The saturated-receptors thing has limited application. The body has plenty of ability to make androgen receptors, and people argue over whether-or-not androgen receptors up-regulate themselves. Of course though, at any point of time, a person may take excessive androgens that they practically "saturate" receptors at that point of time.
It seems as though the limitations come from other feed-back loops, such as Myostatin itself. Yes, taking androgens and other stimulants can increase myostatin as a part of an attempt to obtain homeostasis. Obviously, androgens increase both follistatin and myostatin, creating an escalating race between the two.
So if YK can increase Follistatin without triggering the negative-feedback loops, then it would be well worth displacing the Test/Tren.
For an optimal cycle, people don't need to take so much Tren that they excessively activate the negative-feedback loops, and like I said, it's not so much about occupying the AR, but it's about how to activate the AR. The AR is not just a binary ON/OFF switch. It's a three-dimensional molecule that conforms to the way in which ligands/proteins binds to it; therefore, having different kinds responses.