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(There were steps needed to get from the mRNA to the protein, but we will skip them. online pharmacy steroids Anabolic-insider. )Does each binding of AAS to an AR result in exactly one extra molecule of protein produced? No. Because even though the AR is fully activated by any AAS, that does not mean that it always succeeds in binding to DNA. And differing amounts of mRNA might be produced, because an AR remains active as long as an AAS remains bound to it. online pharmacy steroids Teenage-bodybuilding. If many mRNA molecules are produced, then, generally, they will cause many corresponding protein molecules to be produced. So the amount of extra growth per extra activated AR can vary. The Androgen ReceptorNow, having a broad view of the process, let's take a closer look at the AR itself. online pharmacy steroids Free steroid information. The AR is a large protein molecule, produced from one and only one gene in DNA. There aren't lots of different kinds of receptors, as some authors claim. There are not, for example, ARs specific for oral or injectable anabolics, nor for different esters of testosterone, nor for any different kinds of AAS. The first important question to ask is, "How many ARs do you have? Is the number small or large? Can it be changed?" Since these are, in effect, little machines which are either on or off, and their effect is greater as more are activated, we want as many of them switched on as possible. There are far fewer ARs than most people realize. Some authors who are opposed to AAS doses beyond 200 mg/week say that only this amount will be accepted by the receptors in muscle, and everything past that will "spill over" and go into receptors in the skin and elsewhere. Research shows that muscle tissue has, roughly, 3 nanomoles of ARs per kg. Then your body probably has less than 300 nanomoles of ARs, grand total, let's say. Well, one 2. 5 mg tab of oxandrolone supplies about 8000 nanomoles of AAS. Clearly, that's far more molecules than your body has receptors. A little math shows that all those receptors combined could bind only a small percentage of the molecules of AAS in one little 2. 5 mg tab. So binding to ARs cannot appreciably reduce the concentration of AAS in the blood. Therefore, the ideas that ARs will bind most of whatever dose some author recommends, or that "spill-over" will occur beyond that, are entirely wrong. There just aren't that many receptors. Typical doses of AAS are high enough that a high percentage of the ARs are bound to AAS, whether the dose is say 400 mg/week or 1000 mg/week. If similar percentages of ARs are active - close to 100% in each case -- then why do higher doses give more results? It's a fact that they do, but there is not any large percentage of unoccupied receptors at the moderate dose. Thus, there is little room for improvement there. So at least part of the cause must be something other than simply occupying a higher percentage of receptors. And why did I pick those doses, rather than comparing normal levels with say 400 mg/ week?The fact that the ARs must form dimers to be active has an interesting consequence. The mathematics are such that if two ARs must join together to form an activated dimer, and both must bind a molecule of AAS, then the square must be taken of the percentage. This means that if say 71% of receptors are binding steroid, only 50% of the dimers will be activated. Thus, at low levels, there is more room for improvement than one would think. But if say 95% are occupied, then even after squaring that, there would still only be 10% room for improvement. But actual improvement - increase in effect - seems to be much more than 10%.
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