OK here's the low down:
GH exerts its negative feedback loop in several ways. the first and most well recognised is through IGF-1. IGF-1 exerts its negative feedback loop by inhibiting GHRH production. since the half life of exogeneous GH is 4 hours, and it would seem quite obvious to me, that shutdown induced by IGF-1 even in absurdley high levels would be very short lived. I would say several hours in low GH doses and 24 hours in high doses (IGF-1 has a short half life in the blood).
so in that sense, the pitutary sutdown is a myth. all the studies Ive seen have used ED doses when they could, the only reason for lower frequency was convinience with clinic visits. in the testes cells atrophy on long (AAS) cycles while in the pituitary there has been no documentation of such response, at least not in the studies I found.
now one of the long term shotdown mechanism is through somatostatin, tied strongly to insulin and blood FFA levels. here is where it gets tricky. GH over the long run decreases insulin sensetivity. it is not know yet by the exact mechanism by which blood FFA, bodyfat or insulin levels efect somatostatin, but it is thought to be one of the three or combination thereoff, as high dose IV arginine, a somatostatin regulator was shown to improve GH response to high glucose meal. this is very relevant to bodybuilders who also abuse stimulants and accumulate androgen-related VAT, both adding to insulin resistance.
one other thing is cortisol - IL1(interleukin1) is one of the promoters of GHRH, and high cortisol will supress it (cortisol also decreases insulin sensitivity).
so my advice is to dose as frequently as possible, while trying to keep insulin sensitivity as high as possible, with right choice of food and timing, supplements(KRALA, fish oil, lean extreme), and obviously exercise.
right after the cycle ends, the use of high dose arginine may be benficial, but that is a speculation on my part.
hope this helps
