The secondary mechanisms by which AAS induce growth or muscular hypertrophy deal with a given drugs capacity for conversion or reduction into other hormones. This also applies to the cascading effect resulting from the parent drug and conversion/reduction product. Some of these mechanisms are very synergistic to the growth process and had to be taken into consideration when constructing cycles and protocols for beasts. Others may have inhibited a chosen out come or goal by rendering one or more drugs in a stack useless.
ESTROGENIC CONVERSION RATE: Most AAS are susceptible to conversion into an estrogen. Like different AAS posses different levels of activity, so do different estrogenic conversion products. AAS can be converted into estrogens by two main pathways. The most commonly discussed pathway occurs when a susceptible AAS molecule encounters the aromatase enzyme. The conversion process is called aromatization, of course.
In most cases, individuals with higher levels of body fat will experience greater levels of AAS aromatization due to the fact that lipocytes (fat cells) are primary producers of the aromatase enzyme. This makes sense because estrogens are anabolic to lipocytes and all cells posses certain survival mechanisms.
The second conversion pathway is activated during liver/intestinal deactivation of susceptible AAS. Various P-450 enzymes induce a conversion process that results in a percentage of the AAS being metabolized into estrogens. Some AAS are more or less susceptible to estrogenic conversion and therefore convert at a higher or lower rate or percentage. And the method of administration can effect this as well.
As example, testosterone in its unaltered form converts to estrogens at a much higher rate if ingested than if it is injected. The same is true of some pro-hormones. The estrogenic conversion rate of a drug or its metabolites maybe either beneficial or counter-productive, depending on the intended out come or goal of the protocol.
Estrogens increase GH and IGF-1 production by initiating a cascading effect beginning with the hypothalamus. The synergy between GH, IGF-1, and AAS is well known. The issue of estrogenic value was always a matter of ratio between androgens and estrogens.
Estrogens act to trigger another cascading effect by up-regulating production of an enzyme necessary for glycogen synthesis and intracellular storage in muscle tissue. The resulting increase in cellular glycogen content allows for prolonged ATP production during anaerobic activities such as weight training and subsequent recovery process. Both require a great deal of ATP. (We will discuss that issue in depth later.)
Additionally, each gram of glucose stored as glycogen in muscle tissue brings with it 2.7-3.0 grams of water. This triggers osmotic anabolism similar to "one" positive factor of creatine supplement use. This simply means cells are supersaturated with growth nutrients intracellularly. The osmotic effect also increases localized IGF-1 production due to the increase in pump and stretch realized during conditions of elevated glycogen storage. (Guess that explains the cookies-n-cream ice cream carb-loading during women's periods)
Estrogens increase anaerobic weight-load capacity. This is due to an increase in the whole body water table that results in an increase in muscle integrity and joint stability. Simply said, it allows for a greater and sounder foundation from which to lift weight from. Greater weight-load capacity means more weight used and a greater stimulus for anabolic over-compensation during recovery. GROWTH!
The mitigating effects of estrogens should seem evident. Gyno, increased fat synthesis, and water retention are not pre-contest goals. The issue during mass gaining periods therefore became estrogen control, not elimination.
Reduction to DHT or Derivative: DHT (Dihydrotestosterone) is 3-7 times more androgenic than testosterone. High androgenic AAS tend to promote an increase in total muscle glycogen synthesis. The result is similar to the prior mentioned osmotic effect.
It differs however due to the lack of estrogenic activity which would normally draws water into the entire body water table. In this case, due to no aromatization, the high androgenic value draws water from under the skin and forces it "into" muscle cells. This is why drugs that are structurally similar to DHT such as Parabolan, Halotestin, and Masteron, were used pre-contest to create hardness of the complete musculature and increased viewable vascularity.
Many AAS are susceptible to a percentage of enzymic reduction to either DHT or a metabolite/derivative of DHT. This is the result of a susceptible AAS molecule encountering the enzyme 5-alfa-reductase. The majority of 5-alfa-reductase is found in sex-specific tissues such as hair follicles, and prostate cells. Some does exist in muscle and the vascular system of course.
Once an AAS molecule encounters 5-alfa-reductase, whether in the vascular system or in sex-specific tissues, it is reduced to a derivative of DHT corresponding with its unique chemical structure. As example, Nandrolone reduces to NOR-DHT. Therefore the resulting reduction products may be more or less androgenic than actual DHT. This means the new product can have a more or less potent androgenic effect upon tissues it merges with.
Since different AAS reduce to DHT at different rates or percentages, each can trigger a growth or androgenic mechanism to a greater or lesser degree of a secondary nature. This of course, also is dependent upon the potency of the specific reduction product as well. It should be noted that some DHT reduction products can possess an inhibitory effect upon estrogens.
Of course there are other pathways and mechanisms by which AAS induce the growth process.
• When 17-alfa-alkylated steroids are detoxified/deactivated by the liver there is a significant increase in hepatic IGF-1 production and secretion.
• AAS increase CP (Creatine Phosphate) synthesis.
• AAS increase circulatory amino acid (s) levels by redirecting amino acids away
• from liver oxidation / destruction.
• AAS susceptible to estrogenic conversion suppress cortisol levels and activity by stimulating GH/IGF-1 production.
• AAS inhibit the synthesis of fat by blocking the enzyme lipoprotein lipase which in turn spares calories that can be utilized for the growth process of muscle tissue.
• Some AAS increase muscle cell PGE-1 and PGF-2 receptor-site count/concentrations.
• By stimulating an increase in nitric oxide synthesis, AAS increase vascular endothelial growth factor (VEGF) which is responsible for capillary formation. Nitric oxide also positively effects erectile function. (Think about it)
There are several other mechanisms by which AAS induce or mediate the growth process but for now we will simply accept that a foundation for greater knowledge has been laid down. And it barks like a dog because...
We have discussed the benefits and methodology of Max Androgen Phases that had employed different variants of high anabolic/high androgenic testosterone up in the front of the cycle, and a high anabolic/moderate-to-low androgenic at the cycle exit. Growth potential during these brief protocols was nothing short of miraculous in most cases. Normally Max Androgen Phases were at a point of high activity for 30 days or less, thus functioning within the basic Action/Reaction "initiation" time period of 2 weeks.
Of course, we are speaking of the time frame in which the body normally begins significant response or counter measure to a given stimulus. As example, HPTA inhibition became a concern at the 2 week point when using AAS that aromatize at a higher rate. This is the body's attempt at down-regulating the level of androgens/estrogens circulating in the vascular or lymphatic system. It does so by decreasing natural (endogenous) androgen (testosterone) production.
The main stimulus that acts as the "action" is estrogens produced by way of the activity of the aromatase enzyme upon testosterone. The "reaction" is the down-regulation of HPTA function that results in major post- cycle lean mass tissue loss (total in most cases) and "raisin nuts syndrome". By using the get in, hit hard, and get out structures of Max Androgen Phases, beasts like Frank retained a far greater level of their lean mass gains post-cycle. And their nuts played nice too. But what about longer AAS cycles?
AAS cycles that used testosterones always induced the greatest strength, weight, and lean mass gains for the least financial cost. But prolonged use of testosterones would have resulted in HPTA shut down and reduced (like serious) postcycle lean mass retention. Since long term continuous progress was the goal of any muscular augmentation protocol, this situation was simply unacceptable.
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