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Testosterone enanthate gave a small decrease in subcutaneous fat but a slight increase in visceral fat. bodybuilding clip art Articles on steroids. Nandrolone decanoate also increased visceral fat while decreasing subcutaneous fat. If these activities were via the AR, all three steroids should give the same effects, differing only in potency or the dosage required. There are some interesting studies on sexual receptivity of female rats. bodybuilding clip art Steroid-discussion-boards. Methyltestosterone, methandrostenolone (Dianabol), nandrolone decanoate, and stanozolol all interfered with sexual receptivity (a different result than seen in human bodybuilders) while testosterone propionate did not. 11In male rats,12,13,14 differential activities are also seen. In intact (non-castrated) male rats, testosterone cypionate, nandrolone decanoate, and methandrostenolone (Dianabol) were all able to support male sexual behavior, while methyltestosterone, stanozolol (Winstrol), and oxymetholone eliminated male sexual behavior. bodybuilding clip art Bodybuilding. Again, these results are different than are seen in human bodybuilders. Testosterone cypionate was able to maintain ejaculation in castrated rats, while oxymetholone (Anadrol) was barely able to do so, and stanozolol was unable to do so. This however might have to do with estrogenic activity - use of an aromatase inhibitor was not tried. Oxandrolone was found incapable of supporting reproductive development in the young male rat. 15 Weight of testes, prostate gland, and seminal vesicles were all below controls, and Leydig cells were severely depleted. Again, it was not ruled out that reduced estrogen levels of the oxandrolone-treated animals might have been to blame, so this does not actually prove a non-AR-dependent mechanism for reproductive development. It does indicate that androgens other than testosterone combined with low estrogen levels can result in fertility problems in the rat, and therefore long-term use of nonaromatizing steroids might affect sperm count in the human as well. Virilizing activities in female rat fetuses also showed a trend of potencies different from trends of binding affinities to the AR. 16 The specific test used was measurement of the abridgment of urovaginal septum length: admittedly not so directly relevant for female bodybuilders. The most active AAS was stanozolol, which was more active than methyltestosterone despite having much poor binding affinity to the AR than that steroid. 17In Syrian hamster embryo cells, trenbolone, a more potent agonist of the AR than testosterone, was found unable to transform these cells while testosterone was effective. 26 This indicates that the mechanism cannot be simply via the AR. The AR is not a membrane-associated receptor, but exists within the cell. However, receptors for testosterone have been found in the cell membranes of T cells. The activity of testosterone (increase of amounts of Ca++ within the cell) occurs within seconds (and therefore cannot be via interaction with DNA resulting in increased protein synthesis, since this is a slow process) and was not affected by an AR blocker. 18 This effect has also been seen in Sertoli cells. 19Androgen binding receptors have also been found in cell microsomes - these receptors cannot interact with DNA because of their location. 20,21,22 Stanozolol has been found to have activity in microsomes that testosterone does not. 23,24,25Lastly, while only stanozolol was tested and therefore we cannot know if there is differential activity between different steroids or not, stanozolol induced a type of skeletal muscle injury that was thought perhaps to stimulate growth, and to induce gene expression by an AR independent mechanism. 27 At last, a specific example related to muscle that shows that not all activity is via the AR alone. We might also speculate that AR upregulation (which has been demonstrated to occur under some conditions (see Androgen Receptor Regulation) is probably not itself mediated by the AR. It would be an unstable mechanism to have the number of ARs increase as a result of increasing numbers of activated ARs. More likely there would be another mechanism. We may also speculate that different AAS have different effects on nerves, and these effects (being rapid) are not mediated by the AR. E. g. , fluoxymesterone, while it binds fairly poorly to the AR, is highly potent in stimulating aggression, and this activity occurs quickly. ConclusionWhat to do with this information? Unfortunately we cannot yet identify how many non-AR- mediated activities there may be. There are I think at least two: activity in microsomes and activities in nerves. There may be more.
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