybuilding magazine.

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’t 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’m 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.

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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.

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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.

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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® as a sterile solution for subcutaneous and intramuscular injection. It’s 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.

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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’s just a spineless way of saying, “I don’t 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.

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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 (mechanical stimulation) and eating (insulin action).

Insulin

As eluded to above, insulin stimulated protein synthesis is linked to the production of phospholipases which lead to increased availability of arachidonic acid. This is a two edged sword. Increased availability of arachidonic acid can increase the amount of PGF2a thereby increasing protein synthesis. On the other hand, arachidonic aid directly suppresses GLUT4 production which is the chief glucose transporter in skeletal muscle. High levels of arachidonic acid can reduce glucose transport by up to 50%. It could be that insulin action is more dependant on the cAMP antagonist, cyclic PIP (prostaglandylinositol cyclic phosphate), a proposed second messenger for insulin and alpha-adrenoceptor action, than on PGF2a. PGE2 however is a different story. Prostaglandin E, myo-inositol and one phosphate are components of cyclic PIP. So increased production of PGE2 may increase insulin mediated glucose transport through this mechanism. Taking this into consideration, exogenous PGF2a should not be considered to replace insulin.

Dietary Fatty Acids

Dietary fatty acids significantly effects prostaglandin production. Diets high in omega-3 fatty acids (fish oil, flax oil) decrease prostaglandin production. Diets high in omega-6 fatty acids (corn oil) increase prostaglandin production. Once again you have pros and cons with trying to manipulate PGF2a production with your diet. By increasing omega-3s, you get lower levels of PGF2a and probably a less intense stimulus of protein synthesis immediately after you workout. On the other hand by increasing omega-3s you reduce inflamation, pain, increase GLUT4 content, and a whole host of other factors related to cardiac risk. I don’t think its as clear cut as Dr. Sears (Zone Diet) would have you believe. Trying to manipulate the diet to control prostaglandin kinetics is fraught with complexity making black and white statements difficult to support.

NSAIDs

NSAIDs are non-steroidal anti-inflammatory drugs. An example of such drugs are aspirin, ibuprofen (Motrin), naproxen sodium (Anaprox, Alleve). There are several more but these are the most common to consumers. NSAIDs work by inhibiting the activity of cyclooxygenase. By blocking cyclooxygenase you block prostaglandin production. These drugs have been shown to improve nitrogen balance under conditions of severe physical stress such as after surgery. The effect is abolished when PGE2 is infused linking PGE2 production with the catabolic effect of stress. In the case of PGF2a, the use of NSAIDs also blocks its production in that PGE2 and PGF2a are normally produced in a 1:1 ratio from the same precursor. Using NSAIDS while using exogenous PGF2a may improve the anabolic effect by reducing PGE2 in the presents of elevated PGF2a shifting the ratio towards anabolism.

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PGF2a + IGF-1: The ultimate cocktail for localized muscle growth?!

Say good by to lagging body parts forever. It is a special time to be a bodybuilder. With the advent of PGF2a as a localized anabolic agent along with the newly available rhIGF-1 which has also been shown to build muscle where you want it, the future for genetically challenged bodybuilders looks bright indeed. A brief refresher course on locally injected IGF-1. Non-exercised muscle, when injection with 0.9 – 1.9 micrograms/kg/day of rhIGF-1 was shown to mimic the effects of physically loading the muscle. Much the same effect PGF2a but by different mechanisms. With local IGF-1 injections there is an increase in protein content, cross sectional area and DNA content. The increase in muscle DNA is presumed to be a result of increased proliferation and differentiation of satellite cells which donate their nuclei upon fusion with damaged or hypertrophying muscle cells. Take note that the quantities of IGF-1 needed are extremely small, much smaller than studies that have shown relatively poor results from administering IGF-1 systemically which range from 1.0 to 6.9 milligrams/kg/day.

Now add PGF2a to the mix and whalla! You can virtually mimic the mechanical stimulus of training without even picking up a weight. You have PGF2a to accelerate short term protein synthesis by activating ribosomes and/or eIFs and thereby translation, as well as IGF-1 to activate satellite cells to bind and donate additional nuclei to boost the amount of mRNA to be used by the ribosomes. Because the mechanism of action is different, the two compounds should compliment each other delivering results beyond what either one alone could produce.

Are these compounds going to replace traditional training? Not in the near future. The use of site injectable drugs only reaches the surface musculature. Deeper muscles are only stimulated to grow with traditional training. For strength athletes, strength is dependant on neuromuscular training which is not enhanced by simple muscle hypertrophy without actual lifting in a coordinated fashion. Are these compounds going to replace traditional anabolics? No. The reason is basically the same as with training. Deeper muscle groups are only reached by systemically administered anabolics that are carried throughout the entire body. In addition, androgens are needed to influence genetic expression in favor of whole body skeletal muscle growth. Are these compounds going to change the face of bodybuilding? It is very likely that they will, depending on their availability and cost. I would hope that as competitors become educated about these alternatives that we will no longer see implants in top level competitors. It would also be nice to see people have an option when it comes to pumping their muscles full of “stuff” in hopes that it will improve their symmetry. No doubt the future will bring us even more new and exciting drugs like non-steroidal androgens and compounds that alter the expression of myostatin (GDF . Once again, it is an exciting time in the science of bodybuilding, perhaps now more than any other time since the introduction of testosterone.

Sources:

Arntzen KJ, Brekke OL, Vatten L, Austgulen R Reduced production of PGE2 and PGF2 alpha from decidual cell cultures supplemented with N-3 polyunsaturated fatty acids. Prostaglandins Other Lipid Mediat 1998 Jun;56(2-3):183-95

Chan AC, Allen CE, Hegarty PV. The effects of vitamin E depletion and repletion on prostaglandin synthesis in semitendinosus muscle of young rabbits. J Nutr 1980 Jan;110(1):66-73

Chromiak JA, Vandenburgh HH. Mechanical stimulation of skeletal muscle cells mitigates glucocorticoid-induced decreases in prostaglandin production and prostaglandin synthase activity. J Cell Physiol 1994 Jun;159(3):407-14

Gregory R. Adams & Samuel A. McCue. Localized infusion of IGF-I results in skeletal muscle hypertrophy in rats. Journal of Applied Physiology 84(5): 1716-1722, 1998

Marshall LA, Szczesniewski A, Johnston PV. Dietary alpha-linolenic acid and prostaglandin synthesis: a time course study. Am J Clin Nutr 1983 Dec;38(6):895-900

Marshall LA, Johnston PV Modulation of tissue prostaglandin synthesizing capacity by increased ratios of dietary alpha-linolenic acid to linoleic acid. Lipids 1982 Dec;17(12):905-13

Nasjletti A, Erman A, Cagen LM, Brooks DP, Crofton JT, Share L, Baer PG High potassium intake selectively increases urinary PGF2 alpha excretion in the rat. Am J Physiol 1985 Mar;248(3 Pt 2):F382-8

Olomu JM, Baracos VE. Prostaglandin synthesis and fatty acid composition of phospholipids and triglycerides in skeletal muscle of chicks fed combinations of flaxseed oil and animal tallow. Lipids 1991 Sep;26(9):743-9

Palmer RM. Prostaglandins and the control of muscle protein synthesis and degradation. Prostaglandins Leukot Essent Fatty Acids. 1990 Feb;39(2):95-104

Sadoshima J, Izumo S. The cellular and molecular response of cardiac myocytes to mechanical stress. Annu Rev Physiol 1997;59:551-71

Sadoshima J, Izumo S. Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: potential involvement of an autocrine/paracrine mechanism. EMBO J 1993 Apr;12(4):1681-92

Southorn BG, Palmer RM Inhibitors of phospholipase A2 block the stimulation of protein synthesis by insulin in L6 myoblasts. Biochem J. 1990 Sep 15;270(3):737-9.

Thompson MG, Palmer RM Signaling pathways regulating protein turnover in skeletal muscle. Cell Signal. 1998 Jan;10(1):1-11.

Vandenburgh HH, Shansky J, Solerssi R, Chromiak J. Mechanical stimulation of skeletal muscle increases prostaglandin F2 alpha production, cyclooxygenase activity, and cell growth by a pertussis toxin sensitive mechanism. J Cell Physiol 1995 May;163(2):285-94

Wasner HK, Salge U, Gebel M. The endogenous cyclic AMP antagonist, cyclic PIP: its ubiquity, hormone-stimulated synthesis and identification as prostaglandylinositol cyclic phosphate. Acta Diabetol 1993;30(4):220-32…freak


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