Evidence for cyclooxygenase‐dependent sweating in young males during intermittent exercise in the heat

• Published in: The Journal of physiology Vol. 592; no. 23; pp. 5327 - 5339
• Main Authors: Fujii, Naoto, McGinn, Ryan, Stapleton, Jill M., Paull, Gabrielle, Meade, Robert D., Kenny, Glen P.
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01-12-2014; BlackWell Publishing Ltd
• Subjects: Adult; Body Temperature Regulation - drug effects; Body Temperature Regulation - physiology; Cyclooxygenase Inhibitors - administration & dosage; Cyclooxygenase Inhibitors - pharmacology; Exercise - physiology; Fever - physiopathology; Heat Stress Disorders - etiology; Heat Stress Disorders - physiopathology; Hot Temperature - adverse effects; Humans; Integrative; Ketorolac - administration & dosage; Ketorolac - pharmacology; Male; NG-Nitroarginine Methyl Ester - administration & dosage; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide - physiology; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase - physiology; Prostaglandin-Endoperoxide Synthases - physiology; Skin - blood supply; Sweating - drug effects; Sweating - physiology; Vasodilation - drug effects; Vasodilation - physiology; Young Adult
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2014.280651

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% V̇O2 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% V̇O2 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.
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). Similar results were obtained for the second exercise at moderate heat load (all P < 0.05). However, forearm sweating was similar between the four sites during exercise at high heat load and during recovery regardless of exercise intensity (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.