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Elevated mitochondrial oxidative stress impairs metabolic adaptations to exercise in skeletal muscle.

07:00 EST 1st January 2013 | BioPortfolio

Summary of "Elevated mitochondrial oxidative stress impairs metabolic adaptations to exercise in skeletal muscle."

Mitochondrial oxidative stress is a complex phenomenon that is inherently tied to energy provision and is implicated in many metabolic disorders. Exercise training increases mitochondrial oxidative capacity in skeletal muscle yet it remains unclear if oxidative stress plays a role in regulating these adaptations. We demonstrate that the chronic elevation in mitochondrial oxidative stress present in Sod2 (+/-) mice impairs the functional and biochemical mitochondrial adaptations to exercise. Following exercise training Sod2 (+/-) mice fail to increase maximal work capacity, mitochondrial enzyme activity and mtDNA copy number, despite a normal augmentation of mitochondrial proteins. Additionally, exercised Sod2 (+/-) mice cannot compensate for their higher amount of basal mitochondrial oxidative damage and exhibit poor electron transport chain complex assembly that accounts for their compromised adaptation. Overall, these results demonstrate that chronic skeletal muscle mitochondrial oxidative stress does not impact exercise induced mitochondrial biogenesis, but impairs the resulting mitochondrial protein function and can limit metabolic plasticity.

Affiliation

Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada ; Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada.

Journal Details

This article was published in the following journal.

Name: PloS one
ISSN: 1932-6203
Pages: e81879

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A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).

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Toxic substances isolated from various strains of Streptomyces. They are 20-membered macrolides that inhibit oxidative phosphorylation and mitochondrial ATPases. Venturicidins A and B are glycosides. Used mainly as tools in the study of mitochondrial function.

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