by Ed Barillas, Staff Writer
There is as much disinformation and misinformation about steroids as there is good and solid information among bodybuilders. If you step into any gym you will likely hear some kid yacking to his buddies about how steroids do this or how they do that – you get the picture. Anyway, this soon starts somewhat of a pissing contest as to who knows more about steroids and has about the same kind of imbicilic banter that teenage boys get into about girls and sex. With steroid banter, you hear all the popular terms like Deca, Test, HGH, gyno, zits, raisins, roid, freak, monster, roid-rage, but if by some rare chance they are smart and have been reading this or some other high quality bodybuilding site on the net and in our forums, they may actually get a few details right. More often than not they know just enough to be dangerous. Fortunately, steroids have not proven to be all that dangerous and not only that, most of these guys who are infatuated with steroids will not ever use or even see them other than in magazines.
This kind of ego driven gym talk does not really bother me until they begin giving advice to other clueless people who actually have access to them and that’s where the problems begin. Spewing out steroid lingo gives other less experienced kids the impression that these kids actually know what they are talking about. That is how all of the psuedo-science folklore about steroids perpetuates. This is also why most people who actually use steroids know little about them and this last fact should bother anyone who cares about bodybuilding and/or bodybuilders.
The game plan of this article is to tell you about what Androgens actually do and how this precludes Androgen receptor down regulation. One misunderstood common principle of steroid physiology is the concept of Androgen receptors (AR), sometimes called “steroid receptors”, and the effects of steroid use on their regulation. It is commonly thought that taking Androgens for extended periods of time will lead to what is called AR “down regulation.” The notion for this argument goes something like this – when using steroids during an extended cycle, you eventually stop growing, even though the dose has not decreased. This belief has persisted despite the fact that there is no scientific evidence to date that shows that increased levels of Androgens down regulates the Androgen receptor in muscle tissue.
One can say that AR down-regulation sounds pretty straightforward on the surface. After all, we know that receptor down-regulation happens with other messenger-mediated systems in the body such as adrenergic receptors. It has been shown many a times that when taking a beta agonist such as Clenbuterol, the number of beta-receptors on target cells begins to lower. This is due to a decrease in the half-life of receptor proteins without a decrease in the rate that the cell is making new receptors. This leads to a decrease in the potency of a given dose. As a result, with fewer receptors you get a smaller, or lower, physiological response. This is a natural way for your body to maintain equilibrium in the face of an unusually high level of beta-agonism.
But really this example using Clenbuterol is not an appropriate one. Androgen receptors and adrenergic receptors are very different. Nevertheless, this is the argument for Androgen receptor down-regulation and the reasoning behind it. The differences in the regulation of ARs and adrenergic receptors, in part, show the mistake in the view that AR down-regulate when you take steroids. Where adrenergic receptor half-life is lowered in most target cells with increased catecholamines, AR receptors half-lives are actually increased in many tissues in the presence of Androgens.
If I may show you the flip side to this coin, against AR down-regulation in muscle tissue, I feel that once you consider all of the effects of testosterone on muscle cells you come to realize that when you eventually stop growing it is not because there is a reduction in the number of Androgen receptors.
So how do anabolic steroids produce muscle growth? The basic common answer is that steroids increase protein synthesis. Which is true, but there is more to it than simple increases in protein synthesis. Actually, the answer to the question of how steroids work must include virtually every mechanism involved in skeletal muscle hypertrophy which mechanisms include: Enhanced protein synthesis, enhanced growth factor activity (e.g. GH, IGF-1, etc.), ½ Enhanced activation of myogenic stem cells (i.e. satellite cells) ½ Enhanced myo-nuclear number (to maintain nuclear to cytoplasmic ratio) and ½ New myo-fiber formation.
Starting with enhanced growth factor activity, we know that testosterone increases HGH and IGF-1 levels. In a recent study the effects of testosterone and stanozolol were compared for their effects on stimulating HGH release. Testosterone enanthate (only 3 mg per kg per week) increased HGH levels by 22% and IGF-1 levels by 21% whereas oral stanozolol (0.1mg per kg per day) had zero effect whatsoever on IGF-1 or HGH levels. This study was only 3 weeks long, and although stanozolol did not affect HGH or IGF-1 levels, it had the same effect on urinary nitrogen levels. So what does this difference in the effects of testosterone and stanozolol mean? It means that stanozolol may increase protein synthesis by binding to AR receptors in existing myonuclei, but because it does not increase growth factor levels, it is much less effective at activating satellite cells and therefore may not increase satellite cell activity nor myo-nuclear number directly when compared to testosterone esters.