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Exp Physiol. 2018 Feb 1;103(2):172-178. doi: 10.1113/EP086746. Epub 2017 Dec 20.

Oxidative stress does not influence local sweat rate during high-intensity exercise.

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Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada.
Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba City, Japan.
Faculty of Physical Activity Sciences, University of Sherbrooke, Sherbrooke, Quebec, Canada.
Departments of Medicine, Cardiac Sciences and Community Health Sciences, University of Calgary, Calgary, Alberta, Canada.
Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.


What is the central question of this study? We evaluated whether oxidative stress attenuates the contribution of nitric oxide to sweating during high-intensity exercise. What is the main finding and its importance? In contrast to our previous report of an oxidative stress-mediated reduction in nitric oxide-dependent cutaneous vasodilatation in this cohort during intense exercise, we demonstrated no influence of local ascorbate administration on the sweating response during moderate- (∼51% peak oxygen uptake) or high-intensity exercise (∼72% peak oxygen uptake). These new findings provide important mechanistic insight into how exercise-induced oxidative stress impacts sudomotor activity. Nitric oxide (NO)-dependent sweating is diminished during high- but not moderate-intensity exercise. We evaluated whether this impairment stems from increased oxidative stress during high-intensity exercise. On two separate days, 11 young (24 ± 4 years) men cycled in the heat (35°C) at a moderate [500 W; 52 ± 6% peak oxygen uptake (V̇O2 peak )] or high (700 W; 71 ± 5% V̇O2 peak ) rate of metabolic heat production. Each session included two 30 min exercise bouts separated by a 20 min recovery period. Local sweat rate was monitored at four forearm skin sites continuously perfused via intradermal microdialysis with the following: (i) lactated Ringer solution (Control); (ii) 10 mm ascorbate (Ascorbate; non-selective antioxidant); (iii) 10 mm NG -nitro-l-arginine methyl ester (l-NAME; NO synthase inhibitor); or (iv) 10 mm ascorbate plus 10 mm l-NAME (Ascorbate + l-NAME). During moderate exercise, sweat rate was attenuated at the l-NAME and Ascorbate + l-NAME sites (both ∼1.0 mg min-1  cm-2 ; all P < 0.05) but not at the Ascorbate site (∼1.1 mg min-1  cm-2 ; both P ≥ 0.28) in comparison to the Control site (∼1.1 mg min-1  cm-2 ). However, no differences were observed between treatment sites (∼1.4 mg min-1  cm-2 ; P = 0.75) during high-intensity exercise. We conclude that diminished NO-dependent sweating during intense exercise occurs independent of oxidative stress.


hyperthermia; reactive oxygen species; sudomotor activity

[Indexed for MEDLINE]

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