Wasn't it the other way around, that more AR activation upregulates it? When a blast has to come to an end as the muscle growth has stopped, I think it's the increase in myostatin that ultimately limits gains in lean mass, not AR desensitization.
Yes, there is an up-regulation of the AR but after sustained elevated testosterone levels some desensitization occurs which leads to a decrease in mRNA levels acting as a negative feedback loop. In several cases it was found that the AR content increased but the binding affinity for androgens decreased resulting in a net loss of testosterone utilization. Essentially, after such a long period of exposure the extra testosterone (above a certain point) can become useless, whereas initially when first starting a cycle the extra free testosterone resulted in an almost linear dose-dependent effect curve. So, there's still benefit to an extended cycle (longer than 12 weeks) but the growth experienced isn't near what one expects an the beginning of a cycle... almost a sort of plateau effect. Leaving a 3 month gap or so between cycles resulted in a stronger initial response to the androgens.
On a separate note, Testosterone increases Dopamine levels, so going from blast to cruise/TRT dose will leave the Dopamine receptors downregulated, which will surely impact one's libido, even if temporarily. Other steroids alter neurotransmitters levels differently from Testosterone, and Oestrogen levels also play a role.
Different AAS can be responsible for varying effects on reward pathways. Long-term administration of nandrolone increased dopamine transporter density, In addition, the density of dopamine receptors was affected by AAS administration; D1 receptors were down-regulated in the striatum and nucleus accumbens, and D2 receptors were down-regulated in the nucleus accumbens, but up regulated in the caudate putamen. In a recent study, nandrolone administration decreased the expression of the D1 dopamine receptor in the nucleus accumbens, Furthermore, studies have reported decreased activity of the dopamine-metabolizing enzymes monoamine oxidase A and B and a decrease in the levels of the dopamine metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid after repeated nandrolone administration.
Several studies have reported AAS-induced changes in the levels of opioid peptides and their receptors in the CNS, In addition to dopamine and opioids, the neurotransmitter serotonin plays an important role in the context of reward, and AAS administration induces alterations in the serotonergic system..
Effects of AAS on other signaling systems in the brain, for example the glutamatergic, and various neuropeptidergic systems, have also been demonstrated (Hallberg, 2011; Le Greves et al., 1997; Rossbach et al., 2007). Glutamate is known to bind with high affinity to N-methyl-D-13 aspartate (NMDA) receptors, which are important for neuronal plasticity, including learning and memory...
