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There are studies showing how the body tries to "turn down" the growth process after some time. Desensitizations occur, transcriptional changes. Increased expression of ligases Atrogin-1, MuRF1, down regulation of miR-378, miR-29a, and miR-26a... of course increases in myostatin, etc etc.
Even high protein diets will then cause deficiencies in threonine, histadine, glycine (shared transporters) which is detrimental for various reasons (healing of tissue, growth). Some recover and replete quickly where other aminos take over a week.
My point is that if someone is using steroids that hit non-genomic pathways (strong AR binding affinity) and starts to stall/plateau (inevitable), it would be of interest to then hit the body with either something incredibly strong in AR binding (tren), or attack it from a different pathway (genomic) like Anadrol which has shown some interesting transcriptional activity at the promoter region without having measurable AR binding.
So that is why I said, later in the cycle, Anadrol may be better used. It would be intuitive to target other pathways when the body resists. Just the other day I read about someone using YK-11 or a myostatin inhibitor later in a cycle when myostatin is increased. I don't know much about YK-11 but I liked their though process.
Toggling fasted states to reduce the body's down regulation, more insulin sensitivity, etc. etc.
Dat really liked Anadrol didn't he. I remember you Hilly, from MuscleTalk as well. I think back when Maxiter was posting on there.
This is one note Dat made on the Holterhus study when trying to figure out why some steroids have such high myotropic potential even though their AR binding affinity is so weak:
"They concluded that their results were due to specific ligand-induced conformation changes which determined how the hormone receptor complex can specifically interact with coregulators and neighbouring transcription factors. This meant that transactivation capability (extent of activation) depends on the structure of the response element (a short sequence of DNA within the promoter of a gene that is able to bind a specific hormone receptor complex and therefore regulate transcription). Understanding that a response element binds to this androgen receptor complex at least helps us visualize that different “shaped” receptor complexes may “fit” differently. Coregulators may attach along the way or behave differently and together this “blob” which looks different then another steroid induced “blob” may enter and interact in the nucleus distinctly.
Again this is a new area of understanding and how androgen receptors interact with its coregulators in different tissues is paramount to understanding how anabolic steroids exert their actions. It also clues us in to the possibility of emphasizing an anabolic action (as a totality of a steroid cocktail and timing) over the actions of an androgenic singular compound."
Potts GO, Arnold A, Beyler AL (1976), Dissociation of the androgenic and other hormonal activities from the protein anabolic effects of steroids. In: Kochakian CD (ed). Handbook of Experimental Pharmacology, vol. 43. Springer-Verlag: Berlin, pp 361–401.
^ This was interesting because it showed the anadrol and winstrol having low binding affinity yet much higher myotropic activity. Perhaps this can be used to our advantage with constructing cycles.
About using anadrol for prolonged periods, there are a lot of studies (not about anadrol) showing lag in gene transcription between signaling and expression over weeks. Perhaps a threshold requirement that a longer duration of signalling reaches.
Anything truly myotropic at the level of Anadrol or Anavar should be taken for enough time to accrete enough dry weight muscle tissue, not just that glycogen supercompensation and intracellular water swelling we see in the short term... Since during muscle atrophy, myonuclei that have been donated to the muscle fibers do not degrade like the fiber structure, and some evidence shows it is these myonuclei that play a role in the vague and mysterious "muscle memory" that we experience after we start to workout again...
I imagine taking something that is incredibly myotropic needs a longer duration to actually have more myonuclei donated and more dry weight tissue accretion. I hate to use the word permanent, but there is something to be said about striving for something more than glycogen swelling.
My "claims"? Easily refuted by evidence? What?
My "claim" was the fact that the human body releases various isoforms of GH, not just the 22kda isoform that we inject. My "claim" was that these isoforms are released for a reason.
I then showed the ratios of how the isoforms are released together. How different isoforms bind to different binding proteins. There was discussion about how some isoforms are missing amino acids in the chain, how some bind to receptors differently. There is a different blend of GH isoforms released after exercise...
So my "claims" were that the body probably has good reasons for producing these various isoforms and that we should strive to maintain or enhance those various isoforms...
The foolish statements came from the other poster who said the body is not optimal/efficient and often doesn't have reason for what it does.
This poster argued that the single isoform of GH we inject is all that the body needs and that the other isoforms are not necessary.
So no there was no evidence showing me why the body is wrong and the poster was right.
If anything, it is "hippy", arrogant and unwise to claim the body is producing unnecessary peptides for no reason... that is a very "hippy" vague statement.
If I was a betting man, I would probably bet there is a ton of undiscovered reasons for the various isoforms besides the research posted in that thread. Especially when these variants are consistently produced in specific ratios and in specific circumstances.
That whole argument came down to this:
Person A believes we should try to maintain or enhance the hormones and peptides the body natural produces for all the known and still unknown physiological functions they serve.
Person B believes the body doesn't know what it is doing often and those peptides are unimportant. One synthetic isoform does the same thing as all the varous isoforms and serves all physiological functions and parameters.
The burden of proof is on those who argue against the body. If the body produces hormones or peptides in a pulsatile pattern, the burden of proof is on someone to show why pulsatile pattern is NOT important when taking a long acting hormone or peptide.
If the body produces 6 isoforms of GH in specific ratios and at specific times, the burden of proof is on the party claiming only ONE isoform satisfies the same functions.
Hope this clears things up.
There is a certain logical fallacy that you used against Dat. By mentioning that he is a lawyer you sought to try and discredit the information he provided, even though his background as a lawyer has no bearing.
Have you considered that he used studies by academics/researchers (credentialed) and often double/triple supported theories based on various studies coming together?
If the man used studies by scientists, doctors, researchers etc. and wanted other people to help elucidate information from these studies, please tell me how the information is invalidated?
He followed the scientific observations of our time... the studies and data of our time. In fact, he sometimes found errors in their studies. He did not go off on his own with heretical cult like theories. I can't think of anything he said that wasn't supported with evidence. Your comment on him emphasizes your thought process and with that, I am finally done with this conversation.
wouldn't this mean time off and time on to resensitize would be the best utility.
Like lets say for example youre on 500 test or whatever, then when gains stall in 6-8 weeks you get on drol for 8 weeks to break up the myostatin other genes limiting growth and repeat?
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