In looking over the proposed indirect effects of testosterone, and pondering the effectiveness of the synthetic anabolic/androgenic steroids, we must resist the temptation to believe we can categorize steroids as those which directly, and those which indirectly, promote muscle growth. The belief that there are two dichotomous groups or classes of steroids ignores the fact that all commercial steroids promote not only muscle growth but also androgenic effects. There is no complete separation of these traits at this time, making clear that all activate the cellular androgen receptor. I believe the theory behind direct and indirect steroid classifications originated when some noted the low receptor binding affinity of seemingly strong anabolic steroids like oxymetholone and methandrostenolone. If they bind poorly, yet work well, something else must be at work.
This type of thinking fails to recognize other factors in the potency of these compounds, such as their long half-lives, estrogenic activity, and weak interaction with restrictive binding proteins. While there may possibly be differences in the way various compounds could foster growth indirectly, such that advantages might even be found with certain synergistic drug combinations, the primary mode of action with all of these compounds is the androgen receptor. The notion that steroid X and Y must never be stacked together because they both compete for the same receptor when stimulating growth, while X and Z should be combined because they work via different mechanisms, should likewise not be taken too seriously. Such classifications are based on speculation only, and upon reasonable investigation are clearly invalid.
MECHANISM OF ACTION DIAGRAM:
The mechanism of anabolic action due to the administration of anabolic/androgenic steroids. AAS causes not only direct stimulation of the androgen receptor, but also supports muscle growth by increasing the levels of free androgens, increasing androgen receptor density, inhibiting corticosteroid action, increasing GH/IGF- 1, and suppressing IGF-1 binding proteins.