title: Exercise can be pyrogenic in humans.
abstract: Exercise increases mean body temperature (T(body)) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE(2) can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised T(body) in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), Vo(2 max): 53 ml x kg(-1) x 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 ( approximately 75% Vo(2 max)) followed by 45-min cycling and 60-min seated recovery (28 degrees C, 50% relative humidity). Plasma cytokine (TNF-alpha, IL-10) concentrations were measured at rest and 30-min recovery. T(body) was similar at rest in PLAC (35.59 degrees C) and NSAID (35.53 degrees C) and increased similarly during running, but became 0.33 degrees C (SD 0.26) lower in NSAID during cycling (37.39 degrees C vs. 37.07 degrees C; P = 0.03), and remained lower throughout recovery. Sweating was initiated at T(body) of approximately 35.6 degrees C in both conditions but ceased at higher T(body) in PLAC than NSAID during recovery [36.66 degrees C (SD 0.36) vs. 36.39 degrees C (SD 0.27); P = 0.03]. Cardiac frequency averaged 6 x min(-1) higher in PLAC (P < 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W x 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.
authors.affiliation: School of Physical Education, University of Otago, P.O. Box 56, Dunedin, New Zealand.
authors.forename: Carl D
authors.initials: CD
authors.lastname: Bradford
authors.forename: James D
authors.initials: JD
authors.lastname: Cotter
authors.forename: Megan S
authors.initials: MS
authors.lastname: Thorburn
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Walker
authors.forename: David F
authors.initials: DF
authors.lastname: Gerrard
mesh_terms: D000328:Adult; D015308:Anaerobic Threshold / Q000502:physiology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D015992:Body Mass Index; D001831:Body Temperature / Q000502:physiology; D001833:Body Temperature Regulation / Q000502:physiology*; D002245:Carbon Dioxide / Q000097:blood; D051546:Cyclooxygenase 2 / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D016207:Cytokines / Q000097:blood; D004311:Double-Blind Method; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005542:Forearm / Q000098:blood supply; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D009043:Motor Activity / Q000502:physiology; D010101:Oxygen Consumption / Q000502:physiology; D010809:Physical Fitness / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D012881:Skin Temperature / Q000502:physiology; D013546:Sweating / Q000502:physiology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D016207:Cytokines; D002245:Carbon Dioxide; D051546:Cyclooxygenase 2