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Related Experiment Videos

Exercise can be pyrogenic in humans.

Carl D Bradford1, James D Cotter, Megan S Thorburn

  • 1School of Physical Education, University of Otago, P.O. Box 56, Dunedin, New Zealand.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|January 2, 2007
PubMed
Summary

A COX-2 inhibitor reduced body temperature during exercise by inhibiting prostaglandin production. This indicates that inflammatory processes contribute to heat strain in endurance athletes.

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Area of Science:

  • Exercise Physiology
  • Inflammation and Immunity

Background:

  • Exercise elevates body temperature and plasma cytokine levels.
  • Cytokines stimulate prostaglandin (PG) production via cyclooxygenase (COX) enzymes, and PGE(2) is a known mediator of fever.
  • PGs may contribute to exercise-induced hyperthermia.

Purpose of the Study:

  • To investigate the role of prostaglandin-mediated pyrogenicity in exercise-induced hyperthermia.
  • To test if a COX-2 inhibitor can attenuate the rise in body temperature during exercise.

Main Methods:

  • A double-blind, cross-over study involving 10 male participants.
  • Participants consumed either a COX-2 inhibitor (rofecoxib) or a placebo for 6 days.
  • Thermoregulation was assessed during running and cycling exercise, with measurements of body temperature, heart rate, and cytokine concentrations.

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Main Results:

  • The COX-2 inhibitor significantly lowered mean body temperature during the cycling phase and recovery.
  • Sweating offset occurred at a higher body temperature in the placebo condition compared to the COX-2 inhibitor condition.
  • Cardiac frequency was higher with the placebo, while metabolic rate remained similar between conditions.
  • Cytokine concentrations increased similarly during exercise in both conditions.

Conclusions:

  • Prostaglandin E2 (PGE2) synthesis inhibition reduces exercise heat strain.
  • COX-2 inhibitors attenuate exercise-induced hyperthermia and cardiovascular strain.
  • Inflammatory pathways, mediated by PGs, play a significant role in human exercise thermoregulation and heat strain.