Evidence for cyclooxygenase‐dependent sweating in young males during intermittent exercise in the heat
TL;DR: It is demonstrated that exercise‐induced sweating at a moderate heat production was similarly reduced when COX and NO synthase were inhibited separately and in combination, and that COX inhibitors (e.g. aspirin) may impair core body temperature regulation and thereby increase the risk of heat‐related illness.
read more
Abstract: Key points
Previous studies implicate nitric oxide (NO) in the control of sweating during exercise in the heat; however, it is unclear whether cyclooxygenase (COX) is also involved.
We demonstrated that exercise-induced sweating at a moderate heat production (400 W, ∼40% VO2 max ) was similarly reduced when COX and NO synthase were inhibited separately and in combination.
Alternatively, inhibiting COX and/or NO synthase did not influence exercise-induced sweating at a high heat production (700 W, ∼70% VO2 max ).
We show that both COX and NO are involved in sweating during exercise at moderate heat production and that the effects may not be independent. However, roles for COX and NO are less evident when heat production is elevated.
The results lead to better understanding of the mechanisms of sweating and indicate that COX inhibitors (e.g. aspirin) may impair core body temperature regulation and thereby increase the risk of heat-related illness.
Abstract
Our recent work implicated nitric oxide (NO) in the control of sweating during intermittent exercise; however, it is unclear if cyclooxygenase (COX) is also involved. On separate days, ten healthy young (24 ± 4 years) males cycled in the heat (35°C). Two 30 min exercise bouts were performed at either a moderate (400 W, moderate heat load) or high (700 W, high heat load) rate of metabolic heat production and were followed by 20 and 40 min of recovery, respectively. Forearm sweating (ventilated capsule) was evaluated at four skin sites that were continuously perfused via intradermal microdialysis with: (1) lactated Ringer solution (Control), (2) 10 mm ketorolac (a non-selective COX inhibitor), (3) 10 mm NG-nitro-l-arginine methyl ester (l-NAME; a non-selective NO synthase inhibitor) or (4) a combination of 10 mm ketorolac + 10 mm l-NAME. During the last 5 min of the first exercise at moderate heat load, forearm sweating (mg min−1 cm−2) was equivalently reduced with ketorolac (0.54 ± 0.08), l-NAME (0.55 ± 0.07) and ketorolac+l-NAME (0.56 ± 0.08) compared to Control (0.67 ± 0.06) (all P 0.05). We show that (1) although both COX and NO modulate forearm sweating during intermittent exercise bouts in the heat at a moderate heat load, the effects are not additive, and (2) the contribution of both enzymes to forearm sweating is less evident during intermittent exercise when the heat load is high and during recovery.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
Citations
Human temperature regulation under heat stress in health, disease, and injury.
TL;DR: This review focuses on healthy and disordered human temperature regulation during heat stress, with emphasis on the mechanisms by which various morphological features, intrinsic factors, diseases, and injuries independently and interactively influence deep body temperature during exercise and/or exposure to hot ambient temperatures.
185
Sweating as a heat loss thermoeffector
Daniel Gagnon,Craig G. Crandall +1 more
TL;DR: The role of sweating as a heat loss thermoeffector in humans is reviewed to review the control of sweating can be modified by biophysical factors, heat acclimation, dehydration, and nonthermal factors.
47
Do nitric oxide synthase and cyclooxygenase contribute to the heat loss responses in older males exercising in the heat
Naoto Fujii,Gabrielle Paull,Robert D. Meade,Ryan McGinn,Jill M. Stapleton,Pegah Akbari,Glen P. Kenny,Glen P. Kenny +7 more
TL;DR: In this article, the separate and combined roles of NOS and COX in forearm sweating and cutaneous vasodilatation in older adults during intermittent exercise in the heat were evaluated.
35
Cutaneous vascular and sweating responses to intradermal administration of ATP: a role for nitric oxide synthase and cyclooxygenase?
TL;DR: In this paper, the authors show that in humans in vivo, intradermal administration of ATP induces pronounced vasodilatation which is partially mediated by NOS, but neither COX nor adenosine influences ATP-mediated vasodiliatation, and ATP alone does not induce an increase in sweating.
28
Local infusion of ascorbate augments NO‐dependent cutaneous vasodilatation during intense exercise in the heat
Robert D. Meade,Naoto Fujii,Lacy M. Alexander,Gabrielle Paull,Jeffrey C. Louie,Andreas D. Flouris,Andreas D. Flouris,Glen P. Kenny +7 more
TL;DR: It was shown that local infusion of ascorbate (an anti‐oxidant) improves NO‐dependent forearm cutaneous vasodilatation during high intensity exercise in the heat and provides novel insight into the physiological mechanisms governing cutaneous blood flow during exercise‐induced heat stress.
26
References
PGE1 and PGE2 modify platelet function through different prostanoid receptors.
David Iyú,Madlen Jüttner,Jackie R. Glenn,Ann E. White,Andrew J. Johnson,Susan C. Fox,Stan Heptinstall +6 more
TL;DR: The ability of the selective prostanoid receptor antagonists CAY10441 (IP antagonist), DG-041 (EP3 antagonist) and ONO-AE3-208 (EP4 antagonist) to modify the effects of the prostaglandins on platelet function are investigated to confirm that PGE(2) interacts with EP3 and EP4 receptors, but not IP receptors.
Effects of nitric oxide synthase inhibition on cutaneous vasodilation during body heating in humans
TL;DR: It is demonstrated that NO contributes modestly, but not consistently, to cutaneous vasodilation during body heating in humans, and this indicates that NO is not the only factor responsible for the dilation.
The evaporative requirement for heat balance determines whole‐body sweat rate during exercise under conditions permitting full evaporation
TL;DR: To perform an unbiased comparison of WBSRs (but not necessarily core temperature) between different individuals/groups under conditions allowing full evaporation, future studies should consider using a fixed Ereq irrespective of the % incurred.
Cutaneous Active Vasodilation in Humans Is Mediated by Cholinergic Nerve Cotransmission
Dean L. Kellogg,Pablo E. Pergola,Kenneth L. Piest,Wojciech A. Kosiba,Craig G. Crandall,Mattias Grossmann,John M. Johnson +6 more
TL;DR: It is concluded that cholinergic nerve activation mediates cutaneous active vasodilation through release of an unknown cotransmitter, not through ACh.
Mechanisms of acetylcholine-mediated vasodilatation in young and aged human skin
TL;DR: There was no difference in peak %CVCmax during ACh infusion between age groups, and the response was unchanged by NOS‐I, but an age‐related shift toward COX vasoconstrictors contributing to basal cutaneous vasomotor tone was suggested.