The article is quite flawed sorry.
Phosphoinositide 3-kinase is what is of more interest in that it can cause Myostin inhibition.
The accumulation that Nelson spoke about is correct, as IGF levels peak, they desensitise the receptors.
IGF-1's pro-hypertrophy activity comes predominantly through its ability to activate the Phosphoinositide 3-kinase.
What is of particular note is that P-3-K only increases skeletal muscle size, so by adding in something which causes muscle cell proliferation, and matures satellite muscle cells more increases can come.
IGF1/PI3K also can dominantly inhibit the effects of the protein Myostatin which is a member of the TGF family of proteins.
There is no evidence to conclude that myostain returns to action during a steroid cycle, where p-3-k is activated.
Its more that doses of AAS would need to be steadily increased to keep on causing this selective muscle building signal.
The greater the gains..
And
The longer your on
= The slower the returns, your body adjusts, P-3-K signalling is deactivated and igf levels start to drop, unless the doses are increased accordingly.
That will prevent P-3-K from allowing myostatin to begin to induce muscle inhibition and cellular myotube shrinkage.
Adding in GH at the stage where igf levels start to drop would be of particular benefit as it can enhance muscle cell proliferation.