Crane 2013 PLoS One

From Bioblast
Publications in the MiPMap
Crane JD, Abadi A, Hettinga BP, Ogborn DI, Macneil LG, Steinberg GR, Tarnopolsky MA (2013) Elevated mitochondrial oxidative stress impairs metabolic adaptations to exercise in skeletal muscle. PLoS One 8:e81879.

Β» PMID: 24324727 Open Access

Crane J, Abadi A, Hettinga BP, Ogborn DI, Macneil LG, Steinberg GR, Tarnopolsky MA (2013) PLoS One

Abstract: 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.


β€’ O2k-Network Lab: CA Hamilton Tarnopolsky MA


Labels: MiParea: Respiration 


Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 


Coupling state: LEAK, OXPHOS  Pathway: N, NS  HRR: Oxygraph-2k 


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