Do I know what genes are transcribed in muscle cells?
Uh...not comprehensively. But in the spirit of the question, let me see if I can build a bridge here.
First off, in food deprivation induced muscular atrophy, over 98% of transcripts remain unchanged. The altered values include an upregulation of ubiquitin, (which makes sense seeing as it is the ubiquitin proteaaome pathway that is activated in nutrient deprivation induced atrophy), and 20S and 26S proteasome subunit genes, as well as some glycolotic/oxidative metabolic enzymes, but I cannot name the individual enzymes or their roles. Again, this is a short list, but there is one more, very pertinent, item worth mentioning.
There exists a group of recently identified genes that have been named atrophins. One of these genes, called atrophin-1, is increased 9 times in skeletal muscle during atrophy, but is unchanged everywhere else. How do we know that this is utilized in the actual degredation? Because it contains a certain characteristic, which at present I cannot recall (I am not good at terminology in this area, and moreover, I am uneducated by and large here), but anyway it has a trait that is a characteristic of Ub-protien ligases, as well as a nuclear localization sequence.
Pretty good evidence that this gene is somewhat germain to protien degredation.
Remeber that one (main?) reason that degredation occurs in a nutrient-scarce environment is to supply amino acids for gluconeogenesis. Moreover, not only short chained protiens are degraded, but myofibrillar components are, likewise, degraded via this pathway.
So it would seem that any exogenous compound that amplifies, or for that matter, impacts in any way this mechanism, would indeed play a critical role in the process of protien degredation.
I just recently read the report I am summarizing as a result of this thread, so I think that I can find it in pretty short order. Again, my understanding of the minutia of this issue is very VERY limited, but one can certainly see where I am intrigued by the concept?
Now, about that whole GC reduction issue...
Wheew. Well, I will have to go and dig around a bit, and while I am at it I will try and refresh my learning about this, because I have come off like I actually think I know more than I do, and believe me, that is not my intention here. I simply think that there is good evidence in literature, but moreover, in the empirical realm.
Think about it. What happens if you were to inject, say, 50mg of test, maybe prop for similar lifespan, every day, and restrict your diet to a 20% deficit?
Would the results be superior to the same experiment carried on with trenbelone? Not for me, they aren't. When I do test, if I do not eat sufficient calories, I don't gain any significant amount of muscle at all. Even at 700mg/week. All that happens is I get horny, oily, and a bit stronger (due to water retention primarily). Not only that, when I stop the therapy, my gains, such as they were, vanish. I think this is actually due to the fact that there were no actual gains to speak of.
Now with trenbelone, I can eat 1700 calories a day and gain ten or twelve pounds in a month. On top of that, I will not retain water. My relative strength is indicative of an actual muscular gain, although, admitttedly, not a massive one. But the point is that there is, in fact, muscular gain on restricted calories. And the real kick is that those calories can be pretty wreckless in terms of nutrient dispersal, within reason.
At the end of the therapy, I will lose about 3/4 of what I gained if I simply quit cold turkey, and this will occur over a period of about six weeks. But with proper cessation techniques, I have discovered that the gains actually stick pretty much entirely, or at least they have thus far from my six week fina only cycle earlier this summer. Bear in mind that I actually did quit cold turkey, and started ancillary therapy after four weeks of nothing but vitex and arimidex. My weight gain has remained intact, and my strength has dropped by a amall margin. I think that the weight gain that vanished after trenbelone is not actually muscle loss, but rather, a reduction in blood volume. Again, give me some time to dig up supporting literature.
But in the end, literature can only support what we see with our own eyes. No amount of speculation can change what I know to be a fact for my own body, which is that trenbelone supports muscle in a nutrient scarce environment much better than does testosterone.
Now, away I go to learn and respond! Off to the papers!
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