Our aim was to examine whether 1) growth-inducing exercise altered the pulsatile pattern of GH release, 2) endogenous opiates mediated these changes, and 3) endogenous somatostatin (SRIF) suppressed pulsatile GH secretion in slowly growing sedentary hamsters. To that end, mature female hamsters were either exposed to 2 weeks of voluntary running or prevented from engaging in running activity. Intracardiac catheters were inserted to allow blood collection every 20 min during 6 h. GH and PRL secretory patterns were determined with homologous RIAs for hamster hormones after administration of saline, naloxone, or anti-SRIF serum. It was found that exercise accelerated somatic growth. GH pulse frequency and amplitude were significantly higher in rapidly growing hamsters. The rate of growth was inversely related to basal trough values of GH and PRL. Opiate receptor blockade reduced GH pulse frequency and amplitude to below sedentary values and did not affect PRL secretion. Anti-SRIF serum increased GH pulse frequency and amplitude in naloxone- as well as in saline-injected animals. Our results are consistent with the conclusions that 1) rapid growth, spontaneous or induced by exercise, is associated with increased GH pulse frequency and amplitude and decreased GH and PRL baseline concentrations in hamsters; 2) endogenous SRIF inhibits pulsatile GH secretion in slowly growing hamsters; and 3) endogenous opiates mediate increases in GH pulse frequency and amplitude in rapidly growing hamsters by antagonizing the endogenous SRIF action.