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"experts" on anabolic/androgenic?

brutus69

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so im watching more plates more dates on youtube. derek says the reason 1 guy on 300mg test can be vastly bigger than another on the same dose is the amount of androgen receptors in the muscle, not necessarily how much gear is used.
my question is, and maybe im just an idiot, but...if test or tren, something very androgenic is used, will systemic muscle mass be greater than if u use something more anabolic? like anavar, winny, npp, etc.
they're androgen receptors, not anabolic receptors, is what im thinking. and IF thats the case, and u wanted specific muscles to grow more than others, would more anabolics do the job, since androgens DO cause overall muscle mass increases to some degree with or without training them....or its thought so, as face muscles get bigger, for example. according to some. i havent trained legs in general for 2 years and they're still 1.5 inches bigger than they were before my trt started, as an example.
basically my goal is to grow some muscles and let others shrink some, purely for aesthetic reasons and ive noticed with 700-900 test levels, im not shrinking anywhere even with zero training time.
 

Stewie

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As far as abundance goes per anatomical position within skeletal muscle tissue goes. I'd suspect that has some interplay with hypertrophic response.


We also have to take into account the intraindividual DNA segment known as a CAG (CAG=cytosine, adenine, and guanine) trinucleotide repeat within the nuclear receptor (androgen receptor). There's some suggestive literature denoting varying intraindividual CAG repeat lengths, which may give some explanation to different genetic responsiveness to anabolics. Namely, testosterone.

Skeletal muscle hypertrophy isn't limited to just one particular nuclear receptor, such as the AR. The complexities goes way beyond that.
 

Stewie

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I was going to place this "food for thought" in my previous commentaries. As it was at that time, I had several other things to do.

Nevertheless.

Since we're hypothesizing receptor dynamics of less than stellar effects based on -to saturate or not to saturate, content and abundance- theorism. Which has been a contagious regurgitated conversation for quite some time.

Discussion or lack thereof about post translation of the androgen receptor -the communication that occurs giving the proteins (mRNA-miRNA) towards gene expression- isn't talked about. There's hundreds, upon hundreds of androgen specific genes that are either up-regulated or down-regulated post translation after translocation of the androgen response element, blah, blah, blah to the nucleus where dimerization occurs towards target gene expressions.

What if some of these genes aren't responding appropriately, even though these nuclear receptor(s) (AR), (ER) and (PR) are sending the proper communications?

Do we still place blame upon the receptor or "to saturate or not to saturate, content or abundance" or could there be epigenetic modifications limiting the expression(s) of one or more genes 🤔

If anybody is up for core DNA biopsies or hundreds and hundreds of dollars worth of genetic testing I'm all ears.
 

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