EXERCISE-INDUCED ACTIVATION OF THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS - MARKED DIFFERENCES IN THE SENSITIVITY TO GLUCOCORTICOID SUPPRESSION

Treadmill exercise activates the hypothalamic-pituitary-adrenal axis a nd evokes metabolic responses proportional to exercise intensity and d uration. To determine whether glucocorticoid administration would alte r humoral and metabolic regulation during exercise, we administered 4 mg dexamethasone (DEX) or placebo to 11 normal, moderately trained men (19-42 yr old) in a double blinded random fashion 4 h before high int ensity intermittent treadmill running. Plasma levels of ACTH, cortisol , arginine vasopressin (AVP), lactate, and glucose were measured befor e, during, and after exercise. A wide range of ACTH responses were see n in the DEX-treated group and arbitrarily defined as two subsets of i ndividuals according to their responses to dexamethasone: DEX nonsuppr essors and DEX suppressors. Exercise-induced increases in heart rate a nd circulating concentrations of cortisol, AVP, lactate, and glucose w ere all significantly greater (P < 0.05) in nonsuppressors (n = 4) com pared to suppressors (n = 7) after both placebo and DEX administration . Interestingly, heart rate, AVP, and lactate responses were unaltered by DEX alone in both groups. In summary, this study demonstrates that normal individuals exhibit differential neuroendocrine and metabolic responses to exercise and pituitary/adrenal suppression after pretreat ment with DEX. These findings reflect marked individual differences in the stress response to exercise that may derive from or lead to diffe rential glucocorticoid negative feedback sensitivity in humans.