Banned
Okay I was reading some of these articles tonight and it COMPLETELY went against everything you guys have said on this board and it made me mad and want you to check it out because its ridiculous uneducated people read this and act on it. Not every article is BS but most are, you kinda gotta read through em.
no links
Last edited by EternalStud; 06-17-2010 at 01:01 AM.
Anabolic Voice of Reason
I assume you had some links up, but then realized you cant do that, right?
Correction, guess not...
-Please, no outside links
~Retired~ AR-Platinum Elite-Hall of Famer ~
No links pls
Banned
gotcha....can i just post the articles?Originally Posted by marcus300
~Retired~ AR-Platinum Elite-Hall of Famer ~
Yes you can copy and paste the actual article so long as it doesnt have any links to other BB sites.
Banned
okay awesome....you should take a look at these marcus, very strange and makes little sense....im posting as you read this
Banned
Clenbuterol and Muscle Growth: A New Approach
by Dharkam
Molecular Nutrition Lipid Stabil
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.
I still remember when Clenbuterol was the new wonder drug.
"You know, my rat seems to respond very well to this new stuff."
"Oh, which one?"
"You know this new stuff, Cle something."
"Clenerol, ... no, Clenbuterol. I don’t know why I cannot remember that name"
The friend talking to me was in the habit of trying each new drug or new stack on a rat that he would buy for the occasion, as an experiment before he tried the substances himself. I guess it was his way of being careful.
Clenbuterol (Clen) was supposed to be an incredibly anabolic, non-hormonal compound. Furthermore, it could destroy fat like nothing else. A new category of drugs had just emerged: the repartitioning agents. What a brilliant concept! We could replace fat by muscles after all!
Now, more than 10 years later, while Clenbuterol has not lived up to initial expectations, it is still used extensively in bodybuilding circles. Why? I think it’s time for a review in depth of this drug’s properties and effects. What I am going to reveal may seem very strange, but everything is based on the fact that I have seen kilos of this stuff being swallowed voraciously or injected by eager bodybuilders (not all at once, of course).
Is Clenbuterol a non-hormonal drug?
This was the pitch with Clenbuterol: it was supposed to be a repartitioning agent, not a hormone. I guess the idea came from the fact it was not a steroid and not related to testosterone in any way. Many drug free bodybuilders bought that idea and started using drugs with the help or because of Clenbuterol. Clenbuterol is indeed very closely related to hormones called catecholamines. The best known catecholamines are adrenaline and noradrenaline (a.k.a epinephrine and norepinephrine). So, taking Clenbuterol is a bit like using those hormones except that Clen acts mostly on beta adrenergic receptors and not on alpha adrenergic receptors. Adrenaline and noradrenaline act on both kinds of adrenoceptors. Clen is therefore a beta agonist (beta 2 to be more specific).
Is Clenbuterol anabolic?
The popularity of Clenbuterol came from the amazing muscle building action experienced on some animals. Clen has the ability to quickly and strongly stimulate the muscle protein synthesis processes. It is more potent even than anabolic steroids. Our high hopes with Clen rapidly faded away and were replaced by deep disappointment. We all hoped that something with, less side effects could have replaced the anabolic steroids. Also, Clen arrived when drug testing began to be implemented in bodybuilding. It seemed that a good way to beat the test was to use this magical Clen (it was not yet on the doping list). It is sad but true: Clen has a very low muscle building capacity in humans. Why? And if so why is it still popular?
Does Clen act on beta 2 receptors?
If Clen is a true beta 2 receptor agonist, there is no reason for it not to be anabolic. Human muscles are full of beta 2 receptors ready to react under the order of Clenbuterol. Intense exercise can increase the beta 2 receptor density in muscles, creating a potential synergy. This would mean that training should increase the muscle sensitivity to Clen. The problem is, such results have not been observed, even in animals. In fact, animals given Clenbuterol and then intensively trained show very poor results. Later researchers demonstrated that the muscle building properties of Clen were not derived from a specific activation of beta 2 adrenoceptors as previously thought. Rather, Clen acts on a still unidentified atypical beta receptor. Then, it was thought that Clen would act on the newly discovered beta 3 receptors. Next, action on beta 4 was hypothesized. Both proved to be wrong as far as anabolism is concerned. In order to explain the lack of effect of Clen on anabolism in humans I think it is safe to conclude that we do not possess a significant amount of those atypical beta receptors in our muscles.
Of course, animal studies were performed with huge dosages starting with a rough equivalent of 50-60 tablets of 20 mcg a day. But even in increasing the dosages close to unsafe amounts (using a beta 1 receptor antagonist to minimize the side effects of Clen on the heart), no one ever experienced the strong anabolic action of Clen. And this is not due to a lack of candidates willing to try. We should congratulate those kamikazes as it is thanks to them that major muscle building breakthroughs are revealed.
Some human studies have shown a mild and transient anabolic action of catecholamines. Eating proteins do that too, but believe me it is not with this sort of mild anabolic effect that your muscles are going to be visibly bigger.
Is Clen anti-catabolic?
Controversy still remains as to the capacity of Clen to mediate muscle growth, because of a strong anabolic or a potent anti-catabolic action. If Clen is not anabolic in humans, is it at least anti-catabolic? The answer is yes and no. Let me explain: if you are eating normally, I doubt that Clen exerts any significant anti-catabolic action. In fact, Clen is probably more catabolic than anti-catabolic at high dosages. However, when you’re on a low calorie diet, things are very different, and Clen is then truly an anti-catabolic drug. It may sound paradoxical but it is not at all.
When on a restrictive diet, the main problem for our body is to use the fat from the adipose tissue as energy in order to make up for the caloric deficit. In bodybuilders, this pathway is very inefficient. We eat a high carb diet all year long, which means we train our body to selectively use carbs at the expense of fat. On a diet, our body has not been trained to use fat instead of carbs. It is still good at using carbs and bad at burning fat. So, instead of using fat as energy our body uses a second best source of energy: proteins. And where are those proteins coming from, from our muscles, which are perceived as a protein reserve while we are on a diet. Our muscles shrink while fat remains stuck.
This is where Clen comes in. Clen is able to help our body uses its own fat as energy instead of muscle proteins. The fat burning process is accelerated which mechanically spares our muscles mass. At the end of the diet, thanks to a quicker and more efficient fat usage, we end up leaner and bigger. Not bigger compared to what we were before the diet but bigger compared to what we would have been at the end of the same diet without the Clen. It depends on the length and the severity of the diet, but Clen can make a difference of several kilograms, which is remarkable. Growth Hormone is popular before a competition for the very same reason: it renders the diet both easier and far more effective, preventing excessive muscle shrinkage. For those who still insist that it is possible to diet without sacrificing a significant amount of muscle mass, please take a long look at Dorian Yates' book "Blood and Guts". Before and after pictures are shown while he is on a diet. An expert eye will see that many pounds of pure beef were lost while the amount of fat he got rid of is limited. This is what happens when you get shredded, even if you’re the best in the world (Of course, by diet I don’t mean shedding five pounds before the holidays. I mean a real, shredding diet).
Please understand that this anti-catabolic action of Clen is indirect and will therefore not help you get bigger while you are NOT on a diet. This is why I say Clen can exert some anti-catabolic action or none at all.
Is Clen catabolic? Can this actually help us grow?
This may sound even stranger after what I just said but Clen can truly be a catabolic drug, too. At low dosage, it will go unnoticed. But past a certain amount (equivalent of 15-20 tablets of 20 mcg) chances are you are going to get sore by using Clen. Scientific research in humans demonstrates a potent catabolic effect of Clen as reflected by a rise of serum creatine kinase level. This means that Clen is attacking our muscle cells a bit like heavy training does.
Sound bad?
No!
Is it of any use for bodybuilders? Yes!
For "drug free" bodybuilders, it means that you have got to stay away from this high dosage of Clen. On the other hand, for steroid users, it is unfortunately a very interesting property. Ten years ago, I would not have made such a statement. Almost all the anabolic steroids were still available and one could choose the ones that suited him best. Saying that such a choice does not exist anymore would be an understatement. Prices and availability are inversely progressing. Testosterone is again the steroid of choice (because of a lack of choice). The main problem with testosterone is that after a while a user experiences more and more trouble getting sore while on it. Of course, it depends on the dosage and the capacity of the user to transform the male hormone into female hormones (aromatization).
You see, estrogens protect our muscles from damage. This is good in every sport except bodybuilding. Potent anti-aromatase drugs do exist but their prices prohibit their use. Tamoxifen (Nolvadex) will exert an estrogen-like activity on muscle (and fat too) in many people, which is going to reduce their capacity for muscle growth while helping them to get fat.
Why do we want some muscle damage to occur because of training, simply, because our muscle cells are internally able to manufacture very potent growth factors such as IGF, FGF, Prostaglandins and probably GH too, in case of damage. The more steroids one uses, the higher this manufacturing capacity should be. Furthermore, steroids increase the muscle’s sensitivity to the anabolic actions of those growth factors. This is a shame, since most of those growth factors will only be released (and therefore become active) if the muscle membrane experiences some damage. Training acts like a robber who opens the vault where the growth factors are hidden. Because of the estrogens, this beneficial effect of training is attenuated. Clen can act like this robber to unleash the growth factors. How do we manage this?
Once all the growth factors are released, growth will take place, repairing the damage and inducing a hypertrophic response on top of this. On the other hand, the muscle capacities to reproduce extra amounts of growth factors will be impaired for a short while. Steroids will accelerate recovery from this shortage.
But it means that the high doses of Clen have to be used sporadically, I would say about once a week. It has to be coupled with a traumatic workout on a body part where you want to accelerate growth. You also need to rotate those body parts in order to make sure the restoration of the manufacturing capacities in one muscle is complete before triggering a new release. For example, one week you can train your back in a traumatic fashion (using heavy weights along with forced and negative reps in movements that end with a strong stretch). Next week, do the legs. The following week, it can be chest... The pain due to the soreness will be intense but it will be rewarded by rapid growth. Therefore, the catabolic actions of Clen can be used to trigger growth, but only in synergy with steroids. If you follow this procedure, make sure you use massive amounts of proteins and amino acids, especially BCAA and taurine. Clen will accelerate their destruction and you do not want to experience a shortage in either one.
Banned
Forward: This two-part series introduces a secret anabolic agent which has been used by elite European athletes for a few years. We present the series for information only. Nothing in this series is intended to take the place of advice from a licensed health professional. Consult a physician before taking any medication.
Whenever steroids are discontinued, the muscles tend to shrink. It can be discouraging to see gains in strength and size, won at such a cost, dwindle away. Cycle after cycle, only a fraction of all your gains will be added while the side effects and the risks to your health continue to multiply. It is time we put an end to this vicious cycle.
Why do muscles shrink after a cycle?
Last month, we saw that when steroids are stopped, your natural testosterone level is likely to be lower than normal while your muscles are less responsive to the anabolic effects of androgens. As a result, muscle protein synthesis rate will be depressed. Since muscles are subjected to a constant basal protein degradation, anabolism will be lower than catabolism. Training can actually make this worse by increasing the degradation rate. The result will be a non-renewal of the muscle's contractile proteins. In simple terms, muscle mass will slowly shrink.
Is fighting catabolism the answer?
If muscle protein synthesis rate is depressed, one way to hold on its mass is to attempt to reduce the rate of degradation so that it is equal to or lower than anabolism. This is not an ideal solution, but we have to use all the tools available while we are waiting for a rebound of anabolism. So our task is to attack the main proteolytic (protein-destroying) pathways.
How does muscle breakdown occur?
The most up-to-date theory concerning muscle breakdown involves two distinct steps. First, calcium-dependent proteases called calpains are upregulated by the calcium leaks induced by training. Each of our muscle cells hold on calcium in small pockets called sarcoplasmic reticulum. It is the rapid entry and exit of calcium from the sarcoplasmic reticulum which induces muscle contractions. Repeated contractions induce an impairment of this highly regulated calcium movement. Calcium accumulates inside the cell rather than in its sarcoplasmic reticulum reserve. The first consequence of this loss of homeostasis is the reduction of strength experienced as sets accumulate. The second long term consequence is the upregulation of the activity of calpain. Calpain in turn cuts out large chunks of myofibrils that are called easily releasable myofilaments. This is for the first act.
Second act: Those large pieces of muscle cells will then be attacked by another proteolytic mechanism called the ATP-dependent ubiquitin-proteasome pathway. Ubiquitin is only a marker which detects abnormal, denatured or damaged muscle proteins such as the easily releasable filaments. Then, the proteasome is attracted by these marked proteins because of their association with ubiquitin. Once attacked by the proteasome, a damaged protein is digested into single amino acids ready to be recycled as raw materials for muscle rebuilding or more likely as waste products such as urea. Needless to say, an intense workout rapidly increases the activities of both ubiquitin and the proteasomes.
I cannot stress enough the necessity of the large cuts to the myofibers for the ubiquitin and proteasome to act. If we can reduce the actions of the calpains, we can prevent the proteasome from acting. If the cleaving of muscle fiber doesn't take place, myofibers will be very resistant to the catabolic actions of the proteasome. On the other hand, a small break up of the contractile apparatus will markedly increase the likelihood of degradation by the proteasome. We should nonetheless also attempt to tame the activity of the proteasome. In this way we have two possible ways of acting to prevent catabolism. We'll combine them for maximum effect.
Dantrolene: The weapon against calpains.
We should first attempt to impair the normal functioning of muscle calpains. As calpains are activated by excessive calcium leaks, let's limit this leakage. Dantrolene is an oral drug which belongs to a class of medication called calcium channel blockers [1]. Dantrolene is the most muscle specific member of this class. This is why it is so popular among athletes. It is commonly used as a muscle relaxant. As intracellular calcium release is responsible for muscle contractions, inhibition of this release induces a relaxation of the muscles. This reduces the muscle's need for ATP, which allows a faster recovery of the training-induced diminution of the ATP "stores." By inhibiting the calcium release from the sarcoplasmic reticulum, Dantrolene will impair the normal activation of the calpains by training.
Dantrolene has two major flaws. First, it acts on every muscle and not only specifically on the trained muscles as we would wish for optimal effects. Second, as a muscle relaxant, it will reduce muscle strength if you are not extra careful about the intake timing and dosage. What you want is for Dantrolene to produce its magic right after but not during the workout. If your training lasts less than one hour, you can take Dantrolene before your workout. This way, the drug will kick in at the right time. If you train for more than an hour, it is best to take Drantrolene in the middle of your workout. Start with the 25 mg tablets and build up SLOWLY to the 200 to 300 mg per day. It is ideal if you work out at night as Dantrolene will help you to sleep (it is a relaxant). If you have to drive or to perform something which requires attention while you are supposed to be under the influence of this drug, please do not take it. However most people work out in the evening, so it should not be a problem. If you have to drive home after your workout, take Drantrolene right after your workout so that it kicks in while you are home ready to go to bed.
Dantrolene
Dantrolene (Click for info)
The Ubiquitin-Proteasome Inhibitors: The new kids on the block.
Now that we have impaired the "normal" activity of the calpains, let's act on ubiquitin. So far, the availability of the ATP-dependent ubiquitin-proteasome inhibitors is at best very limited. I am sure it will make you feel much better to learn that newer and more potent inhibitors will be available soon. But what can we do for now on? The most effective so far is a drug called Torbafylline [2]. Another good one is called Amrinone. Both are likely to be hard to get so I suggest a third one which is easier to obtain named Pentoxifylline. Though less potent than Torbafylline, Pentoxifylline will still reduce muscle protein catabolism through an impairment of the proteasome activity.
Some studies have shown that Pentoxifylline and Amrinone prevent the depression of anabolism in skeletal muscles during illness [3]. I would not count too much on this effect in the post-steroid period.
Pentoxifylline can be used in several forms. Injectable versions do exist but they are generally used as infusion. This form contains lots of water and little active ingredient, making it impractical to use. The oral versions exist in both normal and timed release forms. The latter is preferable. At 400 mg per tablet, you will need at the very least 4 to 6 per day. Although I have yet to see a side effect due to Pentoxifylline, start with only one tablet a day and build up from there.
Pentoxifylline
Pentoxifylline (Trental ®)
Insulin and the proteasome.
The anti-catabolic actions of insulin are well known. Insulin acts in part by altering the normal activity of the ubiquitin-proteasome pathway. We now start to uncover a sketch of a potent anti-catabolic stack as insulin will reinforce the favorable effects of Pentoxifylline.
Amrinone and fat loss.
Amrinone is not only a wonderful drug for muscles, it is also a magical molecule for fat loss. It is a specific phosphodiesterase III inhibitor. It is this very specific phosphodiesterase that insulin activates in adipose tissue to prevent fat loss. This means that by using Amrinone, you can lose bodyfat even while on insulin. Stacking Amrinone along with insulin allows you to decrease the catabolic activity of the ubiquitin-proteasome pathway while reducing the likelihood of gaining fat.
Clenbuterol and catabolism.
Several researchers have theorized that Clenbuterol induces muscle growth in animals by reducing protein degradation. In fact, one study demonstrated that Clen was able to reduce the expression of ubiquitin [4]. However a newer study shows that Clen was unfortunately also able to increase the activity of the proteasome. Those two mixed effects are likely to more or less cancel each other. By the same token, Clen was hypothesized to reduce the activity of calpains. I doubt this is true in humans as high doses of Clen increase soreness rather than reduce it, as it would be expected with a moderation of the activity of calpains. New studies support my observations as Clen was shown to increase the basal intracellular calcium leaks explaining why it can provoke muscle soreness at proper dosage with no training at all. As a result, I strongly encourage Clenbuterol users to stack it along with Dantrolene, Amrinone/Pentoxifylline and insulin for maximal effects on muscle mass.
Is there an effective and cheap alternative to boost anabolism?
Now that we have played on catabolic side of the muscle protein turnover, let's jumpstart anabolism. One of the most potent anabolic drugs is also the most neglected and the most despised. Steroids have been around for so many years that bodybuilders do not realize that they are in fact only minor anabolic drugs for muscles. Many other growth factors produced by the muscles themselves are far more potent.
Prostaglandins!
Lutalyse, 19KAmong 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! WARNING: 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.
PGF2a
PGF2 alpha Molecule
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.
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 steroids with PGF2?
If PGF2 is so powerful, why not stack it along with steroids 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. Steroids 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 steroids. 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 steroids along with PGF2. So it is best to use the prostaglandins to grow when you're off the steroids.
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.
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 steroid users...
PGF2 users: Healthy, who knows? Big and lean, yes!
Banned
Manipulating Dietary Cholesterol for Optimum Muscle Growth
by Dharkam
CEM-Meso.com
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.
Vince Gironda, the Iron Guru, used to recommend eating up to three dozen eggs a day in order to pack on mass fast. His rational was that the high cholesterol content would trigger a natural anabolic effect.
Ronnie Coleman, in his last video, Relentless, is taking a cholesterol lowering drug. Yet, such drugs are said to be detrimental to muscles.
Both behaviors seem contradictory!
* Is high or low cholesterol better for muscle growth?
* Why would anyone use a muscle wasting drug?
New research reconciles this paradox revealing that proper cholesterol manipulations can optimize muscle growth.
Acute training impact on cholesterol level
If moderate weight training does not seem to affect cholesterol levels, a traumatic workout will most definitely induce an acute reduction of blood cholesterol level within 2 hours (1). This shortage of cholesterol can last up to several days during the recovery phase. This lowering effect is due to an accelerated uptake of cholesterol by skeletal muscle. It reveals our fibers need this extra cholesterol in order to recover and grow.
Considering the positive impact of cholesterol on muscle growth (see below), it might be a good idea to include cholesterol-rich foods such as whole eggs in you first real post-workout meal. This strategy would make sure your muscles obtain all the cholesterol they need, preventing any potential shortage which would postpone recovery.
Dietary cholesterol intake on muscle growth
Riechman has studied the impact of cholesterol on (resistance) training-induced hypertrophy (2). This research has been conducted on elderly men and women, yet its findings seem relevant to younger subjects:
For 12 week, those people weight trained. When their daily cholesterol intake was inferior to 3.5 mg per kg of lean mass, no hypertrophy was detected. Strength only increased 36%. When their cholesterol consumption was above 5.7 mg/kg, muscle mass increased an average of 2.1 kg. Heavy cholesterol consumers experienced a strength increase of 86%.
Muscle growth and strength gains are closely related to dietary cholesterol intake. Considering a large egg contains around 200 mg of cholesterol, a 220 lbs bodybuilder would need at least 3 whole eggs a day.
Blood cholesterol level on muscle growth
Subjects with serum cholesterol lower than 178 mg/dl did not experienced much growth (+300 g of lean mass). When serum cholesterol was above 238 mg/dl, lean mass increased an average of 2.3 kg. The correlation between serum cholesterol and strength gains is statistically weaker. Subjects with low cholesterol level experienced an increase of 37% Vs 70% for subjects with high levels.
Muscle growth is positively correlated with blood cholesterol level.
Cholesterol lowering drugs on muscle growth
Statins are a class of drugs prescribed to lower the level of cholesterol in the blood. This class of drugs includes lovastatin (Mevacor), simvastatin, (Zocor), fluvastatin (Lescol), pravastatin (Pravachol), rosuvastatin (Crestor) and atorvastatin (Lipitor). The mechanism by which statins lower cholesterol is by blocking the enzyme in the liver, hydroxy-methylglutaryl-coenzyme A (HMCoA) reductase, responsible for producing cholesterol. Statin drugs lower total serum cholesterol levels, including HDL, as well as LDL levels.
Cholesterol intake and blood level represent two independent variables affecting hypertrophy. Subjects who responded the best to weight training were those consuming a cholesterol rich diet AND having a high blood cholesterol level AND using anti-cholesterol statin drugs. It is very surprising to discover that such drugs improved muscle gains as they are associated with myalgia, muscle weakness and muscle wasting in sedentary subjects.
Statin drugs accelerate muscle hypertrophy. The more we train, the more resistant our fibers get. It is increasingly difficult to damage them sufficiently to force them to grow. By rendering our fibers more fragile, statin drugs allow each rep to be more damaging to our muscles. As our muscles cannot seem to strengthen its fibers enough to counteract this fragilizing effect, they have no choice but to keep on growing.
Will cholesterol-related muscle catabolism favor growth?
I am not surprised that catabolic drugs facilitate muscle gains in trained subjects. I have already explained this paradox in a previously published clenbuterol article. Even cholesterol seems to enhance catabolism. Following an acute eccentric workout, soreness as well as strength loss are higher in young men consuming a whole egg diet rather than a low cholesterol diet (1). In response to this exacerbated catabolism, muscle strengthening is much more robust with the whole egg than with the white egg diet (1). This greater anabolic response explains the results observed on elderly. It also suggests that conclusions reached in older subjects apply to young men as well.
It may be important to note that if training-induced catabolism is enhanced by cholesterol lowering drugs, they also protect muscle cells from apoptosis (death) (3). This protective effect may facilitate an additional growth response.
Anabolic steroids and cholesterol
Anabolic steroids can either increase or decrease cholesterol levels depending on the choice of the drug as well as the individual response of the user. For example, orally active 17-alkylated anabolic-androgenic steroid are known to cause and undesirable reduction in HDL cholesterol levels. A severe reduction (which can go as low as having almost no cholesterol) is really bad for 2 reasons:
* Cholesterol is needed for muscle growth (as well as for general health). It is very hard to bring cholesterol production back up to normal even with discontinuation of the steroids.
* An increase in serum cholesterol levels would be a much better scenario as more cholesterol would be available for growth. It would also provide a good reason to get a prescription for the anti-cholesterol drug class of statins.
In conclusion:
* With regards to muscle hypertrophy, It is a good idea to follow a high cholesterol diet (at least 3 whole eggs a day).
* This is especially true if your training is both intense and traumatic.
* Be careful during a low calorie diet as cholesterol intake usually is reduced during this period.
* Cholesterol level tends to decline in summer, so be careful at that time, too.
* Whole eggs are very appropriate and recommended following a workout.
* Steroid users should closely monitor their blood cholesterol level as a decrease may reduce muscle growth.
* Steroid users with high cholesterol levels should consult a physician and may consider the use of statin drugs in order to grow even more rapidly.
References
1. Riechman SE. Dietary Cholesterol Alters Recovery from Eccentric Muscle Damage in Humans. Medicine & Science in Sports & Exercise: Volume 38(5) Supplement May 2006 p S386
2. Riechman SE. Dietary and blood cholesterol and statins increase hypertrophy with resistance training. FASEB J. 2005 19 A1571
3. Urso ML. Changes in ubiquitin proteasome pathway gene expression in skeletal muscle with exercise and statins. Arterioscler Thromb Vasc Biol. 2005 Dec;25(12):2441-4.
Banned
Dharkam's Way - The 'How-To" of PGF2
by Dharkam
CEM-Meso.com
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.
Let me begin by saying that I do not have the answers to many of the questions that you, readers, are asking me. I will try my best to address all of them even if I do not have the exact answer, by using common sense.
The how-to of PGF2
Q: How long should you use PGF2, do you cycle it or is there no need to come off it?
A: Bodybuilders are so used to steroid cycling that it is legitimate to wonder about the necessity of cycling PGF2. After more than 50 years of both continuous usage and scientific research, no one has been able to come up with a universal steroid cycling pattern that could suit everyone. Do not expect that after such a limited experience with PGF2, anyone could come up with an optimal cycling pattern. So let's look at a rational way of cycling. If you are off steroids for 2 months at a time, your PGF2 cycle should last 2 months in order to turn this potential wasting period into an opportunity to pack on lean muscle.
Another way of looking at PGF2 cycling is to use it for as long as you can stand it. PGF2 usage is not as comfortable as steroid use. Most bodybuilders are not motivated enough to inject several times a day for more than 60-90 days at a time. So, here is your cycle length. It is counterproductive for bodybuilders to use drugs reluctantly.
As far as the need to come off is concerned, there is as much need to come off prostaglandins as need to come off steroids. Although everyone should discontinue anabolics from time to time, most pros never do. If you use PGF2 just to look good on the beach, yes, you should come off. If you have to make a living from body, you may not have much choice.
Q: How long does it take to see the first results?
A: Cosmetically speaking, less than a week. Most of the early gains are due to the diuretic properties of prostaglandins. Then you realize that your muscles get very hard even when relaxed. To get a similar hardening effect, you would have needed quite a bit of steroids. You will also remark quickly that the overall shape of your muscles is much more pleasing. To understand what I mean, take a picture of yourself and compare it to the picture of a pro. You will notice that the pro's muscles are fuller and rounder. Again, you could duplicate this with long and heavy cycles of steroids. PGF2 simply speeds up this process. In one or two weeks of PGF2, you can achieve what could have taken one to two years of continuous steroids to obtain as far as muscle roundness is concerned.
Q: What sort of gains can I expect from the use of PGF2, and how much fat can I lose e.g. average man 200 pounds, bodybuilder, with a normal fat layer?
A: Please understand that PGF2 is not a weight gainer. The first use of steroids is usually associated with a tremendous weight gain. Most of it is due to water retention and often fat gains too. You can see this because steroids tend to blow up your face. Most bodybuilders' faces, offseason, look like a fish tank. They are usually very pleased with such impressive gains, but as they try to get rid of the water and the fat to regain a leaner appearance they realize that the net pure muscle gains while on steroids are more modest. This is why you cannot transform yourself into a new Yates with only a few cycles under your belt even if you gain 30 pounds each time.
With PGF2, you may gain 5 pounds of bodyweight. This certainly does not sound like a lot. But you have to add the two or three pounds of extra water you got rid of plus the fat you are shedding. In terms of pure bodyweight gain, this is not very impressive. On the other hand, packing on lean muscles and getting rid of the fat is a better and faster way to get to the top.
As far as fat loss is concerned, it depends of course of your diet and the other drugs you are using (i.e: insulin). It is hard to make any estimate as it is impossible to differentiate the water and the fat losses. Let's say that you can get rid of in between 5 to 10 pounds of water and fat in a matter of 8 - 10 weeks with a moderate cycle.
Q: For how long has PGF2 has been used? How was it discovered?
A: As far as I know, bodybuilders have been using prostaglandins on a regular basis for more than 5 years. Perhaps it was used before that, but I'm not aware of it. Its use has not been reported in the bodybuilding magazines. In fact, I am sure you will keep reading articles claiming prostaglandins are very bad.
About its discovery, I would say that it comes from farmers who have used this substance to grow their animals in a way that was undetectable at any drug test used by various governmental agencies. It may have leaked out from there. If it makes a steer more muscular why not a bodybuilder? But this was the easiest part -- when it was first speculated that PGF2 could be a muscle builder, no one knew whether it would work. There are many potential anabolic substances out there. Very few really work in the real world. Whenever a new substance is tried, the odds are very against it in that its chances of truly working are remote. If it does not work, is it because not enough was used, is it because it was used the wrong way or simply as it does nothing at all? The next issue is how much should be used? What are the side effects? Most of the steroid users may have been a bit scared about their first time even though millions of people have used them before. Imagine what it could be with an obscure veterinary substance that almost no one you are aware of has ever used! Fortunately, PGF2 has already been employed in women so the side effects were more or less known. A very few women did die, but it was not directly because of prostaglandins (not even PGF2) but a concomitant administration with RU 486 for abortion.
Even though the administration modes in women are very strange, PGF2 administration did not result in sudden death. Next, the type of administration had to be decided. All this is not easy, so the science of PGF2 usage is not very advanced. Ten years from now, bodybuilders will probably laugh at the way PGF2 is presently used.
Q: Is there a pro using prostaglandins? If PGF2 is not able to build up a pro rapidly, isn't that a proof of its ineffectiveness?
A: I do not know if any pro is using PGF2 though I would not be surprised if it were so. The early use of PGF2 had to be done on drug free bodybuilders which meant beginners. If someone is already using a tremendous amount of various drugs, how can you tell PGF2 is actually working? You may feel that it is bringing an extra edge but you are not sure, nor do you know how much is due to PGF2 or the synergy between steroids and the prostaglandins. In order to really discover what PGF2 would do, only one variable (one drug) had to be used at a time. A beginner with six months to a year of consistent drug free training under his belt has no reason to experience any sudden and dramatic change on his body.
A speed-up of the muscle building process was the testimony that the prostaglandins were working. Only then, steroid users could experiment with PGF2. First it was used, while off cycle without steroids. This is again certainly not a good way to become a pro fast. But one had to figure out whether PGF2 anabolic actions were strong enough not only to prevent the muscle wasting but rather to continue to gain lean mass while off steroids. Then only, the steroid plus prostaglandin stack could be studied. The amounts of both drugs were varied to see what would happen. To sum up, the discovery of a new drug has nothing to do with building up a pro physique. Once a minimal amount of research is done, only then can pros benefit optimally from it.
What about PGE2?
Q: Isn't PGE2 catabolic? You seem to think otherwise.
Whenever prostaglandins are mentioned, it is usually PGE2 rather than PGF2 that is discussed. The consensus is that PGE2 is bad. The main reason for this is because the early major prostaglandin study performed on muscles did suggest PGE2 was catabolic. In fact, this is what you would probably conclude after a 5 minute search on Medline. In a lesser known study, the very same scientific team admitted that they kind of messed up during their first study. It is very rare to see this study mentioned, including in scientific papers. Later, another team of scientists did indeed prove that they were in error. As most of the information in the bodybuilding world is based on hearsay and repetition, it suffices that one writer suggests PGE2 is bad, for another to repeat. You then have two different writers making the same claim, therefore the readers considered it as gospel. What I've not figured out yet is why only the wrong assumptions get repeated in the muscle magazines while the right information is generally omitted.
To answer your question in a more direct way: I do not consider that PGE2 is catabolic. Newer research shows that it accelerates the muscle protein turnover just like androgens. Understand that it increases both catabolism and anabolism at the same time except that it accelerates synthesis rate more than degradation. An overall gain results.
Drug testing
Q: Will PGF2 show up at drug test?
A: So far, PGF2 is not tested for. I doubt that it will ever be tested. It is a pure muscle builder, not a performance enhancer. In fact, it tends to reduce strength and performance. Furthermore, it may be very hard to test as we naturally produce some and it might be tough to differentiate between natural and exogenous prostaglandins. On the other hand, PGF2 does alter steroid hormones in many ways. For example, it might alter the testosterone/epitestosterone ratio.
Side effects
Q: After some of my own research on PGF2 I have found a few ways of overcoming a few of the side effects. As you said in your paper, the side effects were bronchoconstriction and violent spasms of the intestines and bowel. Could you take salbutamol (Ventolin Inhaler for asthmatics) for relief of the tightening of the chest? And could you also take an anti-spasmodic drug such as Mebeverine Hydrochloride, which is used in irritable bowel syndrome complaints, to relief the spasms of the bowels and intestines?
A: Beta agonists can help reduce the bronchoconstriction (which does not occur in all users) but it is not an ideal solution. First, because it does not completely prevent it. Second, it will increase the tightening of the muscles. This is going to truly impress your fellow bodybuilders as they touch your "relaxed" muscles but it makes it very hard to train.
As far as the intestines are concerned, this is disturbing at first, then you realize there is a rapid reduction of the impact of PGF2 so that it is not so disturbing. You also get used to it. It may be wiser not to mess around with additional drugs.
Q: Are there any drugs or supplements that will prolong the half life of PGF2 in the body?
A: Sure there are. I just do not know which ones.
Aspirin and prostaglandins
Q: I have read that aspirin can effect prostaglandins in the body, is this true or does it not apply to PGF2, and should I avoid any other substance which can effect PGF2?
A: It is true that aspirin is a prostaglandin inhibitor. At normal dosage, it only weakly affects the muscle prostaglandins. But whenever you use aspirin, your muscle insulin sensitivity is reduced because of a lesser secretion of muscle prostaglandins. Several people did report a significant muscle growth after discontinuing aspirin. Prostaglandins will also affect your adipose tissue both directly and indirectly. Because of the aspirin-induced insulin resistance, your insulin secretion will increase in order to make up for the weaker effects in muscles, resulting in an excess of insulin effect within the adipose tissue. Insulin promotes fat aggregation if unopposed. Therefore, I do not recommend continual use of aspirin for bodybuilders unless you want to get smaller and fatter. Of course, the dose also matters. A little bit of aspirin may not hurt much while high doses will.
Paradoxically, for someone who has no adipose tissue problem, it may be interesting to "play" with aspirin. As I said, a muscle gain usually results from aspirin discontinuance. Chances are it is because muscles try to overcome the inhibitory action of aspirin on prostaglandin secretion. Once you stop aspirin, there is a rebound in the muscle production of prostaglandins (i.e: there is an excess of prostaglandins) leading to muscle growth. It may be possible to do small but repeated cycles of aspirin in order to boost growth this way. This is a worthwhile way to pursue. For those who desires to try this more "natural" approach, do not forget to use small doses oral PGE1 in order to minimize the side effects of aspirin on the gastrointestinal tract plus high doses of a prostaglandin precursor such as primrose oil.
DNP and prostaglandins
The following is not a question but rather a remark that I would like to address in a prostaglandin way:
"I feel that DNP, in doses of 2mg/kg can be an effective anabolic agent. I just can't tell all the mechanisms why it works so well."
Whenever one studies prostaglandins, one hears about DNP a lot. DNP causes cellular damages which results in prostaglandin leaks. PGE2 release in particular is severely increased as a result of the addition of DNP. At first, scientists speculated that it was because of the PGE2 elevation that cell damages appeared (the catabolic theory of PGE2). The mere addition of aspirin proved this theory wrong. Whenever aspirin is administered along with DNP, PGE2 release was inhibited yet, cellular damage remained. Therefore, PGE2 release is the consequence and not the cause of the cellular damage. All this to say that DNP will cause muscle damage a bit like training does. But unlike a workout-induced damage, it is not localized to a single muscle group but is rather spread all over. Of course, the body will try to stop or minimize the wasting process that DNP is trying to trigger. Your body will try to calm down the main catabolic pathways DNP puts into play. Once DNP is discontinued, the rate of protein degradation in the muscle will be restricted a a bare minimum while the long-lasting prostaglandin leaks will keep on going. The end result is that the rate of synthesis is boosted while the catabolic pathways are slowed. We are then placed in the most favorable situation possible to build muscles fast.
Q: Can I stack DNP with PGF2 for better thermogenic response?
A: I would say no as I speculate that DNP thermogenic actions require the release of prostaglandins or at least employ similar pathways. To determine this for sure, scientists (do not try this at home) could use very high doses of aspirin a bit before DNP to determine whether the thermogenic response is affected. The same kind of result should be realized with Dantrolene as an inhibitor.
Q: Where is it possible to obtain PFG2? Is it illegal as AS are?
A; Try your best guess on this one!
Q: Does it come in only veterinary form?
A: No, but it is the cheapest and easiest form to get.
Q: What dosage (in cc's) should I use at each injection?
A: All the info I could give you were provided in the part III of the prostaglandin article series. You are on your own for the rest. Of course, I could pretend to know all this. The truth is I do not know how much YOU should use. I do not even know if you should use PGF2 in the first place.
Q: I have never used steroids, is this a prerequisite? It just seems that PFG2 is more in line with my goals of losing bodyfat while developing muscle. I was about to cycle some T enanthate, as my first time, should I do that first?
A: No, you do not have to have several cycles of steroids under your belt to get the most out of PGF2. Although -- you may want to use testosterone first because it is easier. This way you could first get used to the needle manipulations plus all the little things that are part of the education of a bodybuilder.
Ripped off
Q: Thank you so much for your time and knowledge. I also enjoyed your article about prohormone stacking which appeared in the [name of company elided] buyers guide.
A: Thanks, but the trouble is I've never seen this prohormone stack nor did I ever write for them, nor do I recommend any of their products. This is funny as I am not the only one complaining about it. They seem used to this kind of misleading marketing ploy.
Did I make mistakes?
Q: This may be a memory lapse :-), but I thought that Dantrolene was used in some hyperthermia crisis conditions. Someone suggested that it was stacked with Lutalyse, which itself could elevate T. Wouldn't that be contradictory? Or was it the actual intention?
A: True, it is a contradiction to use both a thermogenic with an anti-thermogenic drug if your main goal is to get leaner. My article was entitled "grow off steroids" which was mainly concerned with muscle growth and not as much with fat loss.
Q: Dharkam, Excellent article on PGF2, but where in this world can we find it? I know it's for animal use so I checked two local animal stores, neither of them even heard of it. It sure is a bitch when you read about the new cutting edge shit, but then can't find it til about a year down the road.
A: You may want to go to a store selling bigger animals and not pets. If all the drugs were both freely available and cheaper, bodybuilders would be far bigger. You may feel better by knowing your problem is a problem everyone faces.
From a single unsatisfied reader.
Q: In his article "Grow Even When Off Steroids: Part 2" Dharkam makes a couple of incorrect predictions. Dantrolene taken before a workout will certainly reduce exercise performance effectively cancelling any benefits accrued from its ability as a calcium channel blocker.
A: I sure made more than a couple of mistakes if you do not understand what you read. Here is what I said: "What you want is for Dantrolene to produce its magic right AFTER but NOT during the workout. If your training lasts less than one hour, you can take Dantrolene before your workout. This way, the drug will kick in at the right time." The misunderstanding may come from the fact that you assume oral Dantrolene works as soon as you have swallowed it. As with most of the oral drugs, it takes a while before the molecule starts working.
Q: You recommend amrinone as a Ubiquitin-Protease inhibitor. The anabolic effects of amrinone are due to its effects as a PDE3 inhibitor and the corresponding release of insulin. Dharkam suggests the use of insulin in conjunction with PDE3 inhibitors, but fails to mention what a potentially lethal combination this is. All PDE3 inhibitors cause an increase in insulin tolerance, a release of insulin, and an increase in plasma glucose. If the PDE3 is eliminated while insulin concentrations are excessively high a hypoglycemic coma may result.
[Editor's note: PDE3 = Phosphodiesterase 3]
A: You are discounting the lipolytic properties of Amrinone. Amrinone + insulin is safer than insulin alone. Insulin will deprive the blood of glucose while Amrinone will increase the release of fats (plus glycerol) which will serve as energy replacement leaving what is left of glucose for the brain. Insulin is certainly not safe if you do not know what you are doing -- this is why I recommended oral insulin boosters first, rather than straight insulin. Amrinone was not my first pick either as an anti-catabolic. Alone it is best while on a diet but this was not what the article was mainly dealing with. By the way, if you want everything to be safe do not use drugs and do not get involved in bodybuilding.
Banned
Should Nolvadex be Avoided at All Cost?
by Dharkam
CEM-Meso.com
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.
Nolvadex is the trade name of a drug containing a molecule called Tamoxifen. Its primary use by male bodybuilders is to prevent gynecomastia (the growth of the breast tissue). It was introduced by steroid guru Dan Duchaine 25 years ago. After a quarter of century, it is time for an update about its use. What I am going to demonstrate is it is high time to eliminate Nolvadex from the bodybuilder's drug stacks.
A Little Bit of History
Back in the late 70's, more and more bodybuilders developed strange lumps around their mammary glands. At first, no one really took notice but more and more competitors grew a gynecomastia. In 1981, the M Olympia had a pretty serious gyno. This was shortly after the introduction of this new drug by Dan Duchaine. At the time, it was a pretty good idea as no one else could came up with a solution in order to prevent this growing problem. Nolvadex was popularized by Dan's first Underground Steroid Handbook. Dan even states that "this drug has a lot of potential but hasn't been used enough yet to find it". After more than 25 years of intensive usage, it is my opinion that it is time to forget about Nolvadex. Why? First, because newer and more effective drugs have been developed. Second, because it seems obvious that Nolvadex impairs muscle growth.
Nolvadex and Muscle Growth
After so many years of usage, it seems pretty clear that if Tamoxifen helps prevent the growth of the nipples, it also weakens the anabolic properties of steroids in a majority of bodybuilders. We are frequently said that this weakening effect is due to the anti-estrogenic action of Nolvadex. According to the fantasy, muscles require both testosterone and estrogens to grow at an optimal rate.
This belief is derived from the results of studies showing that without estrogens, testosterone alone possesses minimal anabolic properties. By increasing the density of androgen receptors, estrogens render the muscles much more sensitive to testosterone (1). This has been demonstrated in a very specific muscle called the levator ani. But this muscle does not reflect what happens in the muscles bodybuilders are interested in (2). Estrogens have even been shown to reduce muscle fiber size (3-4). I think this effect of estrogens is closer to what we experience on bodybuilders.
Another popular explanation of the weakening action of Nolvadex is provided by studies which have shown that it reduced the plasma level of IGF-1. I do not think this is a primary explanation.
What Nolvadex Truly Is
Most lifters assume Nolvadex is a pure estrogen antagonist (which would mean it prevents estrogens from acting on their receptors). As far as bodybuilding is concerned, this assumption is very wrong as Nolvadex is both an estrogen receptor agonist and an antagonist. It all depends upon the tissues. Along with the nipples, on which Nolvadex acts mainly as an antagonist, we are also interested by its behaviour on skeletal muscles, on the liver and on the fat cells.
Nolvadex has been shown to behave as estrogens in skeletal muscles (5). This is a very good thing for every athletes except bodybuilders. You see, estrogens protect muscle cells from the training-induced damages (5-6). It means that one can train more without damaging his muscles. Recovery will also be much faster. But for bodybuilders, the training-induced damages are a key ingredient to trigger growth. Nolvadex will therefore reduce the muscle building effects of resistance training.
As for the impact of Tamoxifen on IGF-1, it simply demonstrates another estrogen-like action of Nolvadex. By rendering the liver less sensitive to growth hormone (probably by reducing the liver density of GH receptors), estrogens and tamoxifen diminish the production of IGF-1. This action of estrogens explains why women produce less IGF-1 than men even though the have a higher GH level.
Nolvadex and Muscle Definition
Within 24 to 48 hours, Nolvadex is able to greatly increase muscular definition. As a result, bodybuilders assume Nolvadex will help them reduce their bodyfat level. But this rapid cutting action of Nolvadex is due to an anti-estrogenic action on water retention. Estrogens will make you hold water. Nolvadex will produce the opposite effect. But it says nothing about the impact of Tamoxifen on bodyfat. Depending upon your own production of estrogens and your estrogen receptor density on adipocytes, Nolvadex can act as an antagonist (which would help you lose fat) or an agonist. In that case, Nolvadex will make you fatter especially in the lower body area.
Conclusion: if the introduction of Nolvadex 25 years ago was a brilliant idea, times have changed. Very effective anti-aromatase drugs (such as Letrozole or Anastrazole) have been introduced. They will fight gynecomastia, help prevent the anti-anabolic actions of estrogens, fight fat and water retention. They will also boost natural testosterone production far more effectively than Nolvadex. So, it is up to you to decide whether you wish impair your rate of progression with an outdated drug or move on to the 21st century.
Bibliography:
(1) Max SR. Androgen-estrogen synergy in rat levator ani muscle: glucose-6-phosphate dehydrogenase. Mol Cell Endocrinol. 1984 Dec;38(2-3):103-7.
(2) Rance NE, Max SR. Modulation of the cytosolic androgen receptor in striated muscle by sex steroids. Endocrinology. 1984 Sep;115(3):862-6.
(3) Kobori M, Yamamuro T. Effects of gonadectomy and estrogen administration on rat skeletal muscle. Clin Orthop Relat Res. 1989 Jun;(243):306-11.
(4) Suzuki S, Yamamuro T. Long-term effects of estrogen on rat skeletal muscle. Exp Neurol. 1985 Feb;87(2):291-9.
(5) Koot RW, Amelink GJ, Blankenstein MA, Bar PR. Tamoxifen and oestrogen both protect the rat muscle against physiological damage. J Steroid Biochem Mol Biol. 1991;40(4-6):689-95.
(6) Naessens G, De Slypere JP, Dijs H, Driessens M. Hypogonadism as a cause of recurrent muscle injury in a high level soccer player. A case report. Int J Sports Med. 1995 Aug;16(6):413-7.
Associate Member
very interesting
Thanks
Sapiens Fingit Fortunam Sibi
So much to read, I just finished the Nolvadex part...
Banned
sorry mate, trust me though it's interesting as hell. The guy who writes this contradicts himself a few times back and forth if anyone noticed? thats why i was pissed and confused about these articles.
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