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.

Introduction

As already demonstrated in other studies, an exhaustive exercise is followed by an enhanced formation of oxygen free radicals by muscle fibers in animals (Alessio et al., 2000, Bejma and Ji, 1999, Best et al., 1999, Kolbeck et al., 1997, Koren et al., 1980, Reid, 1996, Suzuki et al., 1983) and humans (Alessio, 1993, Ashton et al., 1998, Ebbeling and Clarckson, 1989, Lovlin et al., 1987, Sen, 1995, Suzuki et al., 1996, Viguie et al., 1993, Viinika et al., 1984). Both these result in lipid peroxidation of cell membranes, leading to the cell inability to maintain ionic gradients and in tissue inflammation (Fitts, 1994). The post-exercise oxidative stress is first explored through measurements of blood markers which indicate the formation of lipid hydroperoxides, as the thiobarbituric acid reactive substances (TBARS) (Alessio, 1993, Ashton et al., 1998, Bejma and Ji, 1999, Best et al., 1999, Ebbeling and Clarckson, 1989, Joanny et al., 2001, Lovlin et al., 1987) and second through measurements of the consumption of endogenous antioxidants (Joanny et al., 2001, Sen, 1995), estimated by the decrease in plasma reduced ascorbic acid (RAA) and in erythrocyte reduced glutathione (GSH). RAA is the sole endogenous antioxidant that protects completely the membrane lipids against peroxidative damage (Frei et al., 1989, Glascott et al., 1996, Rokitzki et al., 1994), and GSH is the substrate of glutathione peroxidase, an erythrocyte enzyme which protects the cells against the damage caused by oxygen free radicals (Lew and Quantanilha, 1991). We already showed (Joanny et al., 2001) that the occurrence of a post-exercise oxidative stress is indicated by an increased concentration of TBARS and a decreased concentration of RAA and GSH. However, the human literature gives no information on the kinetics of exercise-induced oxidative stress following a forearm exercise, the existing studies concerning only leg exercise.

The oxidative stress is responsible for the activation of the cyclo-oxygenase enzyme which promotes the formation of arachidonic acid and consecutive inflammatory reactions (Ebbeling and Clarckson, 1989, Reid, 1996). The acetylsalicylic acid (ASA) is commonly used to block cyclo-oxygenase and the consecutive inflammation. Moreover, biochemical studies have also suggested that ‘ASA may function as a hydroxyl radical scavenger’ (Aubin et al., 1998, Sagone and Husney, 1987) but it does not exert any protective effect on superoxide ion and H₂O₂ formation (Simchowitz et al., 1979). However, hydroxyl radicals have no chemical specificity virtually and react with the first molecule they encounter. We found no data in the literature on the eventual protective effects of ASA on the post-exercise oxidative stress. Thus, there are no assessments of the efficacy of ASA administered systemically to compete against endogenous hydroxyl radical targets as membrane lipids, glutathione, etc.

In the present study, we chose a protocol constituted by periods of dynamic handgrips in order to estimate the kinetics of the post-exercise TBARS, RAA and GSH changes. We addressed two questions: (1) does the oxidative stress occur after fatiguing dynamic contractions of a small forearm muscle group and, if so, what are the kinetics of its blood markers? and (2) are there any protective effects of acetylsalicylic acid against this oxidative stress?