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Author | Topic: Long but worth it...might want to print it. |
Curious Pro Bodybuilder (Total posts: 395) |
![]() ![]() ![]() Many steroid users would like us to think that if they grow so fast while medicated, it is not so much because of the drug but rather due to their innate ability to train. This is probably why they never dare to go off steroids. Is there really any usefulness in cycling anabolics? I doubt that any pro ever goes off! Why shouldn't up-and-coming amateurs and contenders for the pros do the same? Is it useful to cycle steroids? Such has been the situation until now. I will show you not only how to prevent this wasting phase but also how to grow while off steroids. Of course, this will be a quite unorthodox method but it is highly effective. Let's first review the classic strategies employed when off steroids. Why does muscle mass shrink when steroids are discontinued? If you don't understand how steroids work, there is no way you can prevent the loss of mass when you go off them. Whenever our muscles are exposed to too much androgen, the number of testosterone receptors rapidly diminishes. On top of this, the receptors left lose some of their ability to trigger the anabolic process. You could say that the muscles become testosterone resistant as an analogy with the insulin resistance associated with the early phase of some diabetes. By the same token, whenever our testes are exposed to too much androgens, their own production of testosterone lessens. So at the end of a cycle, your 'nads may have shrunk a little or a lot. This depends mostly on your age. The young bodybuilders being less likely to end up with a little peanut than the more mature weightlifters. To sum up, at the end of your cycle your muscles are resistant to the building properties of androgens and you are not producing much testosterone to stimulate those receptors anyway. It's is an ideal situation for a rapid muscle shrinkage. This will not be due to an acceleration of catabolism but rather to a strong deceleration of the protein synthesis rate. As anabolism drops below the catabolic rate, the degraded muscle proteins will not be renewed, hence the loss of mass. A further complication is that in many people (but not all) anabolics tend to reduce the cortisol elevation associated with training stress, the secretion of this wasting hormone may tend to increase. This will further depress the anabolic drive. Should a minimal intake of steroids be maintained? In order to counteract this great wasting period, bodybuilders taper off their steroid use. It is rare that they stop cold turkey, especially after a serious cycle. The rationale is, maintain a reduced supply of androgens so that a) the muscles have a chance to recover some of their lost sensitivity to testosterone and b) the testicles can grow back a little. This may work to some extent but it mostly just postpones the wasting rather than preventing it. A possible strategy here can be to only partially discontinue steroids in order to artificially keep a high level of androgen in the blood. The issue of the lost muscle sensitivity is not addressed but at least you do not end up with a zero androgen level in your blood and all the problems inherent to this situation (loss of libido, depression, feminization, etc.). This may seem an unusual way of stopping steroids but it is in fact very popular. It is why someone can tell you that he is completely off steroids when he is still using 3 to 5 d-ball a day plus one or two vials of testosterone a week. He is not lying to you when he says he is off as he truly believes it himself. It is just a matter of semantics here. This is the person's minimum (zero or off) dosage. I am not going to argue on this as it is a universal strategy which has proved its efficacy. The main advantage is that it prevents the muscle shrinkage. In fact, you can keep on making progress while "off." It also protects from the wide endocrine fluctuations associated with a classical steroid cycling. The main disadvantage is you will not recover your muscle sensitivity to testosterone completely. More importantly, your endocrine system and especially your testes do not stand a chance of recovering homeostasis. Which nutritional strategies should be adopted? Attempt to maintain the muscle mass even if it means adding some fat. Attempt to maintain the muscle mass even if it means adding some fat. The main drawback of this strategy is it will not entirely stop the mass loss, and also one is likely to rapidly pack on fat. If you are too fat already, it is not a practical strategy. On the other hand, if you're lean and do not gain fat easily, then this is certainly the way to go. Trim the fat added during the steroid cycle even, if some lean mass is sacrificed. The main drawback here is the risk of losing all the lean mass added during the previous cycle. So, do not go on a super-strict diet. Drugs such as clenbuterol will come handy at this point. Add mass and shed fat if willing to utilize some innovative strategies. What about HCG? The role of anti-aromatase. Teslac (Testolactone) used to be a popular anti-aromatase. Studies have shown that it was able to rapidly and effectively boost testosterone output. Strangely enough, it never gave much muscle mass. Even the scientists were proud to say that it was not a virilizing drug. The problem was discovered recently. Some of the Teslac was confused with testosterone by the measuring apparatus. So it was in fact in great part a false testosterone elevation explaining the lack of effects (Cummings1998). Cytadren or Orimeten (Aminoglutethimide) is the most popular anti-aromatase among bodybuilders because it is relatively cheap. The problem is, it is not super effective, nor is it devoid of side effects. The most common are skin rash and drowsiness. You may feel tired all day long. This is supposed to subside after a while but in many experiencing this side effect, it does not. If you want to go with Cytadren, start with a half tablet at night. If everything goes well, add another half after training (assuming you do not train at night). You should end up using 3 half tablets per 24 hours at regular intervals if possible. Cytadren is the cheapest anti-aromatase and can be used during and after a cycle if your budget permits it. Femara (Letrozole) is a newly developed anti-aromatase. Due to its price, I suggest to start it toward the end of your cycle. Use it for 3 to 5 days at the recommended dose of 2.5 mg. Then use one every other or every 3 days at night. If it is still too expensive, try half a pill every other day. It means that with one box you can cover 4 months. If you can afford it, take half a pill a day. What about Arimidex (Anastrozole)? I do not have much experience with it, so allow me not to talk about it. What about Lentaron (Formestane)? Are anti-DHT medications useful? Saw Palmetto: Recommended as an anti-DHT, saw Palmetto can weaken the potency of your steroid cycles. While off cycle, this plant extract will reduce the effects of what is left of your own testosterone. AVOID! Pro-hormones: is it the right moment to use them? Anti-cortisol: not the right answer. Insulin: beware of the potential fat gains. GH: an expensive weak anabolic. IGF-1: probably too tricky to use optimally. Ephedrine is welcome if not already overused. Clenbuterol: do not expect too much out of it. Thyroid hormones: be careful about the potential lean mass losses. To conclude, many alternatives to steroids are available when off cycle. Unfortunately, none is truly affordable and effective for muscle retention. As far as fat loss drugs are concerned, several effective ones are available but they will not do much good for our muscle size. Up to now, anyway. Next month, I will tell you more about drugs which can not only prevent the losses associated with steroid discontinuance but will also build muscle mass despite the shortage of androgen. They will also play some nasty tricks on your fat mass which will shrink as you get bigger.
Grow even when off steroids! Why do muscles shrink after a cycle? Is fighting catabolism the answer? How does muscle breakdown occur? 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. 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. 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.
Amrinone and fat loss. Clenbuterol and catabolism. Is there an effective and cheap alternative to boost anabolism? Prostaglandins! 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: PGF2 and anabolism.
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 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? What about stacking steroids with PGF2? 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? Dosages. 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! ------------------ IP: Logged |
ajc1977 Pro Bodybuilder (Total posts: 663) |
![]() ![]() ![]() Good post bro... ------------------ IP: Logged |
Future One Amateur Bodybuilder (Total posts: 74) |
![]() ![]() ![]() I read this before, I think that site is down now... ------------------ IP: Logged |
Anabolicum Mister Pro Bodybuilder (Total posts: 420) |
![]() ![]() ![]() ![]() Easier said than done. IP: Logged |
THE APE Pro Bodybuilder (Total posts: 137) |
![]() ![]() ![]() Another killer post from one of the vets.Thanks for putting the time into that bro.Very informative. IP: Logged |
quenepo Pro Bodybuilder (Total posts: 912) |
![]() ![]() ![]() ![]() Long post but thanks for the info. ------------------ IP: Logged |
big_guy1 Pro Bodybuilder (Total posts: 1244) |
![]() ![]() ![]() ![]() nice post..good info..thanks bro big-guy IP: Logged |
pizza man Pro Bodybuilder (Total posts: 365) |
![]() ![]() ![]() pretty good info IP: Logged |
giantset Pro Bodybuilder (Total posts: 260) |
![]() ![]() ![]() ![]() There is some good info in that article but I say BALLOCKS to his initial theory of receptor "disappearance" in the prescence of androgens. There have been studies done in Germany I believe, that show that the use of androgens in pre-pubescent males can actually enhance androgen receptors. I am not convinced that receptors do "downgrade". Also, no one was advocating that steroids reduce cortisol. Increased testosterone and more stressful workouts increase cortisol levels. Steroids however increase protein synthesis to a rate much higher than cortisol can break muscle down and thus you gain muscle more rapidly. If receptors do downgrade in the prescence of increased androgens then why don't the effects of hormone replacement therapy eventually diminish? If receptor downgrade were true then how could they ever recover when bridging between cycles? The truth is they couldn't because there would still be elevated levels of androgens and the receptors would magically vanish or become inactive. I still think that the best way to prevent muscle atrophy post cycle is to finish with a more anabolic steroid or to bridge cycles with low levels of test or a more anabolic steroid. The pros bridge and it certainly appears that their androgen receptors are working quite well. Later, IP: Logged |
ColumboWeiser Pro Bodybuilder (Total posts: 115) |
![]() ![]() ![]() ![]() great info...Bump IP: Logged |
JSNAKE33 Amateur Bodybuilder (Total posts: 84) |
![]() ![]() ![]() ![]() I liked that post.... Good for the newbies to read..... ~~~~~~~~~~~~~~~~~~~~~SNAKE IP: Logged |
Curious Pro Bodybuilder (Total posts: 395) |
![]() ![]() ![]() Yes it would be...and there are plenty of them. ------------------ IP: Logged |
Your_Moms_Kneepads Pro Bodybuilder (Total posts: 196) |
![]() ![]() ![]() Curious, Aweosome post. One question? What source of information says that Cytadren is the most popular anti-aromatase used today. I have to differ. Tamoxifen is by far the most used antiaromatase today. ------------------ IP: Logged |
cowbell Pro Bodybuilder (Total posts: 497) |
![]() ![]() ![]() ![]() good info here!!! your are right though, it was long. nice post ![]() IP: Logged |
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