madman
Super Moderator
4. Summary
Replicating real life AAS abuse patterns which involve vastly supraphysiologic multidrug regimens and other high risk behaviours in scientific studies is neither possible nor ethical. Therefore the scientific evidence validating the perceptions of the sporting community is relatively limited and are largely derived from clinical studies in non-athlete populations using modestly supraphysiologic androgen dosing, and from animal experiments. There are multiple potential mechanisms by which AAS may enhance physical performance with possibly synergistic effects on different organs and systems. While there is unequivocal evidence that AAS can increase muscle mass and strength in a dose dependent fashion, the evidence for performance enhancing effects via actions on the vasculature, erythropoiesis and the central nervous system is comparatively less well established. Indeed, there is considerable evidence that AAS effects on these same tissues cause toxicity (Basaria, 2010) that might be detrimental to optimal athletic performance. At the cellular level, while most data support the importance of classical androgen receptor signalling for mediating the performance enhancing effects of AAS, more rapid non-genomic mechanisms may also contribute.
Replicating real life AAS abuse patterns which involve vastly supraphysiologic multidrug regimens and other high risk behaviours in scientific studies is neither possible nor ethical. Therefore the scientific evidence validating the perceptions of the sporting community is relatively limited and are largely derived from clinical studies in non-athlete populations using modestly supraphysiologic androgen dosing, and from animal experiments. There are multiple potential mechanisms by which AAS may enhance physical performance with possibly synergistic effects on different organs and systems. While there is unequivocal evidence that AAS can increase muscle mass and strength in a dose dependent fashion, the evidence for performance enhancing effects via actions on the vasculature, erythropoiesis and the central nervous system is comparatively less well established. Indeed, there is considerable evidence that AAS effects on these same tissues cause toxicity (Basaria, 2010) that might be detrimental to optimal athletic performance. At the cellular level, while most data support the importance of classical androgen receptor signalling for mediating the performance enhancing effects of AAS, more rapid non-genomic mechanisms may also contribute.
