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Corticotropin-releasing hormone is not the sole factor mediating exercise-induced adrenocorticotropin release in
1Department of Military Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
Insights
Corticotropin-releasing hormone (CRH) alone does not fully explain ACTH release during exercise. Other factors, possibly vasopressin, contribute to the stress response, indicating a complex hormonal interplay.
Area of Science:
- Endocrinology
- Exercise Physiology
- Neuroendocrinology
Background:
- The hypothalamic-pituitary-adrenal (HPA) axis regulates the body's stress response.
- Corticotropin-releasing hormone (CRH) is a key mediator of adrenocorticotropic hormone (ACTH) release from the pituitary gland.
Purpose of the Study:
- To investigate if CRH is the sole trigger for ACTH release during high-intensity exercise.
- To identify potential additional factors involved in exercise-induced ACTH secretion.
Main Methods:
- Ten healthy adults (5 men, 5 women) participated in a randomized, double-blind study.
- Subjects received either a 6-hour infusion of ovine CRH or a saline placebo.
- High-intensity intermittent running was performed after 4 hours of infusion.
- Plasma ACTH, cortisol, heart rate, lactate, epinephrine, and norepinephrine were measured.
Main Results:
- CRH infusion significantly increased plasma ACTH and cortisol levels.
- Exercise led to a substantial rise in ACTH, even with elevated baseline CRH levels.
- Post-exercise ACTH and cortisol responses were significantly higher during CRH infusion compared to placebo.
- No significant differences in heart rate or key metabolic/catecholamine markers were observed between conditions.
Conclusions:
- CRH is not the sole factor mediating ACTH release during exercise.
- Additional neurohormonal factors, such as vasopressin, likely contribute to exercise-induced ACTH secretion.
- The findings highlight the complex regulation of the HPA axis during physical stress.
Abstract:
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 microgram/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 less than 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 less than 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.