title: Effect of voluntary exercise on H2O2 release by subsarcolemmal and intermyofibrillar mitochondria.
abstract: Previous data have demonstrated that, to handle the oxidative stress encountered with training at high intensity, skeletal muscle relies on an increase in mitochondrial biogenesis, a reduced H(2)O(2) production, and an enhancement of antioxidant enzymes. In the present study, we evaluated the influence of voluntary running on mitochondrial O(2) consumption and H(2)O(2) production by intermyofibrillar mitochondria (IFM) and subsarcolemmal mitochondria (SSM) isolated from oxidative muscles in conjunction with the determination of antioxidant capacities. When mitochondria are incubated with succinate as substrate, both maximal (state 3) and resting (state 4) O(2) consumption were significantly lower in SSM than in IFM populations. Mitochondrial H(2)O(2) release per unit of O(2) consumed was 2-fold higher in SSM than in IFM. Inhibition of H(2)O(2) formation by rotenone suggests that complex I of the electron transport chain is likely the major physiological H(2)O(2)-generating system. In Lou/C rats (an inbred strain of rats of Wistar origin), neither O(2) consumption nor H(2)O(2) release by IFM and SSM were affected by long-term, voluntary wheel training. In contrast, glutathione peroxidase and catalase activity were significantly increased despite no change in oxidative capacities with long-term, voluntary exercise. Furthermore, chronic exercise enhanced heat shock protein 72 accumulation within skeletal muscle. It is concluded that the antioxidant status of muscle can be significantly improved by prolonged wheel exercise without necessitating an increase in mitochondrial oxidative capacities.
authors.affiliation: Unité Mixte Recherche 5123 CNRS, Université Claude Bernard, Lyon, France.
authors.forename: S
authors.initials: S
authors.lastname: Servais
authors.forename: K
authors.initials: K
authors.lastname: Couturier
authors.forename: H
authors.initials: H
authors.lastname: Koubi
authors.forename: J L
authors.initials: JL
authors.lastname: Rouanet
authors.forename: D
authors.initials: D
authors.lastname: Desplanches
authors.forename: M H
authors.initials: MH
authors.lastname: Sornay-Mayet
authors.forename: B
authors.initials: B
authors.lastname: Sempore
authors.forename: J M
authors.initials: JM
authors.lastname: Lavoie
authors.forename: Roland
authors.initials: R
authors.lastname: Favier
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism*; D015227:Lipid Peroxidation; D008297:Male; D008931:Mitochondria, Muscle / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010101:Oxygen Consumption; D010805:Physical Conditioning, Animal; D051381:Rats; D017208:Rats, Wistar; D012402:Rotenone / Q000494:pharmacology; D012420:Running; D019802:Succinic Acid / Q000378:metabolism
chemical_list: D000975:Antioxidants; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D012402:Rotenone; D019802:Succinic Acid; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D003576:Electron Transport Complex IV