Although I don't normally respond to trolls or jerks like you, I am making an exception. You can carry this on if you want, but unless you have something current and persuasive, just go away for the sake of the others. I can see through your BS, if others can't.
The whole article you cite is about the half lives of ARs and the possible up-regulation of ARs, written 20 years ago, when the RNA strands and subsequent DNA strands forming a template through transcription were not well understood and hypothesizes drawn were suspect. The whole article actually struggles to explain why, on one hand the transcriptional activity appears to increase androgens in the presence of induced androgens while on the other hand imposing a self mediated stopping point, or down-regulation. Otherwise the more AAS you introduce and the longer you stayed on, the larger you would become with cancerous like growth of the ARs. Even the author of your citation admitted that the data, including his studies, were, “unfortunately the data are equivocal.”
Even the study, which used isotopically dense amino acids to determine the rates of receptor appearance failed to adequately and accurately distinguish between sensitivity and appearance, but surmised through basal transcription data that not only was sensitivity increased (which I agree) but that production was also increased (something that lacks empirical data on). The logical explanation, assuming you’re following me thus far, is that in the presence of increased androgens the sensitivity of receptors is increased, but not the production of additional cells, but possibly the regeneration of the receptors or extension of half lives.
This would explain two flaws in that 20 year old study. First, DNA, vice receptors, are genetically programmed and the mere introduction of increased androgens would not increase cell production or alter a persons DNA, but could desensitize the numerous cells that androgens would normally not bind to. It would also logically explain why we do not grow into the Hulk with more the introduction of increased androgens. The growth we experience at the on-set of AAS is the most growth a person will see. Subsequent cycles show only slightly more muscle alteration, but the initial growth, due to increased AR sensitivity, is responsible for the rapid growth. The explanation given in the article is weak at best and struggles to balance the dichotomy of increased AR production but only to a point, then abstract mediation takes over, something that makes no sense at all.
The transcriptional activity of AR is affected by coregulators that influence a number of functional properties of AR, including ligand selectivity and DNA binding capacity. Unless they are rendered mutant, they are constrained by genetic predisposition and the increased production of AR’s is something that has not been adequately concluded.
Having said that, let’s take up the argument about AR competition. We all know, or hope we do, that there will always be more receptors than androgens,but looking at the viable host receptors, tren will bind tighter to the AR than will test. And with five times the affinity to bind, it will be the dominant participant. Androgens have a very short window in which to bind. It’s not as if there are enough receptors to go around, so all androgens get a host receptor. It doesn’t work that way. If a person is on tren he needs to let the tren work and do its job. Your position that the only reason a person lowers his test is to reduce sides is ironically correct. Do you see the irony?