E2 inhibits IGF-1 and might attenuate the circulating IGF-1 responses to GH (9), primarily based on the premise that estrogen might down-regulate hepatic GH receptors, alter the hypathopituitary–adrenal axis (HPTA), and impede tissue responsiveness to GH (16). In light of this, we were interested in determining the effects of Novedex XT supplementation on serum GH and cortisol. For the placebo and Novedex groups, we observed no changes in serum cortisol; although not significant, over the course of the supplementation period there was an average 45% decrease in serum GH in the Novedex group. Although we did not measure
serum IGF-1, in the context of incomplete inhibition of aromatase activity with Novedex XT, it is plausible that the suppression in the HPTA and potential GH-receptor down-regulation might have affected the hepatic release of IGF-1, thereby possibly negating any observable increases in fat-free mass. This assumption can be partly supported by previous data showing that complete E2 suppression with anastrozole had no effect on serum GH but decreased IGF-1 (16) and that a 38% suppression of E2 with exemestane had no effect on IGF-1 (15).