You guys are approaching this from too narrow an angle. Here's my take:
Does receptor down regulation occur in almost all neuroendocrine models? Yes. It is much mire thoroughly studied and described in different neurotransmitter models (dopamine pathway, norepinephrine and serotonin for example. Receptors becoming "tolerant" to something is a simplistic way to say our bodies will recognize that a particular ligand (this is the term for whatever the substance is that binds to said receptor) is present in far greater quantities than normal, and your body be ill then try to maintain homeostasis, or will try to prevent this over abundance of a substance from disrupting its normal balance by one of a few different mechanisms. It will either reduce the number of receptors available for the ligand to bind to (downregulation), or it will increase the activity of the enzyme that clears the substance from the synaptic cleft (the area closest to the receptor), which will effectively reduce the amount of substance that is able to bund to the receptors. These twi processes occur is almost any situation where there is an uber abundance of a chemical. A great example of this is opiate abuse (or any drug, really). When you take painkillers regularly, the "tolerance" you feel is due to a literal invagination of the Mu receptor. So the receptor is essentially re-absorbed by the body in an attempt to prevent too many Mu (opioid) receptors from being bound and activated. The end result of tolerance to the drug is what you "feel". Fewer receptors available = more ligand (PKs) required to achieve the same effect. This has been replicated and proven in almost every neurotransmitter pathway.
Now, that said, the endocrine ( hormone) system has less conclusive data behind it, but there is NO doubt that the two systems are extremely similar in structure, sequence, and function. The main diffrrnec is that hormones take a much longer time to exert eltheir effects, and oftentimes there are confounding variables that make this very hard to study in a truly objective fashion. Do I believe that the exact same receptor downregulatiin occurs? Absolutely. (Even though some less-than-reputable studies suggest an upregulation). OSL brings up a very good point that myostatin increases maybalsi be impacting the overall result. The data are still inconclusive, but in my opinion, and in almost anyone else who is in this field will agree, that it is very very likely that the endocrine system experiences the exact sane receptor fatigue that we see with neurotransmitters. It's simply harder to elucidate the actual mechanism, because if the slow nature of any hormone' action on the body. If I were a betting man, would I throw my life savings on the table right now if I had to bet that the endocrine system receptors are impacted just as all the neurotransmitter pathways are? Yeah, I definitely would. Anyone who tried to make an argument to the contraty will either not know what is what, or will be deluding themselves.
NOW, with that said, does receptor fatigue from extended use of a specific AAS result in anytjings that you as a very un-objkextive user can dedinitevely recognize? Probably not, which is why any argument on it is stupid. I have had way to long of a day to go dig up citations right now, bit I feel qualified to make this post. Reps for anyone who can show otherwise. Proving a causal link between hormone-induced receptor fatigue is a rabbit hole that most avoid, I can definitely day that I have spent a pretty ridiculous amount of ferretting this out, and I know enough to known that own bodies are.
You cm neat this and keep the gains rolling by changing the hell out of your routine
