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Physiol Rep. 2018 Sep;6(17):e13844. doi: 10.14814/phy2.13844.

Cyclooxygenase-1 and -2 modulate sweating but not cutaneous vasodilation during exercise in the heat in young men.

Author information

1
Human and Environmental Physiology Research Unit, University of Ottawa, Ottawa, Canada.
2
Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

Abstract

We recently reported that the nonselective cyclooxygenase (COX) inhibitor ketorolac attenuated sweating but not cutaneous vasodilation during moderate-intensity exercise in the heat. However, the specific contributions of COX-1 and COX-2 to the sweating response remained to be determined. We tested the hypothesis that COX-1 but not COX-2 contributes to sweating with no role for either COX isoform in cutaneous vasodilation during moderate-intensity exercise in the heat. In thirteen young males (22 ± 2 years), sweat rate and cutaneous vascular conductance were measured at three forearm skin sites that were continuously treated with (1) lactated Ringer's solution (Control), (2) 150 μmmol·L-1 celecoxib, a selective COX-2 inhibitor, or (3) 10 mmol L-1 ketorolac, a nonselective COX inhibitor. Participants first rested in a non heat stress condition (≥85 min, 25°C) followed by a further 70-min rest period in the heat (35°C). They then performed 50 min of moderate-intensity cycling (~55% peak oxygen uptake) followed by a 30-min recovery period. At the end of exercise, sweat rate was lower at the 150 μmol·L-1 celecoxib (1.51 ± 0.25 mg·min-1 ·cm-2 ) and 10 mmol·L-1 ketorolac (1.30 ± 0.30 mg·min-1 ·cm-2 ) treated skin sites relative to the Control site (1.89 ± 0.27 mg·min-1 ·cm-2 ) (both P ≤ 0.05). Additionally, sweat rate at the ketorolac site was attenuated relative to the celecoxib site (P ≤ 0.05). Neither celecoxib nor ketorolac influenced cutaneous vascular conductance throughout the experiment (both P > 0.05). We showed that both COX-1 and COX-2 contribute to sweating but not cutaneous vasodilation during moderate-intensity exercise in the heat in young men.

KEYWORDS:

NSAIDs; cAMP; endothelium-dependent vasodilation; microcirculation; prostanoids; thermoregulation

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