Androgen receptors (AR) don't get "fried" (whatever that means) but they do get downregulated as a consequence of their rate of binding exceeding their rate of synthesis. It isn't really a homeostatic mechanism it just a physical limit.
The AR is a protein molecule embedded in the membrane or cytoplasm of various androgen sensitive cells (eg. skeletal muscle cells). The AAS that you are ingesting and injecting -- and their androgenic/anabolic metabolites -- eventually bind with the AR and form what is termed a steroid-receptor complex (SRC). The SRC migrates to the nucleus of the cell to eventually produce the androgenic/anabolic response i.e. growth. So the AR that was once in the cytoplasm of the cell waiting to bind to a steroid is no more, it is now in the nucleus of the cell causing proteins to be synthesised. The AR that became an SRC has to be replaced if the cell is to retain its androgen responsiveness. Sythesising AR takes time and materials (amino acids) it doesn't happen "automagically". When the rate of SRC formation exceeds the rate of AR synthesis the cell experiences a net reduction in AR and the cell consequently loses androgen sensitivity, the same amount of androgen now produces less of an androgenic/anabolic response, i.e. it becomes downregulated.
Dosing protocols such as blast 'n' cruise are intended to avoid the downregulation that occurs as a result of constant high doses. The "crusing" period gives the muscle cells a chance to restore their AR and to even proliferate ARs i.e. add new ones.
(I am really tired at the moment (leg day) so this may not be as lucid as intended. I will revisit the matter tomorrow and may add diagrams if this will aid clarity.)
.gif "IP Gear")
