Difference between revisions of "Crane 2013 PLoS One"
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|year=2013 | |year=2013 | ||
|journal=PLoS One | |journal=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'' <sup> | |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''<sup>+/-</sup> mice impairs the functional and biochemical mitochondrial adaptations to exercise. Following exercise training ''Sod2''<sup>+/-</sup> mice fail to increase maximal work capacity, mitochondrial enzyme activity and mtDNA copy number, despite a normal augmentation of mitochondrial proteins. Additionally, exercised ''Sod2''<sup>+/-</sup> 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. | ||
|mipnetlab=CA Hamilton Tarnopolsky MA | |mipnetlab=CA Hamilton Tarnopolsky MA | ||
}} | }} | ||
Revision as of 11:37, 27 April 2015
| 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. |
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.
• O2k-Network Lab: CA Hamilton Tarnopolsky MA
Labels: MiParea: Respiration
Organism: Mouse
Tissue;cell: Skeletal muscle
Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS
HRR: Oxygraph-2k
