Anabolic Steroid and Testosterone Effects

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.

Testosterone Forms

A very small amount of testosterone is actually in the free form stage, in which interaction with cellular receptors is possible. The majority will be bound to the proteins SHBG (sex hormone binding globulin, also referred to as sex steroid binding globulin and testosterone-estradiol binding globulin) and albumin, which temporarily prevent the hormone from exerting activity. The distribution of testosterone in men is typically 45% of testosterone bound to SHBG, and about 53% bound to albumin. The remaining 2% of the average blood concentration exists in a free, unbound state.

The level of free testosterone available in the blood is likewise an important factor mediating its activity, as only a small percent is really active at any given time. It must also be noted that as we alter testosterone to form new anabolic/androgenic steroids, we also typically alter the affinity in which our steroid will bind to plasma proteins. As the higher percentage we have of free hormone, the more active the compound should be on a milligram for milligram basis.

The level of SHBG present in the body is also variable, and can be altered by a number of factors. The most prominent seems to be the concentration of estrogen and thyroid hormones present in the blood. Generally there is a reduction in the amount of this plasma binding protein as estrogen and thyroid content decreases, and a rise in SHBG as they increase. A heightened androgen level due to the administration of anabolic/androgenic steroids has also been shown to lower levels of this protein considerably.

Lowering the level of plasma binding proteins is also not the only mechanism that allows for an increased level of free testosterone. Steroids that display a high affinity for these proteins may also increase the level of free testosterone by competing with it for binding. Obviously if testosterone finds it more difficult to locate available plasma proteins in the presence of the additional compound, more will be left in an unbound state.

So clearly if the level of free-testosterone can be altered by the use of different anabolic/androgenic steroids, there also exists the possibility that one steroid can increase the potency of another through these same mechanisms. Binding proteins act to protect the steroid against rapid metabolism, ensure a more stable blood hormone concentration and facilitate an even distribution of hormone to various body organs. It remains although very clear however, that manipulating the tendency of a hormone to exist in an unbound state is an effective way to alter drug potency.

Estrogen Aromatization





Dihydrotestosterone (DHT) conversion




