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Oxidative stress does not influence local sweat rate during high‐intensity exercise
Author(s) -
Meade Robert D.,
Fujii Naoto,
Poirier Martin P.,
Boulay Pierre,
Sigal Ronald J.,
Kenny Glen P.
Publication year - 2017
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep086746
Subject(s) - chemistry , oxidative stress , nitric oxide , microdialysis , sweat , exercise intensity , medicine , endocrinology , antioxidant , vitamin c , oxidative phosphorylation , heart rate , biochemistry , blood pressure , extracellular
New FindingsWhat 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 ( V ̇O 2 peak)] or high (700 W; 71 ± 5%V ̇O 2 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 m m ascorbate (Ascorbate; non‐selective antioxidant); (iii) 10 m m N G ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME; NO synthase inhibitor); or (iv) 10 m m ascorbate plus 10 m m 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.