While tremendously beneficial to the cutting phase and often considered essential to competitive bodybuilders during contest prep, Trenbolone Acetate is also a phenomenal off-season bulking steroid . When we refer to this hormonal compound as versatile, that is truly an accurate statement. There are very few anabolic steroids that can promote mass like Trenbolone Acetate. More importantly, the effects of Trenbolone Acetate in this regard are not only strong but are far cleaner than most traditional bulking steroids. This hormone will not and cannot promote water retention, meaning each and every pound of weight gained due to use will be lean muscle mass. Of equal importance will be this steroid’s ability to help the individual control fat gain during a period of growth. To achieve true growth, this will require total caloric intake to be slightly above maintenance levels. How far above will vary from one man to the next, and while many often take it too far, this phase will still require a slight surplus. Unfortunately, this necessary surplus will promote body fat gains but due to the metabolic factors that surround Trenbolone Acetate they will be minimized. This is not a license to eat like there’s no end in sight, you can still gain a lot of fat if you continually gorge but you should be able to make better use of your total caloric intake. Those who supplement with Trenbolone Acetate during off-season periods of growth should gain less body fat than they would have without it.
Because steroids are lipophilic, they diffuse easily through the cell membranes, and therefore have a very large distribution volume. In their target tissues, steroids are concentrated by an uptake mechanism which relies on their binding to intracellular proteins (or " receptors ", see below). High concentration of steroids are also found in adipose tissue, although this is not a target for hormone action. In the human male, adipose tissue contains aromatase activity, and seems to be the main source of androgen-derived estrogens found in the circulation. But most of the peripheral metabolism occurs in the liver and to some extent in the kidneys, which are the major sites of hormone inactivation and elimination, or catabolism (see below).
FIGURE 2. Major Pathways of Steroid Biosynthesis.
The pathways outlined here are common to the adrenals, the gonads and, to some extent, to the fetoplacental unit. The first committed step is the conversion of cholesterol to pregnenolone, catalysed by the P-450scc enzyme, which is under pituitary hormone control (ACTH or LH depending on the tissue). Cholesterol side-chain removal is blocked specifically by aminoglutethimide , a steroid biosynthesis inhibitor. From pregnenolone, steroid biosynthesis can proceed either through the so-called "delta-5" pathway (17α-hydroxypregnenolone, dehydroepiandrosterone, testosterone), or through the "delta-4" pathway (progesterone onwards). Progesterone is the starting point for mineralocorticoid synthesis, whereas glucocorticoids are derived from its metabolite, 17α-hydroxyprogesterone. Estrogens are formed from androgens (androstenedione and/or testosterone). Most reactions are irreversible (as denoted by a single arrow). Reversible reactions (double arrows) depend on cofactor availability (. the NADP/NADPH ratio). [Abbreviations used here for the various enzymes are listed in the figure].