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But if androgen receptor density is such a dominant driver of anabolic response, how do you reconcile this with the fact that chronic low-grade inflammation (particularly via IL-6/STAT3 and TNF-/NF-B signaling) can suppress AR nuclear translocation even when receptor count is high and that in some individuals this blunts hypertrophy more dramatically than CAG-repeat length or hormone levels themselves?
Middle East Curr
Oral Supplements: Absorption varies widely due to digestive factors
I also came across a study published in the Journal of the International Society of Sports Nutrition
Instead of efficiently storing incoming calories as fat, treated adipocytes become more metabolically active, breaking down stored triglycerides and releasing them for energy use