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, VO 2max 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.
Intense physical exercise increases systemic 11 beta-hydroxysteroid dehydrogenase type 1 activity in healthy adult subjects
SABA, ALESSANDRO;
2010-01-01
Abstract
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, VO 2max 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
