The adolescent growth spurt is associated with a sex steroid hormone-dependent rise in GH production; both androgens and estrogens are implicated as positive regulators of the somatotropic axis during puberty. The issue is complicated by the fact that testosterone may act both directly via the androgen receptor and indirectly, after its aromatization to 17beta-estradiol, through the estrogen receptor. Recently, a number of investigators have studied the effects of the administration of androgen and estrogen receptor antagonists, as well as nonaromatizable androgens, on GH secretion. These reports suggest that estrogen receptor-dependent processes play a facilitatory role in the pubertyassociated rise in GH secretion. If androgen receptor-mediated events are involved in the control of the somatotropic axis, their role is likely inhibitory. A hypothalamic site of action of the sex steroids is postulated.