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Physiology and Pharmacology of Temperature Regulation

Exercise can be pyrogenic in humans

¹School of Physical Education and ²Dunedin School of Medicine, University of Otago, New Zealand

Submitted 31 December 2005 ; accepted in final form 24 July 2006

Exercise increases mean body temperature (_body) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE₂ can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised _body in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), O_{2 max}: 53 ml·kg^–1·min^–1 (SD 5)] consumed rofecoxib (50 mg/day; NSAID) or placebo (PLAC) for 6 days, 2 wk apart. Exercising thermoregulation was measured on day 6 during 45-min running (75% O_{2 max}) followed by 45-min cycling and 60-min seated recovery (28°C, 50% relative humidity). Plasma cytokine (TNF-, IL-10) concentrations were measured at rest and 30-min recovery. _body was similar at rest in PLAC (35.59°C) and NSAID (35.53°C) and increased similarly during running, but became 0.33°C (SD 0.26) lower in NSAID during cycling (37.39°C vs. 37.07°C; P = 0.03), and remained lower throughout recovery. Sweating was initiated at _body of 35.6°C in both conditions but ceased at higher _body in PLAC than NSAID during recovery [36.66°C (SD 0.36) vs. 36.39°C (SD 0.27); P = 0.03]. Cardiac frequency averaged 6·min^–1 higher in PLAC (P < 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W·m^–2; P = 0.56). A modest increase in both cytokines across exercise was similar between conditions. COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans.

body temperature regulation; sweating; inflammation; fever; cyclooxygenase inhibition

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