Document Detail


The post-exercise oxidative stress is depressed by acetylsalicylic acid.
MedLine Citation:
PMID:  12380009     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Jean Steinberg; Marc Gainnier; Fabrice Michel; Marion Faucher; Christiane Arnaud; Yves Jammes
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Respiratory physiology & neurobiology     Volume:  130     ISSN:  1569-9048     ISO Abbreviation:  Respir Physiol Neurobiol     Publication Date:  2002 Apr 
Date Detail:
Created Date:  2002-10-16     Completed Date:  2003-01-29     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  101140022     Medline TA:  Respir Physiol Neurobiol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  189-99     Citation Subset:  IM    
Affiliation:
Laboratoire de Physiopathologie Respiratoire (UPRES EA 2201), Faculté de Médecine, Institut Jean Roche, Université de la Méditerranée, Boulevard Pierre Dramard, 13916 Marseille, France.
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MeSH Terms
Descriptor/Qualifier:
Adult
Ascorbic Acid / analysis,  blood
Aspirin / pharmacology*
Cyclooxygenase Inhibitors / pharmacology*
Dose-Response Relationship, Drug
Exercise / physiology*
Glutathione / analysis,  blood
Humans
Kinetics
Lactic Acid / blood
Male
Oxidative Stress / drug effects*
Potassium / blood
Thiobarbituric Acid Reactive Substances / metabolism
Time Factors
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Thiobarbituric Acid Reactive Substances; 50-21-5/Lactic Acid; 50-78-2/Aspirin; 50-81-7/Ascorbic Acid; 70-18-8/Glutathione; 7440-09-7/Potassium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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