Even though in isolation, synthesized and actively experimented with for many decades now, and at this point the primary mode of anabolic action with all anabolic/androgenic steroids is to be a direct activation of the cellular androgen receptor and increase in protein synthesis. By supplementing external anabolic usage the increase of hormone levels, so does the androgen receptor activation, and finally the protein synthesis effect.
An indirect mechanism is one that is not directly brought about by activation of the androgen receptor. But the affect androgens might have on other hormones, or even the release of locally acting hormones or growth promoters inside cells. Muscle mass disposition involves not only protein synthesis, but other factors as well such as protein breakdown and tissue nutrient transport. In recent years insulin, a hormone that increases transport of nutrients into muscle cells. In which a second way of transport indirectly of protein breakdown to cause muscle growth.
Anti-Glucocorticoid Effect of Testosterone:
Glucocorticoid one of the most important mechanisms of androgen action, these hormone actually have the exact opposite effect on the muscle cell than androgens, namely sending an order to release stored protein. In this process it is called catabolism (breakdown of muscle tissue.) Muscle growth is achieved when the anabolic effects of testosterone are more pronounced overall than the degenerative effects of cortisol.
When steroids are administered a much higher androgen level can place glucocorticoids at a notable disadvantage. In terms, when you do AAS the catabolism effect is shortened leaving room for more muscle adaptation to protein synthesis absorption. With the affect reduced, fewer cells will be given a message to release more protein, and on the long run more will be accumulated. Primarily mechanism believed to bring this effect out is androgen displacement of glucocorticoids bound to the glucocorticoid receptor site. It is also suggested that androgens may indirectly intefere with the DNA binding to the glucocorticoid response element.
Testosterone and Creatine Effect:
Creatine, as creatine phosphate (CP), plays a crucial role in the manufacture of ATP (adenosine triphosphate), which is a main store of energy for the muscle tissues. As the muscle cells are stimulated to contract ATP molecules are broken down into ADP (adenosine diphosphate), which releases energy. The cells then undergo a process using creatine phosphate to rapidly restore ADP to its original structure, in order to replenish ATP concentrations.
With increased levels of CP available to the cells, ATP is replenished at an enhanced rate and the muscle is both stronger and more enduring. This effect will account for some portion of the early strength increases seen during steroid therapy. Personally, the result of creatine and anabolic/androgenic steroids used in combination would result in a boosted strength and size gain, and as well increasing the recovery time during exercises.
Testosterone and IGF-1:
Insulin-Like Growth Factors, also has an indirect mechanism of test action on muscle mass. It has been demonstrated that increases in IGF-1 receptor concentrations in skeletal muscles are noted when elderly men are given replacement doses of testosterone. It looks like androgens are necessary for the local production and function of IGF-1 in skeletal muscle cells, independent of circulating growth hormone and IGF-1 levels. IGF-1 does have a minor effect in the muscle tissue growth in conjunction with steroid cycles.