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Preservation of Pulsatile Luteinizing Hormone Release during Postpartum Lactational Amenorrhea^*

WALLACE C. NUNLEY, RANDALL J. URBAN, WILLIAM S. EVANS and JOHANNES D. VELDHUIS

Interdisciplinary Graduate Biophysics Program Charlottesville, Virginia 22908
The Departments of Obstetrics and Gynecology, University of Virginia Health Sciences Center Charlottesville, Virginia 22908
The Departments of Internal Medicine, University of Virginia Health Sciences Center Charlottesville, Virginia 22908
The Departments of NSF Science Center for Biological Timing, University of Virginia Health Sciences Center Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Dr. Johannes D. Veldhuis, Division of Endocrinology and Metabolism, Box 202, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908.

To evaluate the pulsatile mode of immunoactive LH release during physiological lactational amenorrhea, we withdrew blood samples at 10-min intervals for 24 h from breastfeeding women (n = 9) at both 3 weeks and 3 months postpartum. Nonlactating women (n = 7) were sampled similarly in the early follicular phase of the normal menstrual cycle. Objective LH pulse analysis revealed that the mean frequencies of pulsatile LH release were similar at both times postpartum and in menstruating young women. By 3 months postpartum, mean serum PRL concentrations had declined 50%, and serum LH peak areas doubled. In contrast, LH interpulse interval, peak duration, and maximal, incremental, and fractional LH pulse amplitude did not change significantly. When deconvolution analysis was used to assess pituitary responses to two pulses of exogenous GnRH at 3 months (vs. 3 weeks) postpartum, we found significant increases in maximal LH secretory rates and the total mass of LH secreted. There was no change in the duration or timing of the evoked LH secretory burst and/or the estimated half-life of endogenous LH. In summary, during lactational amenorrhea, pulsatile LH release occurs at a mean frequency no different from that in the normal early follicular phase. As hyperprolactinemia wanes, there is increased pituitary responsiveness to exogenously administered GnRH and a doubling of spontaneous serum LH concentration peak areas. Such amplitude changes are consistent with the hypothesis of increased endogenous GnRH drive (e.g. augmented GnRH secretion per burst and/or increased pituitary responsiveness to available GnRH) during recovery of the postpartum hypothalamopituitary-ovarian axis.

^* This work was supported in part by NIH Grant RR-00847 (to the Clinical Research Center of the University of Virginia), Research Career Development Award 1KOR-HD-00634 (to J.D.V.), NIH Research Career Development Award 1KO4-HD-00711 (to W.S.E.), NIH Diabetes and Endocrinology Research Center Grant DK-38942, NIHsupported Clinfo Data Reduction Systems, the Pratt Foundation, and the NSF Science Center for Biological Timing.

Current address: Charlotte Memorial Hospital and Medical Center, Post Office Box 32861, Charlotte, North Carolina 28232-2861.

Current address: Division of Endocrinology, Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas 77550.

Received November 5, 1990.

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