@Type-IIx
“Benefits from aromatization do not come from high E2, but rather in situ aromatization.”…
Could you elaborate on that?
Without simply dumping a ton of notes with references on this matter on you, I should organize it into a coherent work of some sort.
Put simply, my "thesis" on myotrophic mechanisms of AAS is that these drugs, through:
I. modulating glucocorticoids and muscle IGF-I isoforms (mIGF-I)
II. aromatization
III. ligand dependent- and independent- AR action exert classical genomic effects, mRNA-mediated translation for protein synthesis, as well as rapid nongenomic action
Downstream of aromatization (so with aromatizing androgen only, i.e., Test, Nand, Dbol, a few others) you see a. enhanced growth factor activity (e.g. GH, IGF-1, etc.), b. enhanced activation of myogenic stem cells (i.e. satellite cells) [this occurs via secondary messenger activation]... and perhaps with all androgens, the potential for c. new myofiber formation ["Hyperplasia"] (working on this... I also have a lot to say about rhGH and this).
With aromatization, there are various benefits. That is, benefits from the process itself (in situ aromatization), rather than with its products (chiefly E2, other aromatic products like 17methyl-E2 with MENT)
The chief consideration with aromatizing androgen, is that its estrogen products pose a net negative in the human male. Rather, the aromatization process itself is what we want (and in fact, tamoxifen prevents the T-induced augmentation of serum IGF-I levels).
E2 increases serum IGFBP-1 levels, which reduce free IGF-I availability and (endogenously) unleashes GH secretion by feedback withdrawal. This is why women have 1.5-3x the GH levels of their male counterparts, yet a diminshed IGF-I response (virtually no benefits from rhGH unless they triple the dose... worse with oral estrogens/birth control generally).
The literature points to E2 being of miniscule if any benefit to men.
Benefits from aromatizing androgen (Test!) including augmented glucose metabolism (increased G6PD/Akt activity), potential myostatin attenuation come from in situ aromatization: the process of T/aromatizing androgens being converted to estrogens. Unfortunately, the products themselves through compensatory mechanisms tend to negatively feed back on anabolism.
Sure there are some benefits of estrogens per se (but E2 and the more potent methylestrogens suck!)... there is some interest in an ERx [as yet undetermined] or of course ER-β, which is a very interesting receptor for us: whereas ER-α primarily regulates blood lipids, ER-β primarily regulates muscle tissue remodeling. E2 is just a shit ligand for this (it's why I am intrigued by the potential of phytoecdysteroids).
This falls quite far outside the classical view of primarily AR/ligand-dependent action but is in line with the latest research.
There is certainly an inverse U-shaped curve plotting E2 vs. muscle anabolism. More E2 is definitely not better.