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Corticotropin-Releasing Hormone Is not the Sole Factor Mediating Exercise-Induced Adrenocorticotropin Release in Humans^*

Department of Military Medicine, Uniformed Services University of the Health Sciences Bethesda, Maryland 20814
The Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health Bethesda, Maryland 20892

Address all correspondence and requests for reprints to: Patricia Deuster, Ph.D., Department of Military Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814–4799.

To determine whether CRH is the sole mediator of ACTH release during exercise, five men and five women were given, in a subject-blinded random manner at separate visits, both a 6-h infusion of ovine CRH (1 µg/kg·h) and a saline infusion as a placebo. After the fourth hour of each infusion, when plasma concentrations of ovine CRH were sufficiently elevated to saturate the capacity of the corticotroph to respond further to CRH, each subject completed a high intensity intermittent run. Plasma ACTH and cortisol levels increased significantly during the CRH infusion from 4.6 ± 0.8 (mean ± SE) to 8.6 ± 1.6 pmol/L and from 361 ± 39 to 662 ± 70 nmol/L, respectively (P < 0.05). Despite elevated preexercise cortisol levels during the CRH infusion, plasma ACTH rose to 32.0 ± 8.5 pmol/L after exercise. During the saline infusion, plasma ACTH rose from 3.4 ± 0.6 pmol/L before exercise to 18.1 ± 4.2 after exercise. Time-integrated responses for postexercise values of ACTH and cortisol were higher during the CRH infusion than during the saline infusion (P < 0.05). No significant exercise-induced differences in heart rate or plasma concentrations of lactate, epinephrine, and norepinephrine were observed between the two tests. The findings suggest that some factor(s) in addition to CRH causes ACTH release during exercise. Vasopressin, produced by the magnocellular and/or parvocellular neurons of the hypothalamus, is a likely candidate.

^* The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army or the Uniformed Services University of the Health Sciences. Presented in part at the 1988 Annual Meeting for the American Federation for Clinical Research.

Received October 22, 1990.

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