The primary mechanism by which AAS trigger growth or muscular hypertrophy begins when an AAS molecule merges with an androgen receptor-site on the exterior of a cell. If the cell contains adequate ATP reserves, the receptor-site/molecule complex travels to the interior of the cell where it delivers a "make new proteins" message via DNA/mRNA transcription. Basic, but it barks because it "is" a dog. This is the primary anabolism mechanism since it directly stimulated protein synthesis.
The other primary mechanism by which AAS increase net cellular proteins concerns cortisol. When AAS molecules merge with a cortisol receptor-site, nothing happens. (Huh?) That is the point. Since the AAS molecule acts as a cortisol receptor-site antagonist, it triggers no response while also locking cortisol molecules out of the receptors it occupies. The result is an increase in net proteins due to retention. And that is an anti-catabolic effect, so it is called the primary anti-catabolic mechanism.
However, there are several factors that determine the potential magnitude of total net anabolism achieved by any AAS. These factors correlate with a drug's total potency.
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