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.
Testosterone is the primary male sex hormone. It is manufactured by the Leydig cells
in the testes at varying amounts throughout a person life span. The effects of this
hormone become most evident during the time of puberty, when an increased output of
testosterone will elicit dramatic physiological changes in the male body.
This includes the onset of secondary male characteristics such as a deepened voice,
body and facial hair growth, increased oil output by the sebaceous glands, development
of sexual organs, maturation of sperm and an increased libido. Indeed the male reproductive system will not function properly if testosterone levels are not significant. All such effects are considered the masculinizing or "androgenic" properties of this hormone.
Increased testosterone production will also cause growth promoting or "anabolic" changes
in the body, including an enhanced rate of protein synthesis [leading to muscle accumulation]. Testosterone is clearly the reason males carry more muscle mass than women, as the two sexes have vastly contrasting amounts of this hormone. More specifically, the adult male body will manufacture between 2.5 and 11 mg per day
while females only produce about 1-4 mg. The dominant sex hormone for women is actually estrogen, which has a significantly different effect on the body. Among other things, a lower androgen and high estrogen level will cause women to store more body fat,
accumulate less muscle tissue, have a shorter stature and become more apt to bone weakening with age [osteoporosis].
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.
Once this messaging process is completed the complex will be released and the receptor
and hormone will disassociate. Both are then free to migrate back into the cytosol for
further activity. The testosterone molecule is also free to diffuse back into circulation
to interact with other cells. The entire receptor cycle, including hormone binding,
receptor-hormone complex migration, gene transcription and subsequent return to
cytosol is a slow process, taking hours and not minutes to complete. In studies
using a single injection of nandrolone for example, it is measured to be 4 to 6 hours
before free androgen receptors migrate back to the cytosol after activation.
It is also suggested that this cycle includes the splitting and formation of new
androgen receptors once returned to cytosol, a possible explanation for the many
observations that androgens are integral in the formation of their own receptor sites.
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.