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's cells in the testes at varying amounts throughout a person's 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 11mg per day while females only produce about ? 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 cell's nucleus where it will attach to a specific section of the cell's 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 actin 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 will hormone 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 3alpha- hydroxysteroid 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 cells 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 action 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 favored 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 (See: Estrogen Aromatization).
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. 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.
Anabolic Steroid is the familiar name for synthetic substances related to the male sex hormones (androgens). Anabolic Steroid promote the growth of skeletal muscle (anabolic effects) and the development of male sexual characteristics (androgenic effects). Also Steroid has some other effects. The term Anabolic Steroid will be used through-out this report because of its familiarity, although the proper term for these compounds is anabolic-androgenic Steroid.
Different types of Anabolic Steroid were developed in the late 1930s primarily to treat hypogonadism, a condition in which the testes do not produce sufficient testosterone for normal growth, development, and sexual functioning. The primary medical uses of Steroid are to treat delayed puberty, some types of impotence, and wasting of the body caused by HIV infection or other diseases.
During the 1930s, scientists discovered that anabolic Steroid could facilitate the growth of skeletal muscle in laboratory animals, which led to use of Steroid first by bodybuilders and weightlifters and then by athletes in other sports. Steroid abuse has become so widespread in athletics that it affects the outcome of sports contests.
Although testosterone had been isolated, synthesized and actively experimented with for many decades now, there is still some debate today as to exactly how steroids effect muscle mass. At this point in time the primary mode of anabolic action with all anabolic/androgenic steroids is understood to be direct activation of the cellular androgen receptor and increases in protein synthesis. As follows, if we are able to increase our androgen level from an external source by supplementing testosterone or a similar anabolic steroid, we can greatly enhance the rate in which protein is retained by the muscles. This is clearly the primary cause for muscle growth with all anabolic/androgenic steroids. As our hormone levels increase, so does androgen receptor activation, and ultimately the rate of protein synthesis.
But other indirect mechanisms could possibly affect muscle growth outside of the normally understood androgen action on protein synthesis. 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 a hormones or growth promoters inside cells (perhaps mediated by other membrane bound receptors). We must remember also that muscle mass disposition involves not only protein synthesis, but also other factors such as tissue nutrient transport and protein breakdown. We need to look at androgenic interaction with these factors as well to get a compete picture. Concerning the first possibility, we note that studies with testosterone suggest that this hormone does not increase tissue amino acid transport. This fact probably explains the profound synergy bodybuilders have noted in recent years with insulin, a hormone that strongly increases transport of nutrients into muscle cells. But regarding protein breakdown we do see a second important pathway in which androgens might affect muscle growth.
Testosterone (and synthetic anabolic/androgenic steroids) may help to increase mass and strength by having an anticatabolic effect on muscle cells. Considered one of the most important indirect mechanisms of androgen action, these hormones are shown to effect the actions of another type of steroid hormone in the body, glucocorticoids (cortisol is the primary representative of this group) Glucocorticoid hormones actually have the exact opposite effect on the muscle cell than androgens, namely sending an order to release stored protein. This process is referred to as catabolism, and represents a breaking down of muscle tissue. Muscle growth is achieved when the anabolic effects of testosterone are more pronounced overall than the degenerative effects of cortisol. With intense training and a proper diet, the body will typically store more protein than it removes, but this underlying battle is always constant.
When administering anabolic steroids however, a much higher androgen level can place glucocorticoids at a notable disadvantage. With their effect reduced, fewer cells will be given a message to release protein, and more will be accumulated in the long run. The primarily mechanism believed to bring this effect out is androgen displacement of glucocorticoids bound to the glucocorticoid receptor. In-vitro studies have in fact supported this notion by demonstrating that testosterone has a very high affinity for this receptor and further suggesting that some of its anabolic activity is directly mediated through this action It is also suggested that androgens may indirectly interfere with DNA binding to the glucocorticoid response element Although the exact underlying mechanism is still in debate, what is clear is that steroid administration inhibits protein breakdown, even in the fasted state, which seems clearly indicative of an anti-catabolic effect.
In addition to protein synthesis, a rise in androgen levels should also enhance the synthesis of creatine in skeletal muscle tissue& 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 muscles. As the muscle cells are stimulated to contract, ATP molecules are broken down into ADP (adenosine diphosphate), which releases energy. The cells will then undergo a process using creatine phosphate to rapidly restore ADP to its original structure, in order to replenish ATP concentrations. During periods of intense activity however, this process will not be fast enough to compensate and ATP levels will become lowered. This will cause the muscles to become fatigued and less able to effort a strenuous contraction. With increased leves 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. Although perhaps not itself technically considered an anabolic effect as tissue hypertrophy is not a direct result, androgen support of creatine synthesis is certainly still looked at as a positive and growth supporting result in the mind of the bodybuilder.
It has also been suggested that there is an indirect mechanism of testosterone action on muscle mass mediated by Insulin-Like Growth Factor. To be more specific, studies note a clear link between androgens and tissue release of 15, and responsiveness to, this anabolic hormone. For example, it has been demonstrated that increases in (GE-i receptor concentrations in skeletal muscle are noted when elderly men are given replacement doses of testosterone . In essence, the cells are becoming primed for the actions of IGF-i, by testosterone. Alternately we see marked decreases in (GE-i receptor protein levels with androgen deficiency in young men. It also appears that androgens are necessary for the local production and function of (GE-i in skeletal muscle cells, independent of circulating growth hormone and IGF-1 levels Since we do know for certain that (GE-i is at least a minor anabolic hormone in muscle tissue, it seems reasonable to conclude that this factor, at least at some level, is involved in the muscle growth noted with steroid therapy.
In looking over the proposed indirect effects of testosterone, and pondering the effectiveness of the synthetic anabolic/androgenic steroids in these regards, 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 that 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 however, such as their long half-lives, estrogenic activity and weak interaction with restrictive binding proteins (See: Free vs. Bound Testosterone). 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 primarily 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 seem clearly invalid.
With the wide variety of anabolic/androgenic steroids available, planning the most appropriate cycle may seem like a difficult task to the steroid novice. Even if we have settled on a particular drug or drug combination, it is still easy to question whether or not we are using them in the most effective manner. This is one of those topics which can get more confusing with research, as you will find the popular literature filled with various stacking, cycling, tapering and receptor response (upregulation/downregulation) theories. If you have looked through this site in the hopes it will provide you some new and unusual ways to take anabolic/androgenic steroids, you will probably be disappointed. I have actually developed the opinion that athletes usually place too much importance on cycle construction. Experimenting with fancy dosing patterns, rotation schedules and (especially) tapering routines, hoping they will bring about enhanced results, is in my opinion a very unreliable practice. In this section I will therefore be ignoring the more lavish intake regimens, and focus on the more fundamental aspects to using these drugs. This is obvious when you look at the sample cycles included, which you will notice display little fluctuation in drug dosages from start to finish. They are not fashioned as such due to laziness, but simply because my personal experience has led me to a place where picking a dosage and sticking with it (unless there is an obvious need to adjust) seems to make the most sense. Of course it is ultimately up to the individual to find out what works best for him or her, as nobody can rightly claim that there is one "correct" way for everyone to use steroids. Here are a few things to think about when deciding on the right cycle for your needs.
It is an extremely common practice for an athlete to take more than one individual steroid during a cycle. By taking a combination of steroids, the user is of course seeking to enhance the amount/quality of muscle mass gained from drug therapy. While I'm sure it is no surprise that stacking is generally an effective practice, you should probably give some thought to expected goals and side effects before simply combining steroids. If you are looking to gain considerable mass for example, the use of two strong androgens like testosterone and Anadrol 50® would be one of the more potent cycles to attempt. But this combination would also lead to very harsh side effects, and may be too uncomfortable far some individuals. In this case it may be a good suggestion to combine a milder anabolic with a base androgen instead. A stack such as Deca-Durabolin® and Dianabol would still produce very formidable muscle mass gains, but would provide to user much less water/fat retention, gynecomastia, hair loss/growth and acne than the former.
On the other hand, "anabolics" are typically the favored class of steroids for cutting/dieting phases of training. This is because most have little or no tendency for estrogen conversion, which as you know makes them less apt to induce fat and water accumulation. It is important to remember however that these steroids can still suppress endogenous testosterone production during a cycle. Since the administered drugs) may not provide the body enough androgen content to compensate for this loss, this type of cycle may sometimes interfere with aggression and libido (Deca is a common offender). In such a state the user might become depressed and unmotivated (see: side effects, depression), seriously reducing the quality (results and comfort) of the cycle. It is therefore usually a good idea to include some type of androgen during this type of cycle, especially if you have experienced such problems before. The preference would be a nonaromatizing androgenic compound like Proviron®, Halotestin® or trenbolone, which will not increase the likelihood for fat/water retention. In the absence of excess estrogen, the heightened androgen level brought about by these drugs can actually enhance the removal of body fat, and noticeably increase the look of hardness/density to the physique (provided the user's body fat percentage is low enough to make this visible). (f such compounds were unavailable, perhaps a weekly (low dosage) shot of testosterone would prove sufficient to ward off any problems.
Finally, is also good to remember that it is not absolutely necessary to take more than one steroid at a time. The term you hear most often is synergy, which implies that two (or more) steroids used together will often compliment (and amplify) each other, providing a greater muscle gain than if they had been used consecutively. Though not well understood, a number of studies do suggest that different modes of action might exist for steroids outside of the androgen receptor (which would seem to support the notion that cooperative or synergistic effects can be seen with different drug arrangements). Athletes also seem to know that certain drug combinations work extremely well together (Deca & Dianabol, testosterone and Anadrol 50®, trenbolone and Winstrol® etc.), which is a testament to the notion of drug synergy. But this should not be confused with the idea that you cannot make gains on one drug alone. An athlete new to the world of steroids could make exceptional gains on a cycle of testosterone, Anadrol 50® or Dianabol for example, without ever needing to add a second drug. Heavily increased dosages and multidrug stacks are likewise most prominent among those who are already very familiar with steroid use, and find they are necessary in order to continue to gain or maintain muscle mass.
There are many different opinions as to exactly what dosage an individual should use of any particular drug in order to elicit optimal results. Some seem to find they make exceptional gains on relatively low dosages of most steroids, while others insist they need to administer very large amounts of androgens for the proper level of bulk. While I would be no means claim to have the solution for everybody, I would say those most steroids seem to work their best in a particular range of dosage, and usually fall short of expectations as we go higher or lower. On the one hand we may find that going below what is considered to be a normal dosage for a specific drug will cause a very poor gain to be achieved, the hormone level perhaps not rising enough above normal to stimulate a considerable response. For example, 200-800mg of testosterone enanthate per week is typically sufficient for a man to receive very formidable gains, while 50-100mg may not provide very noticeable results at all (of course this is all common sense). On the other extreme, athletes generally find that unusually large doses (let's say 10002000mg per week) will provide a relatively low quality increase over that of the normal dosage range. Yes, the amount of muscle mass may be considerably more than expected with a typical dose, but this will probably not be proportionate with the gain of new body fat and water weight. The user will typically be stuck with a much more noticeable level of side effects, while receiving a poor return (as in solid muscle mass) on his money. When steroids were abundant and cheap in the 1980', megadosing among recreational steroid users was not all that uncommon. No doubt paying $20 per week as opposed to $5 was not a very difficult decision to make. But today high prices will usually prevent the widespread practice of such excessive dosing, as such a cycle could cost hundreds of dollars each week. The side note to this is that one can reach an extreme level of development where year round high dosage steroid use is a necessity to maintain an anabolic state.
There are also many arguments as to how long one should stay on a steroid cycle before taking a break. Opinions range from those of cautious individuals, who are often vehement about short cycles and long off-periods, to the seriously hard-core user who suggests year round use for optimal results. Since it is really up to the individual to choose the cycle that is best for him or her, I can only provide some very basic advice. For starters, it is very important to watch your intake duration when on stronger or more toxic substances. This includes all c17 alpha alkylated orals, or high-dose cycles of easily aromatized steroids. These compounds place the most stress on your organs, and likewise should be utilized for only limited intervals (preferably less than 8 weeks). Afterwards a break of at least as much time (preferably more) should be taken to give the body ample time to rest/recover. For those who refuse to follow such advice, blood work and regular health checkups should be an absolute necessity.
When taking milder anabolics like Deca-Durabolin®, Primobolan or Equipoise, one might opt to take the drugs for a longer duration. This is due to the fact that these compounds do not act in an extremely dramatic manner, and instead promote a slow but consistent buildup of muscle tissue. With this understanding it is not unusual for an athlete to find a cycle of three, even four or more months to be the most appropriate. If used for only a short duration, the individual might find the overall gains to be uninspiring. Year round, on-all-the-time steroid use should be avoided if at all possible, as one should respect the natural hormonal balance your body strives for. The body really should be given time to regain a natural hormonal balance every so often, to ensure that there is little possibility of future problems. Although many believe the effects of these drugs to be 100% fully reversible, it is not impossible to see problems with virility, libido etc. after the body had been overloaded with hormones for many years. The health risks associated with elevated cholesterol levels, high blood pressure or liver toxicity are of course also important reasons the athlete should limit the duration of steroid intake.
One of the most fundamental beliefs among steroid users is that tapering, or the practice of slowly reducing their drug dosage when discontinuing a cycle, is an absolute necessity when wishing to preserve your newly gained muscle mass. It is rare to find an athlete who does not religiously dedicate (at least) three or four weeks to a tapering schedule after every serious cycle. The obvious belief is that the body will notice the lowering androgen level, and compensate by resuming the manufacture of testosterone. Unfortunately you will see that this theory is in fact, extremely flawed. This is because in order for the production of testosterone to be fully restored, the body will really need to recognize an androgen deficit, not just a drop in steroid dosage. Since for example even one Dianabol tablets could provide the equivalent of a days androgen supply for the average male, tapering from five, to four, to three etc. will accomplish relatively nothing. In the three or four weeks the athlete will spend doing this, his body is still reading "androgen overload", and is not attempting to restore the output of testosterone. This will of course hold true for all anabolic steroids, not just the strong androgens. Anecdotal evidence suggests that even tapering with mild anabolics such as Primobolan or Anavar (normally thought of as mild in terms of testosterone suppression) is enough to prevent or delay a hormonal rebound.
So if tapering is useless what should the athlete do in order to properly discontinue a steroid cycle? Of course the obvious answer is to pay much closer attention to ancillary drug use than tapering. The proper application of testosterone stimulating compounds like HCG, Clomid®, Nolvadex® and/or cyclofenil are the most critical, as these can greatly aid in the balancing of body hormones. [The popular methods for using all the above medications are laid out under their individual profiles.] In the few cycles I have illustrated in this section you will notice that I have not even bothered to lower the drug dosages before the ancillary drugs are added. Simply put, there is no need to. In my opinion going "cold turkey' is just the most logical option.
Sample steroid stacks are provided to demonstrate common and/or effective drug combinations in use by bodybuilders. For most of these cycles, the dosages used are in the moderate range. They are intended to represent a balance of peak effectiveness with tolerable side effects, and are also designed so that they can be assembled with very basic and common black market items. For most novice steroid users, stacks like these provide more than a sufficient level of steroid for very dramatic results. Some even find that they can make substantial progress on much less. These represent only common guidelines toward typical use, and by no means are indented to be the perfect cycles for everybody. You will also notice that I have not provided cycles geared towards women. This is quite simply because I think women should be extremely cautious with these drugs. Those absolutely determined to use them should certainly avoiding multiple drug combinations, especially as a novice to these agents.
