Testosterone is the active androgen in muscle
Skeletal muscle is unique from other androgen dependent tissues in the body. It actually contains little or no 5-AR, so little or no DHT is actually formed in the muscle. In addition to this, any DHT that is formed, or that is already present in the blood and travels to the muscle, is quickly deactivated by an enzyme called 3alpha-hydroxysteroid reductase (3a-HSD).
So at least as far as muscle is concerned, testosterone is the primary active androgen. This is not to say that administering exogenous DHT is not without any anabolic effect. It actually does have some anabolic activity in the muscle, albeit significantly weaker than that of an equal amount of testosterone. This is due to its quick breakdown by 3a-HSD into the weak metabolite 5alpha-androstan-3a,17b-diol. If this enzyme were somehow blocked, it is likely that DHT would exhibit very potent anabolic effects on muscle.
It is important to understand that even though testosterone is the active androgen in muscle, and DHT exhibits relatively little direct anabolic effects on muscle in men, DHT is still very important for the full performance enhancement effects from testosterone. What I specifically mean here are the effects of DHT on the central nervous system, which lead to increased neurological efficiency (strength), and increased resistance to psychological and physical stress - not to mention optimal sexual function and libido.
I have heard several anecdotal reports of individuals who have stacked testosterone with proscar (a 5-AR inhibitor) and have noticed significantly reduced performance enhancement effects. What???s going on here? We know it couldn???t be due to the inhibition of the direct anabolic activity of testosterone on muscle anabolism. Most likely it is due to the reduction of androgenic effects in other parts of the body that contribute to the ergogenic effects, specifically the CNS, which is stimulated by androgens to increase neural output leading to greater strength and greater recoverability. Another possibility is a reduction in the production of androgen dependent liver growth factors (such as IGF-1), since DHT is an important androgen in the liver.
