Endurance and strength exercise effects on cortisol metabolism

Introduction Intense physical exercise is known to increase the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. In addition to the widely investigated effects on the HPA axis, physical activity has been shown to modulate glucocorticoid (GC) sensitivity at the target cell level. In recent years, attention has been drawn to 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 and 2 as major determinants of tissue sensitivity to GCs. In the present work we show that intense physical exercise (of either endurance or strenght type) is able to increase acutely systemic 11beta-HSD type 1 activity, and suggest that such an increase represents an early step of the stress response to exercise. Methods. Fifteen healthy, trained males (age: median 29, range 20-36 years, BMI 24.6, 20.7-34.3 kg/m2) were assessed on three non consecutive days: at rest, during an endurance and a strength sessions. Preliminarily, maximal oxygen uptake (VO2max) and maximal power (one-repetition maximum, 1RM) were assessed. During each session, between 10.00 and 16.00 h, 6-h urine and 4 salivary samples were collected. Urinary total tetrahydrocortisol, tetrahydrocortisone, cortisol and cortisone were measured with HPLC-tandem mass spectrometry; urinary unconjugated cortisol and cortisone were measured by HPLC-UV. Salivary cortisol were measured by RIA and ELISA, respectively. Results Both endurance and strength exercises caused an increase in tetrahydrocortisol/ tetrahydrocortisone ratio (endurance: mean\ub1SE 1.90\ub10.07 vs. 1.63\ub10.06, P