Abstract

To investigate the neuroendocrine changes that regulate initiation of normal menstrual function after parturition, serum LH, FSH, and PRL concentrations were determined at 20-min intervals for 12-24 h in eight nonlactating postpartum women on a weekly basis between postpartum days 10-26. Sleep was monitored by EEG. On postpartum day 10, serum LH concentrations were similar to early follicular phase levels in normal cycling women, while FSH concentrations were lower than early follicular phase levels. Mean LH pulse frequency during each postpartum interval was 3.6 +/- 0.6 (+/- SE), 4.4 +/- 0.6, and 4.1 +/- 0.8 pulses/12 h on postpartum days 10-11, 17-21, and 24-26, respectively. Because mean serum LH levels and LH pulse frequency did not change significantly between postpartum days 10 and 26, the results from the two or three studies in each woman were combined for the purpose of comparing LH pulse characteristics during the waking and sleeping periods. During the waking hours, mean LH pulse frequency (6.1 +/- 0.5 pulses/12 h) was significantly greater than during sleep (4.1 +/- 0.4 pulses/12 h; P less than 0.02). The amplitude of the serum immunoreactive LH pulses (P less than 0.05) and bioactive LH levels (P less than 0.05) were significantly higher during sleep than during the waking period, with five of the eight women having higher sleep-associated immunoreactive LH and bioactive LH levels between postpartum days 17-26. These changes were associated with an increase in the bioactive to immunoactive LH ratio from 3.3 +/- 0.4 (awake) to 4.5 +/- 0.5 (sleep; P less than 0.05). Although serum PRL levels remained elevated during the puerperium, the diurnal pattern of PRL secretion was conserved. With each successive week postpartum, serum PRL concentrations declined. These results suggest that the increment in LH secretion (and, by inference, increased GnRH secretion) during sleep is a feature of postpartum pituitary-ovarian reactivation. Although the mechanism(s) responsible for the increase in GnRH secretion is not known, this hormonal pattern is analogous to that during early puberty and during recovery from anorexia nervosa and hypothalamic amenorrhea. Taken together, these findings provide evidence to support the concept of a centralized preprogrammed scheme for pituitary-gonadal reactivation.

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