title: The post-exercise oxidative stress is depressed by acetylsalicylic acid.
abstract: In order to assess whether oxidative stress occurs after fatiguing dynamic contractions of a small forearm muscle group, we estimated the kinetics of changes in some of its biomarkers (thiobarbituric acid reactive substances or TBARS; plasma reduced ascorbic acid or RAA; erythrocyte reduced glutathione or GSH). We also tested the hypothesis that acetylsalicylic acid (ASA) may compete with endogenous radical targets, attenuating the post-exercise oxidative stress. Seven male subjects successively performed a 3-min dynamic handgrip exercise with the dominant and then the contralateral forearm. Blood samples were taken from an antecubital vein in each exercising forearm. Biochemical analyses, including the concentration measurements of lactic acid, potassium, and oxidative stress markers were performed at rest and then during the 30-min period of recovery following each exercise. The same day, exercises were repeated after ingestion of a single dose (10 mg/kg) of ASA, and the same exercises were performed after a 3-day ASA treatment (30 mg/kg/day). In control condition, the changes in TBARS, RAA and GSH were already significant immediately after the end of the forearm exercise. They culminated after 5 min, and control values were recovered by a 30-min rest period. We verified that repeated bouts failed to alter the post-exercise variations. ASA did not modify the lactic acid production significantly, though the 3-day ASA treatment significantly reduced the efflux of potassium (-74%, P < 0.05), and the post-exercise variations of TBARS (-45%, P < 0.01), RAA (-44%, P < 0.01) and GSH (-48%, P < 0.01). These results suggest that the dynamic handgrip exercise is a good model for studying the post-exercise oxidative stress and also that ASA seems to offer an efficient protection against oxidative stress and the changes in membrane permeability to potassium.
authors.affiliation: Laboratoire de Physiopathologie Respiratoire (UPRES EA 2201), Faculté de Médecine, Institut Jean Roche, Université de la Méditerranée, Boulevard Pierre Dramard, 13916 Marseille, France.
authors.forename: Jean
authors.initials: J
authors.lastname: Steinberg
authors.forename: Marc
authors.initials: M
authors.lastname: Gainnier
authors.forename: Fabrice
authors.initials: F
authors.lastname: Michel
authors.forename: Marion
authors.initials: M
authors.lastname: Faucher
authors.forename: Christiane
authors.initials: C
authors.lastname: Arnaud
authors.forename: Yves
authors.initials: Y
authors.lastname: Jammes
mesh_terms: D000328:Adult; D001205:Ascorbic Acid / Q000032:analysis / Q000097:blood; D001241:Aspirin / Q000494:pharmacology*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D015444:Exercise / Q000502:physiology*; D005978:Glutathione / Q000032:analysis / Q000097:blood; D006801:Humans; D007700:Kinetics; D019344:Lactic Acid / Q000097:blood; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D011188:Potassium / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors
chemical_list: D016861:Cyclooxygenase Inhibitors; D017392:Thiobarbituric Acid Reactive Substances; D019344:Lactic Acid; D005978:Glutathione; D001205:Ascorbic Acid; D001241:Aspirin; D011188:Potassium