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Department of Obstetrics and Gynecology, Northwestern University Medical School, Northwestern Memorial Hospital Chicago, Illinois 60611 Department of Reproductive Medicine, School of Medicine (T-002) General Clinical Research Center, Universityof California San Diego, La Jolla, California 92093
Address requests for reprints to: R. W. Rebar, Department of Obstetrics and Gynecology, Prentice Women's Hospital and Maternity Center, Northwestern University Medical School, 333 East Superior Street, Chicago, Illinois 60611.
Because we previously found increased basal serum cortisol levels in women runners,we examined adrenocortical function in amenorrheic running women (AR), eumenorrheic running women (R), and normal nonexercising women (NC) in further detail. Mean 24-h urinary cortisol levels were significantly elevated (P < 0.001) in six AR [45.1 ± 7.2 (±SEM) µg/24 h] andeight R (38.5 ± 6.9 µg/24 h) compared to four NC (13.9 ± 2.8 µg/24 h). After adrenal suppression with 2 mg dexamethasone, integrated responses and absolute maximal elevations in serum cortisol levels in response to 10 µg/m2 exogenous ACTH (1-24) administered as an iv bolus dose, were not significantly different among six AR,six R, and six NC. This dose of ACTH results in maximal steroid release. The disappearance ratesof cortisol (5 mg, iv) after dexamethasone suppression were similar in four AR, five R, and fourNC and corresponded to a two-compartment model with mean half-lives of 4.9 and 93.8 min, respectively. Cortisol-binding globulin levels werealso similar among the groups. These data document higher cortisol secretion and suggest increased ACTH secretion in running women.
* This work was supported in part by NIH Grants HD-12303 and HD-19542 and the UCSD General Clinical Research Center NIH/Division of Research Resources (Grant RR-00827). Presented in part at the 32nd Annual Meeting of the Society for Gynecologic Investigation, March 1985.
Received July 12, 1985.
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