Quote (noob_whacker @ Apr 18 2015 06:11pm)
could you please explain this, in lower level terms?
Ok just to answer your question
test exerts anabolic effects in cardiac myocytes via the androgen receptor (ofc). Will stimulate canonical signaling pathways, including mTOR to ramp up p synth.
One of the main ways test works in skeletal muscle cells is via increasing satellite cell kinetics. So this mechanism won't take place in other muscle tissues, just skeletal. But it's still anabolic in the others.
As for smooth muscle, eh, I doubt this is as notable if there is hypertrophy occuring. I mean, there's constant turnover of vascular smooth muscle cells anyway right? Plus, testosterone is generally protective for them, which is also why it's typically noted that test/androgens are ameliorative for vascular conditions (or also one of the reasons why, in aging/hypogonadal men, the low test puts them at higher risk for cardiovascular problems).
Quote (cloudkicker @ Apr 18 2015 06:47pm)
depends if cardiac and smooth muscle cells express receptors that will bind testosterone. usually there are isoforms for different tissue types.
and i believe test is a nuclear hormone (not 100%) so it wont be expressed on cell surface if that is correct
Yeah androgen receptors are nuclear hormones and mediate most of its effect.
Interestingly, there's also non-genomic signaling pathways via test. For instance, SHBG can activate cAMP/PKA pathways via binding to the cell surface. Or even to directly cause Ca2+ influx via an interaction with certain Ca2+ channels. Pretty cool imo. Everything is so diverse. It's easy to memorize/understand ALL of the canonical signaling of various factors and receptors. What's hard is all the (typically more newly discovered) non-canonical signaling and unforeseen crosstalk