An Introduction to Testosterone

Anabolic steroids are a class of medications that contain a synthetically manufactured form of the hormone testosterone, or a related compound that is derived from [or similar in structure and action to] this hormone. In order to fully grasp how anabolic steroids work it is therefore important to understand the basic functioning of testosterone.



The actual mechanism in which testosterone elicits these changes is somewhat complex. When free in the blood stream, the testosterone molecule is available to interact with various cells in the body. This includes skeletal muscle cells, as well as other skin, scalp, kidney, bone, central nervous system and prostate tissues. Testosterone binds with a cellular target in order to exert its activity, and will therefore effect only those body cells that posses the proper hormone receptor site [specifically the androgen receptor]. This process can be likened to a lock and key system, with each receptor [lock] only being activated by a particular type of hormone [key]. During this interaction the testosterone molecule will become bound to the intracellular receptor site [located in the cytosol, not on the membrane surface], forming a new "receptor complex". This complex (hormone + receptor site) will then migrate to the cells nucleus where it will attach to a specific section of the cells DNA, referred to as the hormone response element. This will activate the transcription of specific genes, which in the case of a skeletal muscle cell will ultimately cause [among other things] an increase in the synthesis of the two primary contractile proteins action and myosin [muscular growth]. Carbohydrate storage in muscle tissue may be increased due to androgen action as well.


In the kidneys, this same process works to allow androgens to augment erythropoiesis [red blood cell production]. It is this effect that leads to an increase in red blood cell concentrations, and possibly increased oxygen transport capacity, during anabolic/androgenic steroid therapy. Many athletes mistakenly assume that oxymetholone and boldenone are unique in this ability, due to specific uses or mentions of this effect in drug literature. Stimulation of erythropoiesis in fact occurs with nearly all anabolic/androgenic steroids, as this effect is simply tied with activation of the androgen receptor in kidney cells. The only real exceptions might be compounds such as dihydrotestosterone and some of its derivatives`, which are rapidly broken down upon interaction with the 3alphahydroxysteroid dehydrogenase enzymes [kidney tissue has a similar enzyme distribution to muscle tissue, see "anabolic/androgenic dissociation" section] and therefore display low activity in these tissues.

Adipose [fat] tissues are also androgen responsive, and here these hormones support the lipolytic [fat mobilizing] capacity of cells5. This may be accomplished by an androgen-tied regulation of beta-adrenergenic receptor concentrations or general cellular activity [through adenylate cyclase]. We also note that the level of androgens in the body will closely correlate [inversely] with the level of stored body fat. As the level of androgenic hormones drops, typically the deposition of body fat will increase. Likewise as we enhance the androgen level, body fat may be depleted at a more active rate. The ratio of androgen to estrogen action is in fact most important, as estrogen plays a counter role by acting to increase the storage of body fat in many sites of action8. Likewise if one wished to lose fat during steroid use estrogen levels should be kept low and steroid choice is important. This is clearly evidenced by the fact that non-aromatizing steroids have always been favoured by bodybuilders looking to increase the look of definition and muscularity while aromatizing compounds are typically relegated to bulking phases of training due to their tendency to increase body fat storage. Aromatization is discussed in more detail in a following section.

As mentioned, testosterone also elicits androgenic activity, which occurs by its activating receptors in what are considered to be androgen responsive tissues [often through prior conversion to dihydrotestosterone See: DHT Conversion]. This includes the sebaceous glands, which are responsible for the secretion of oils in the skin. As the androgen level rises, so does the release of oils. And as oil output increases, so does the chance for pores becoming clogged [we can see why acne is such a common side effect of steroid use]. The production of body, and facial hair is also linked to androgen receptor activation in skin and scalp tissues. This becomes most noticeable as boys mature into puberty, a period when testosterone levels rise rapidly, and androgen activity begins to stimulate the growth of hair on the body and face. Some time later in life, and with the contribution of a genetic predisposition, androgen activity in the scalp may also help to initiate male-pattern hair loss. It is a misconception that dihydrotestosterone is an isolated culprit in the promotion of hair loss however; as in actuality it is the general activation of the androgen receptor that is to blame [See: DHT Conversion]. The functioning of sex glands and libido are also tied to the activity of androgens, as are numerous other regions of the central nervous/neuromuscular system.