We show that in an experimentally enforced estradiol-predominant milieu, postmenopausal compared with premenopausal women maintain 1) decreased fasting GH and IGF-I concentrations, 2) reduced basal and pulsatile GH secretion, and 3) attenuated GH secretion after maximal stimulation by the paired secretagogues l-arginine/GH-releasing peptide (GHRP)-2, l-arginine/GHRH, and GHRP-2/GHRH. These foregoing outcomes are selective, because menopausal status did not determine mean GH secretory-burst frequency or peptide-induced waveform shortening. Abdominal visceral fat mass predicted up to 25% of the variability in fasting and stimulated GH secretion in the combined cohorts under fixed systemic estradiol availability. Accordingly, as much as three-fourths of interindividual differences in burst-like GH secretion among healthy pre- and postmenopausal women arise from age-related mechanisms independently of short-term systemic estrogen availability and relative intraabdominal adiposity.