Heat acclimation affects circulating levels of prostaglandin E2, COX-2 and orexin in humans

- Short-term passive heating induced heat acclimation (HA).
- After HA, body temperature decreased, whereas sweat volume increased.
- We examined circulating levels of key thermoregulatory molecules.
- PGE2, COX-2, and orexin decreased significantly compared to those at pre-acclimation.

We examined serum levels of prostaglandin E2 (PGE2), cyclooxygenase (COX)-2 and orexin before and after heat acclimation (HA) to test the hypothesis that decreased basal body temperature due to HA correlate with circulating levels of these key thermoregulatory molecules. Nine healthy human male volunteers were recruited (age, 21.9 ± 2.7 years). The subjects were exposed to half-body immersion in hot water (42 ± 0.5 °C) at the same time of day (2-5 p.m.) on alternate days for 3 weeks. The HA protocol included 10 bouts of 30 min immersion. All experiments were performed in an automated climate chamber (temperature, 26.0 ± 0.5 °C; relative humidity, 60 ± 3.0%; air velocity, <1 m/s). Tympanic and skin temperatures were measured, and mean body temperature was calculated. The difference in body weight was used to estimate total sweat loss. Serum levels of PGE2, COX-2 and orexin were analyzed before and after HA. Body temperature decreased significantly (P < 0.05) after HA, whereas sweat volume increased significantly (P < 0.01). Serum PGE2, COX-2 and orexin concentrations decreased significantly compared to those at pre-acclimation (P < 0.001, P < 0.01, P < 0.01, respectively). Our data suggest that decreased basal body temperature after HA is associated with decreases in thermoregulatory molecules, such as PGE2, COX-2 and orexin.