The effects of undernutrition on the timing of puberty and regulation of LH secretion by the inhibitory and stimulatory feedback action of estradiol were examined in female sheep. The first experiment determined that maintenance of low BW (ca., 20 kg, four lambs) between 10 and 45 weeks of age prevented initiation of ovulation at the usual time (30 weeks of age). Ad libitum feeding of such growth-retarded lambs (n = 7) resulted in rapid catch-up growth and onset of reproductive cycles. The second experiment determined the effects of level of nutrition on tonic LH secretion in the presence and absence of inhibitory steroid feedback. Detailed LH patterns were obtained from agonadal lambs (ovariectomy at 20 weeks) that either remained undernourished (ca., 20 kg, 10-39 weeks of age) or were initially undernourished (10-27 weeks) and subsequently fed ad libitum (28-39 weeks). In undernourished lambs (n = 7), LH pulse frequency was slow, and only an occasional LH pulse was detected in the absence of steroid negative feedback; chronic treatment with low levels of estradiol (Silastic capsule), beginning at ovariectomy, prevented pulsatile LH secretion (six lambs). Ad libitum feeding (six lambs) produced a progressive severalfold increase in LH pulse frequency. Estradiol during ad libitum feeding (six lambs) markedly reduced amplitude of LH pulses and retarded the increase in LH pulse frequency. The third experiment, conducted at 40 weeks of age, determined the response to the stimulatory feedback action of estradiol. LH surges were readily induced in undernourished (20 kg) ovariectomized lambs (peak height 51 +/- 16 ng/ml, n = 6 of seven); chronic pretreatment with estradiol markedly reduced the magnitude of the LH surge (peak height 7 +/- 3 ng/ml, four of six). These findings raise the possibility that severe undernutrition prevents ovulation in the lamb by impairing the system governing GnRH secretion and its production of high-frequency LH pulses for follicular development to the preovulatory stage and its establishment of sufficient pituitary LH reserves for release by estradiol stimulatory feedback.