Intense physical exercise increases systemic 11β-hydroxysteroid dehydrogenase type 1 activity in healthy adult subjects

Intense physical exercise activates the hypothalamic–pituitary–adrenocortical axis but little is known about changes in glucocorticoid sensitivity at the target cell level. No data are available on the acute effects of exercise on 11β-hydroxysteroid dehydrogenase (11β-HSD) type 1 activity, which generates biologically active cortisol from inactive cortisone and is expressed also in skeletal muscle. Fifteen healthy, trained males (age mean ± SE 28 ± 1) were assessed on three non-consecutive days: at rest, during an endurance and strength sessions. During each session, between 1000 and 1600 hours, 6-h urine and four salivary samples were collected. Urinary total tetrahydrocortisol (THF) + alloTHF, tetrahydrocortisone (THE), cortisol (F) and cortisone (E) were measured with HPLC-tandem mass spectrometry; urinary-unconjugated F and E were measured by HPLC-UV. Salivary cortisol and interleukin (IL)-6 were measured by RIA and ELISA, respectively. Both endurance and strength exercises caused an increase in (THF + alloTHF)/THE ratio (mean ± SE 1.90 ± 0.07 and 1.82 ± 0.05 vs. 1.63 ± 0.06, P < 0.01 and P = 0.03, respectively), consistent with increased systemic 11β-HSD type 1 activity. No relationship was found with age, BMI, \( V{{{\text{O}}_{2\max } }} , \) maximal power load or perceived exertion. No significant change was apparent in F/E ratio, an index of 11β-HSD type 2 activity. No effect of exercise on salivary cortisol and IL-6 was observed, whereas a significant effect of sampling time was found. Intense physical exercise acutely increases systemic 11β-HSD type 1 activity in humans. Such an increase may lead to higher cortisol concentration in target tissues, notably in skeletal muscle where it could contribute to limit exercise-induced muscle inflammatory response.