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loooking to get some info
any good info on pgf2?
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1abbig
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Dino Strong
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(Total posts: 39) posted January 12, 2000 06:27 PM
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Here is a good PGF-2 article that came from the Underground Supplements Newsletter. i hope this helps.
There is quite a bit of interest in PGF2 right nowise I will clear a few things up first. I get my Lutalyse from a friend who is vet, I can only get personal use for the moment but will look into things further if there is a demand, this is a big if? I don’t even know if it’s on any banned lists in
My own country let alone the U.S.A. My stats are as follows on the 13/01/99: weight: 221 pounds fat: round about 10/11% height: 6ft 2in I will start of with 2mg a day and build up too 8mg.
As a few of you have shown interest in my real life trials with PGF2, I will report every week and tell you how I’m getting on. This report is fairly long but I hope it helps others who might be thinking of using PGF2. These are my results so take them for what they are. I started on the 13/01/99 with my first injection of 1/2 a mg of diniprost (pgf2); each 1-ml of Lutalyse contains 5mg of diniprost (pgf2). I used a 22Ga*3/4 needle, you should use insulin pins, which I will use when I get some. As with any new drug that you inject, I was careful not to use too much just in case I had a bad reaction to it, also I was shitting myself just like the first time with DNP! I injected into the bicep so I would know how painful this stuff really is. As soon as I started to inject, the pain started. If you could imagine your most painful injection, this is what it’s like every time you use it. I had no bad reactions or the side effects, so I thought "that what does not kill you makes you stronger". The next day I intended to use 8mg,so I started with 2mg in each leg, 10 minutes after injection I started to feel my chest and throat tighten so I used my Ventilin inhaler and this really did help. It still was not a pleasant feeling but I had it under control. A few moments later, the
muscle spasms started in my intestines and bowels. The pain was not too bad, but I didn’t like the short stabs of pain my abdominal area was giving me so I quickly took one of my anti-spasmodic diarrhea tablets. These started to kick in 10 minutes later and all you get is a dull sensation of the
pain. I have used it for 4 days now and I have not had the shits once. All you get is a little bit more wind. If your going to use pgf2, I would recommend using the drugs I have stated. They really worked wonders for me! As for training I didn’t feel it effected me at all apart from the fucking great pumps it gives you. Your muscles feel nice and hard all day even when you wake up, just like a good cycle of steroids would give you. I have been on for 4 days now, so I’ll give you my opinion; both-- good and bad.
The bad side is the side effects, which I dealt with pretty well; the worst problem is the amount of injection you have to do in a day. I solved this by injecting 2 or 3ml at a time in each muscle, say for example you injected in your legs. Do 2 or 3ml in each leg. This saves time and pain, because I don’t want to be a slave to the needle. I found its best to inject first thing in the morning and last thing at night when you have not got much food in your digestive system. Any injections in the day are a bonus, you have to be practical about this because most of us have to go work in the day and it’s hard to find time to inject. Some might say you are not going to get the best out of pgf2 doing it this way but this is the practical way. If you can stand injecting 7 or 8 times a day fine, but you must like the fucking pain, because this stuff makes your muscle throb with pain for about an hour, and then it goes away after a day. I felt the rise in my body temperature and it did feel like I was on DNP. But this only lasted for about an hour. Maybe my temperature was still
elevated for a few hours more but this was no problem. PGF2 has got to go along way to beat DNP in the race for the nastiest drug of all time, but its close. The reason I could inject so much into my system at once was because I was using my drug stack to help negate the side effects. The good side has yet to be seen but I am very confident this stuff will work. Remember I’m still learning every day!
TRANSDERMAL PGF2a
The experiment I’m doing now is to use PGF2 transdermally. The insert to Lutalyse (pgf2) states that you should take extreme caution when handling Lutalyse as it can easily be absorbed through the skin. So I thought that maybe it could be applied to the skin without injecting. But as PGF2 has a half-life of around 10 minutes, it might not reach your muscles in time to do its work. But maybe it would be a better fat burner when applied transdermally, as PGF2 is supposed to kill fat cells when it comes in contact with them. I’m applying 2mg of PGF2 with Duchaines "Yo-Be-Lean"; I’ve been rubbing this mixture into my abdominal area until it all disperses. When I apply the mixture the area becomes very hot for 10 to 20 minutes, yohimbe and PGF2 seems like its working and the theory sounds pretty good but I will tell you if its worked after I have given it about a month. If anyone has any better ways to improve this mixture in any way please post here and
tell me what you think. Maybe it will turn out to be a load of bull but who knows?
REPORT 3
After nearly two weeks on, I’m very, very pleased with the results. I’m not taking any steroids or
creatine, and I have not changed my diet in any way. My actual body weight gain has been nearly 5 pounds of muscle as far as I can tell. What with the constant pump I get, my overall appearance has improved greatly. I am using up to 2mg in each body part at a time for a total of 8mg a day. I have tried going higher but 2mg at a time are my limit in any one sight of injection. The body parts that have been hit the most have improved to no end. The improvement is ver visible. This stuff does not take weeks or months to work, it starts right away, and if you can live with the side effects this is worth trying. On the subject of transdermal PGF2a, I am still not sure the PGF2a gets to the muscle before it’s out of the body. This is why I sent e-mail to Dharkham asking this same question. I’m still waiting for a reply. If anyone wants any info on how to use or obtain PGF2a, e-mail me and I will try to answer you.
REPORT 4
To recap things; on the 13/01/99 I started using PGF2a, my starting body weight was 221 pounds. After nearly 2 weeks of use, I was up 5 pounds. My report follows from here. As of 31/01/99 my body weight is 238 pounds, that’s 17 pounds of body weight gain in 17 days! As fucking amazing as it sounds, I began to notice all of this weight was not muscle, but a slight retention of water under the skin. I still got those great pumps you get from using pgf2a, maybe this is why? For the last two weeks, I had been using 10mg of pgf2a a day. The side effects seem to becoming less and less every time I use it. Or maybe I do not notice it so much? I experimented with a few
things as well, such as injecting a body part in the morning and training it that same night. I had no problems with this at all, if anything, I got a better work out because I could feel the muscle better. I’m not saying it does not hurt but it’s a pain I can live with and if you cannot stand a bit of pain in your workouts, then don’t use pgf2a, simple. I also injected straight after training and
still had no problems with the pain, these sensations only last about an hour anyway. I feel this is the best way to take pgf2a as your getting this growth promoter in the place where it’s needed the most, in the trained muscle. This is what I found and the next man might have different results but I found it OK. Other observations that I noticed apart from the slight water retention (maybe this is a one off and will not happen to you) was that it gave me amazingly hard erections, not a bad side effect if you ask me! I know Dharkham states in his article that people using steroids and pgf2a have to cut back on their poundage but, because I have been off for quite awhile now, my strength gains seemed to increase with pgf2a use.
All right, this is where the fun begins. On the 31/01/99 I decided to go on a weeks diet to see what actual muscle gains I had made. I went on the loose theory that if all the weight I had gained was mostly water; I would have a body weight under that than which I had started on 13/01/99. When I diet, I go for it 100%. I use everything in my power to lose those pounds of fat. Here is the list of supplements that I used:
400MG OF DNP EVERY NIGHT BEFORE BED.
YO BE LEAN+5MG OF PGF2A RUBBED ON MY ABS AND LOWER BACK EVERY NIGHT (THIS
REALLY DID VISIBLY WORK IN MY OPINION).
E/C STACK TWICE ADAY WITHOUT THE ASPIRIN (THIS HARMS THE EFECTIVENESS OF
THE PGF2A).
AND THE GREAT NEW DIET BY "ANIMAL"--ANIMALOBOLICS, IN A NUTSHELL YOU TRAIN
THE NIGHT BEFORE THEN RELOAD WITH CARBS STRAIGHT AFTER YOUR WORKOUT, THEN CARB DEPLETE UNTIL THE NEXT NIGHT. ONLY TAKING PROTEIN AND FATS. NOT EVER RAISING YOUR INSULIN LEVELS SO YOU KEEP IN LIPOSIS.
If you want more info on this fucking brilliant way to diet look on the "underground library message board", it’s well worth the read. And I cannot possibly do justice to it in a few lines of words. All right let’s get back to the diet. I weighed myself this morning and had a very pleasant surprise. I scaled in at 228 pounds of lean body weight. As I had hardly any carbs in my system or the water weight, which comes with carb stores, I had gained 7 pounds of lean body mass since my pgf2a experiment. So when I ingest carbs again and rehydrate my muscles, this figure will go
up. I am very, very pleased with the look that pgf2a has given me. I will continue to use pgf2a to gain muscle and hardness. I cannot wait to try a mild cycle with this stuff; God knows how much muscle you can gain? I will report back next issue, as I do not know if I will do another weeks diet
or not. I only intended to do one week but the ease of animals diet has made me want more. It’s the best diet I have been on ever! I’m still working on a new supplement to take with your pgf2a which stops calcium leaks in your muscles which should equate to less muscle being broken down when you train. See ya
THE ENGLISHMAN
i know there is one that ranger did as well, but can not find it yet
Moderator
(Total posts: 39) posted January 12, 2000 06:27 PM
--------------------------------------------------------------------------------
Here is a good PGF-2 article that came from the Underground Supplements Newsletter. i hope this helps.
There is quite a bit of interest in PGF2 right nowise I will clear a few things up first. I get my Lutalyse from a friend who is vet, I can only get personal use for the moment but will look into things further if there is a demand, this is a big if? I don’t even know if it’s on any banned lists in
My own country let alone the U.S.A. My stats are as follows on the 13/01/99: weight: 221 pounds fat: round about 10/11% height: 6ft 2in I will start of with 2mg a day and build up too 8mg.
As a few of you have shown interest in my real life trials with PGF2, I will report every week and tell you how I’m getting on. This report is fairly long but I hope it helps others who might be thinking of using PGF2. These are my results so take them for what they are. I started on the 13/01/99 with my first injection of 1/2 a mg of diniprost (pgf2); each 1-ml of Lutalyse contains 5mg of diniprost (pgf2). I used a 22Ga*3/4 needle, you should use insulin pins, which I will use when I get some. As with any new drug that you inject, I was careful not to use too much just in case I had a bad reaction to it, also I was shitting myself just like the first time with DNP! I injected into the bicep so I would know how painful this stuff really is. As soon as I started to inject, the pain started. If you could imagine your most painful injection, this is what it’s like every time you use it. I had no bad reactions or the side effects, so I thought "that what does not kill you makes you stronger". The next day I intended to use 8mg,so I started with 2mg in each leg, 10 minutes after injection I started to feel my chest and throat tighten so I used my Ventilin inhaler and this really did help. It still was not a pleasant feeling but I had it under control. A few moments later, the
muscle spasms started in my intestines and bowels. The pain was not too bad, but I didn’t like the short stabs of pain my abdominal area was giving me so I quickly took one of my anti-spasmodic diarrhea tablets. These started to kick in 10 minutes later and all you get is a dull sensation of the
pain. I have used it for 4 days now and I have not had the shits once. All you get is a little bit more wind. If your going to use pgf2, I would recommend using the drugs I have stated. They really worked wonders for me! As for training I didn’t feel it effected me at all apart from the fucking great pumps it gives you. Your muscles feel nice and hard all day even when you wake up, just like a good cycle of steroids would give you. I have been on for 4 days now, so I’ll give you my opinion; both-- good and bad.
The bad side is the side effects, which I dealt with pretty well; the worst problem is the amount of injection you have to do in a day. I solved this by injecting 2 or 3ml at a time in each muscle, say for example you injected in your legs. Do 2 or 3ml in each leg. This saves time and pain, because I don’t want to be a slave to the needle. I found its best to inject first thing in the morning and last thing at night when you have not got much food in your digestive system. Any injections in the day are a bonus, you have to be practical about this because most of us have to go work in the day and it’s hard to find time to inject. Some might say you are not going to get the best out of pgf2 doing it this way but this is the practical way. If you can stand injecting 7 or 8 times a day fine, but you must like the fucking pain, because this stuff makes your muscle throb with pain for about an hour, and then it goes away after a day. I felt the rise in my body temperature and it did feel like I was on DNP. But this only lasted for about an hour. Maybe my temperature was still
elevated for a few hours more but this was no problem. PGF2 has got to go along way to beat DNP in the race for the nastiest drug of all time, but its close. The reason I could inject so much into my system at once was because I was using my drug stack to help negate the side effects. The good side has yet to be seen but I am very confident this stuff will work. Remember I’m still learning every day!
TRANSDERMAL PGF2a
The experiment I’m doing now is to use PGF2 transdermally. The insert to Lutalyse (pgf2) states that you should take extreme caution when handling Lutalyse as it can easily be absorbed through the skin. So I thought that maybe it could be applied to the skin without injecting. But as PGF2 has a half-life of around 10 minutes, it might not reach your muscles in time to do its work. But maybe it would be a better fat burner when applied transdermally, as PGF2 is supposed to kill fat cells when it comes in contact with them. I’m applying 2mg of PGF2 with Duchaines "Yo-Be-Lean"; I’ve been rubbing this mixture into my abdominal area until it all disperses. When I apply the mixture the area becomes very hot for 10 to 20 minutes, yohimbe and PGF2 seems like its working and the theory sounds pretty good but I will tell you if its worked after I have given it about a month. If anyone has any better ways to improve this mixture in any way please post here and
tell me what you think. Maybe it will turn out to be a load of bull but who knows?
REPORT 3
After nearly two weeks on, I’m very, very pleased with the results. I’m not taking any steroids or
creatine, and I have not changed my diet in any way. My actual body weight gain has been nearly 5 pounds of muscle as far as I can tell. What with the constant pump I get, my overall appearance has improved greatly. I am using up to 2mg in each body part at a time for a total of 8mg a day. I have tried going higher but 2mg at a time are my limit in any one sight of injection. The body parts that have been hit the most have improved to no end. The improvement is ver visible. This stuff does not take weeks or months to work, it starts right away, and if you can live with the side effects this is worth trying. On the subject of transdermal PGF2a, I am still not sure the PGF2a gets to the muscle before it’s out of the body. This is why I sent e-mail to Dharkham asking this same question. I’m still waiting for a reply. If anyone wants any info on how to use or obtain PGF2a, e-mail me and I will try to answer you.
REPORT 4
To recap things; on the 13/01/99 I started using PGF2a, my starting body weight was 221 pounds. After nearly 2 weeks of use, I was up 5 pounds. My report follows from here. As of 31/01/99 my body weight is 238 pounds, that’s 17 pounds of body weight gain in 17 days! As fucking amazing as it sounds, I began to notice all of this weight was not muscle, but a slight retention of water under the skin. I still got those great pumps you get from using pgf2a, maybe this is why? For the last two weeks, I had been using 10mg of pgf2a a day. The side effects seem to becoming less and less every time I use it. Or maybe I do not notice it so much? I experimented with a few
things as well, such as injecting a body part in the morning and training it that same night. I had no problems with this at all, if anything, I got a better work out because I could feel the muscle better. I’m not saying it does not hurt but it’s a pain I can live with and if you cannot stand a bit of pain in your workouts, then don’t use pgf2a, simple. I also injected straight after training and
still had no problems with the pain, these sensations only last about an hour anyway. I feel this is the best way to take pgf2a as your getting this growth promoter in the place where it’s needed the most, in the trained muscle. This is what I found and the next man might have different results but I found it OK. Other observations that I noticed apart from the slight water retention (maybe this is a one off and will not happen to you) was that it gave me amazingly hard erections, not a bad side effect if you ask me! I know Dharkham states in his article that people using steroids and pgf2a have to cut back on their poundage but, because I have been off for quite awhile now, my strength gains seemed to increase with pgf2a use.
All right, this is where the fun begins. On the 31/01/99 I decided to go on a weeks diet to see what actual muscle gains I had made. I went on the loose theory that if all the weight I had gained was mostly water; I would have a body weight under that than which I had started on 13/01/99. When I diet, I go for it 100%. I use everything in my power to lose those pounds of fat. Here is the list of supplements that I used:
400MG OF DNP EVERY NIGHT BEFORE BED.
YO BE LEAN+5MG OF PGF2A RUBBED ON MY ABS AND LOWER BACK EVERY NIGHT (THIS
REALLY DID VISIBLY WORK IN MY OPINION).
E/C STACK TWICE ADAY WITHOUT THE ASPIRIN (THIS HARMS THE EFECTIVENESS OF
THE PGF2A).
AND THE GREAT NEW DIET BY "ANIMAL"--ANIMALOBOLICS, IN A NUTSHELL YOU TRAIN
THE NIGHT BEFORE THEN RELOAD WITH CARBS STRAIGHT AFTER YOUR WORKOUT, THEN CARB DEPLETE UNTIL THE NEXT NIGHT. ONLY TAKING PROTEIN AND FATS. NOT EVER RAISING YOUR INSULIN LEVELS SO YOU KEEP IN LIPOSIS.
If you want more info on this fucking brilliant way to diet look on the "underground library message board", it’s well worth the read. And I cannot possibly do justice to it in a few lines of words. All right let’s get back to the diet. I weighed myself this morning and had a very pleasant surprise. I scaled in at 228 pounds of lean body weight. As I had hardly any carbs in my system or the water weight, which comes with carb stores, I had gained 7 pounds of lean body mass since my pgf2a experiment. So when I ingest carbs again and rehydrate my muscles, this figure will go
up. I am very, very pleased with the look that pgf2a has given me. I will continue to use pgf2a to gain muscle and hardness. I cannot wait to try a mild cycle with this stuff; God knows how much muscle you can gain? I will report back next issue, as I do not know if I will do another weeks diet
or not. I only intended to do one week but the ease of animals diet has made me want more. It’s the best diet I have been on ever! I’m still working on a new supplement to take with your pgf2a which stops calcium leaks in your muscles which should equate to less muscle being broken down when you train. See ya
THE ENGLISHMAN
i know there is one that ranger did as well, but can not find it yet
1abbig
New member
here is some info from Macro
By Bryan Haycock CSCS
Introduction
In the January 1st issue of Mesomorphosis (Volume 2, Number 1 1999), we 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’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.
--------------------------------------------------------------------------------
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.
--------------------------------------------------------------------------------
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 (GDF8). 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.
------------------
MP
By Bryan Haycock CSCS
Introduction
In the January 1st issue of Mesomorphosis (Volume 2, Number 1 1999), we 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’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.
--------------------------------------------------------------------------------
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.
--------------------------------------------------------------------------------
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 (GDF8). 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.
------------------
MP
Italianboy
New member
Hey buddy,how much you kept from it?I've started to use it but i can't suffer any longer...and somebody said that all the results are momentary.Scotsman said:
I can get it at a great price(20$for 30ml) and if you say it is worth,I'll go on again soon
Willyumyum
New member
Here's a excerpt from an article on gear from testosterone.net:
Lutalyse? More like Loserlyse
Hey, man, what do you think of spot injections of Lutalyse for stubborn areas? I hear it's the bomb. Of course, it makes you feel like shit, but it's not dangerous, is it?
"Arrggghhh! Lutalyse is a veterinary drug that's coming into vogue with serious hardcore bodybuilders who'll stop at nothing to gain an "advantage" (even if it's not a real advantage). Lutalyse is made by Upjohn and is a prostaglandin (PGF2Aa).
PGF2a possibly mediates the endogenous insulin levels and is also a de facto thermogenic, as body temperature is increased after the administration of exogenous PGF2a. Unlike other fat burners, which only decrease the size of fat cells, PGF2a actually destroys them. Fat cells die when exposed to PGF2a.
Side effects associated with PGF2a use are an elevation in body temperature, vomiting, labored breathing and severe abdominal pain/cramping. As PGF2a vasoconstricts the blood vessels in the lungs, the user will feel a tightening in the chest. If you're an asthmatic, use of PGFa could very well put you into full respiratory arrest followed by death. Because PGF2a increases insulinogenic effects, hypoglycemia is a potential side effect.
PGF2a has a very short half-life in the body (only minutes) and most of it is metabolized in the lungs, thus making frequent injections necessary. PGF2a will almost always cause a very strong contraction of the intestine and bladder, emptying the stomach and intestines of all its contents. That's a nice way of saying you'll have explosive diarrhea.
Rumor has it that PGF2a will make training near impossible because of the pump that is created from this drug alone. One of the logistical drawbacks of PGF2a is the difficulty of administration. As it has such a short half-life, injections will be needed quite frequently. Lutalyse comes in a 5 ml (5 mg/ml) multi-dose vial. A single aspirin can render the effects of Lutalyse nonexistent, so most people who use this drug avoid aspirin and aspirin analogs.
Legit use of Lutalyse is by "Farmer Joe." Farmers and ranchers will use this drug to induce abortions in barnyard animals. One-hundred percent of the idiots, uh, I mean, users, I spoke with told me that Lutalyse made them feel terrible. In short, this stuff could kill you, a lot faster that steroids ever could. I wouldn't suggest anyone try this stuff.
Look, if you're an IFBB professional, you certainly don't want or need my advice. But if you're an average person looking to pack on some mass, this is just not worth the risks. Interleukin-15 and Epidural Growth Factor are peptide hormones that are also emerging as "noveau drugs" for the bodybuilding elite. Only a person with a death wish would try either of them (or Lutalyse)."
so basically... don't use it unless you wanna risk dying and/or an assload of pain...
YUM
Lutalyse? More like Loserlyse
Hey, man, what do you think of spot injections of Lutalyse for stubborn areas? I hear it's the bomb. Of course, it makes you feel like shit, but it's not dangerous, is it?
"Arrggghhh! Lutalyse is a veterinary drug that's coming into vogue with serious hardcore bodybuilders who'll stop at nothing to gain an "advantage" (even if it's not a real advantage). Lutalyse is made by Upjohn and is a prostaglandin (PGF2Aa).
PGF2a possibly mediates the endogenous insulin levels and is also a de facto thermogenic, as body temperature is increased after the administration of exogenous PGF2a. Unlike other fat burners, which only decrease the size of fat cells, PGF2a actually destroys them. Fat cells die when exposed to PGF2a.
Side effects associated with PGF2a use are an elevation in body temperature, vomiting, labored breathing and severe abdominal pain/cramping. As PGF2a vasoconstricts the blood vessels in the lungs, the user will feel a tightening in the chest. If you're an asthmatic, use of PGFa could very well put you into full respiratory arrest followed by death. Because PGF2a increases insulinogenic effects, hypoglycemia is a potential side effect.
PGF2a has a very short half-life in the body (only minutes) and most of it is metabolized in the lungs, thus making frequent injections necessary. PGF2a will almost always cause a very strong contraction of the intestine and bladder, emptying the stomach and intestines of all its contents. That's a nice way of saying you'll have explosive diarrhea.
Rumor has it that PGF2a will make training near impossible because of the pump that is created from this drug alone. One of the logistical drawbacks of PGF2a is the difficulty of administration. As it has such a short half-life, injections will be needed quite frequently. Lutalyse comes in a 5 ml (5 mg/ml) multi-dose vial. A single aspirin can render the effects of Lutalyse nonexistent, so most people who use this drug avoid aspirin and aspirin analogs.
Legit use of Lutalyse is by "Farmer Joe." Farmers and ranchers will use this drug to induce abortions in barnyard animals. One-hundred percent of the idiots, uh, I mean, users, I spoke with told me that Lutalyse made them feel terrible. In short, this stuff could kill you, a lot faster that steroids ever could. I wouldn't suggest anyone try this stuff.
Look, if you're an IFBB professional, you certainly don't want or need my advice. But if you're an average person looking to pack on some mass, this is just not worth the risks. Interleukin-15 and Epidural Growth Factor are peptide hormones that are also emerging as "noveau drugs" for the bodybuilding elite. Only a person with a death wish would try either of them (or Lutalyse)."
so basically... don't use it unless you wanna risk dying and/or an assload of pain...
YUM
Last edited:
Scotsman
New member
The gains I saw weren't awe inspiring but it definately help lagging body parts to catch up quickly. Also since pgf2 eliminates fat cells the leaness of the injection area helps bring out muscle detail. In my opinion it is great to use from time to time to help with leaness and muscle detailing. Though you won't see tremendous size gains from using it on its own. If you can tolerate the burning and shortness of breath and all the other wonderful post injection happenings the carry on. I like using it and will continue to do so.
