Cellular/gene basis of action of Anabolic-Androgenic Steroids, VS neural activity;

[JohnBoy2000]

Androgen receptor - Wikipedia

en.wikipedia.org

I guess the core concepts are covered on its wiki page but, specifically in relation to enhancing sports performance and decreased test production with age in relation to cellular or nerve firing slowing with age, I'm just drawing comparisons there and, seems as I'm not really to enlightened about the mechanics of hormonal therapy, figured this would be a good spot to get insights.

So it appears that testosterone basically yields affects by way of influencing gene expression (transcription).
i.e. increasing gene expression = increase in muscle growth.

Basically I'm contending that cell firing is the determinant of hormonal regulation/activity, i.e. that hormonal activity is essentially a 2nd messenger to CNS firing (via the HPA axis), and therapies like testosterone replacement would be less necessary if an effective modality/method/therapy to maintain or halt the slowing of excitatory cellular activity (nerve firing) was established.

Hypothetical as such a modality/method/therapy is unknown, but I'm contending the concept itself could be sound.

i.e. Cell firing > hormonal replacement, in relation to performance and image enhancement.

 

[JohnBoy2000]

I also find it interesting that other thread where the dude claims discontinue AAS use has resulted in decreased blood flow.

Vasoconstriction (blood flow) would be intertwined with nerve activity additionally.

AAS influence nerve activity right down to actually ion channel function (thus nerve firing).

Androgen binding to cytoplasmic androgen receptors can cause rapid changes in cell function independent of changes in gene transcription, such as changes in ion transport.

Androgen receptor - Wikipedia

en.wikipedia.org

In relation to hair loss, by example - restricted scalp blood flow and androgen affects appear the two main hypothesis as to determining factor.