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 . 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.
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 . 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 . 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.
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 . 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.
Among the most potent growth factors produced locally in the muscles are the prostaglandins. These quasi-hormones use fats as their raw materials. Several classes of prostaglandins exist. We will mainly focus on the most potent one, namely the prostaglandin F2 alpha or PGF2 for short.
If you apply PGF2 to a muscle cell, you are going to trigger a very strong anabolic response. PGF2 has been used by veterinarians for years not only to get animals pregnant but also to make them grow. A few daredevils figured out that if it was making animals more muscular, it would make bodybuilders bigger too. This was a big leap of faith as many drugs produce wonderful effects in animals only to fail miserably in bodybuilders. Clenbuterol is a good example of this: ultra potent in animals, deceptive in humans. Amazingly enough, this time it worked wonders.
WARING: What I am going to reveal is true for men ONLY. Women will not get any benefit from what I will describe below. Further, no women should EVER touch this drug which will induce a very severe pain in their ovaries. As men do not have ovaries, this is something that will not happen to them.
PGF2 and anabolism.
Many studies have demonstrated an anabolic effect of PGF2 in skeletal muscles of both humans and animals. Paradoxically, PGF2 usage is still reserved to a bodybuilding elite and no one is willing to divulge the precious secret edge. One of the most remarkable effects of PGF2 is that it mediates the major part of the anabolic effects of insulin. By using PGF2, you can use far less insulin and get a far stronger muscle building effect.
PGF2 and weak bodyparts.
The cardinal rule of PGF2 is to inject as far away as possible from the intestine. You see, PGF2 induces a very strong contraction of the intestine and the bladder (both smooth muscles). The major candidate as a site of injection was the front shoulders. But by repeating injections in the shoulders, bodybuilders soon ended up with grossly overdeveloped front delts. They looked like walking monkeys. The rest of their body was growing too, but not as fast as the muscles closest to the sites of injections.
What this means is that if you want to develop a weak muscle, just inject PGF2 locally and watch the muscle grow. We are talking about a real muscle growth and not an artificial swelling like Synthol or Esiclene would induce. Calves are a muscle of choice. In fact, even if your calves failed to grow no matter how much steroid and training you administered, PGF2 will solve your problem. After a single cycle of PGF2, unresponsive calves start to respond to both training and steroids even if they never did before.
The localized growth induced by PGF2 may appear magical, but there is a simple explanation. The life cycle of the injected PGF2 is terribly short (minutes). Most of it will be destroyed in your lungs. If you hit your right calf for example, this muscle will be exposed to a maximal concentration of PGF2. As the prostaglandin rapidly leaks out of the calf and passes into the blood, it will quickly reach the lungs where most of it will be destroyed. What is left of the PGF2 will be dispatched evenly though your whole body. It means that the other muscles will be exposed to far less of the anabolic effects of PGF2. So unless you want to make a weak point grow, you should rotate the sites of injections frequently which as we will see is not a problem.
PGF2 is not to be confused with steroids.
You’ve probably realized by now that PGF2 produces growth in a radically different way from steroids — although I do not exclude that part of the anabolic actions of androgens are mediated by a local release of PGF2. The way PGF2 should be used is therefore radically different from that of androgens. Steroid use is rather comfortable. You inject or swallow them once in a while and wait for the growth to occur. This is not the case with PGF2. Their main drawback is precisely their difficulty of administration. Steroids once injected survive several days in your body. PGF2 will last only several minutes though their stimulatory actions on anabolism will be far longer lasting (hours). It means that frequent injections are compulsory. Ideally this would be five times per day, 30 minutes after meals.
You will also notice that once you have injected PGF2, the muscle which received it gets sore almost immediately. If the muscle was already sore from training, that painful sensation may become very intense. You definitely do not want to repeat injections at the very same location, hence the necessity for rotation. By the same token, you will notice that you cannot inject in a muscle and then train this muscle. PGF2 is algesic (a pain mediator). Therefore, the timing of injections is key. You should wait for at least 2 to 3 days after you have trained a muscle to inject it. Then you will have to wait for 24 hours before training this muscle. If your muscle is already sore, I advise against using it as a site of injection as long as it hurts.
You will also learn that it is more comfortable to hit the outer part of the muscle than the inner part. For example, it is less painful to hit the outer head of the triceps than the inner head that touches your lats. Some bodyparts such as the biceps, the back, etc. are especially sensitive to the pain sensation PGF2 will induce.
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.
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!