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The Role of Exercise-Mediated Mitochondrial ROS Production in the Regulation of Oxidative Phosphorylation

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dc.contributor.advisor Holloway, Graham
dc.contributor.author Barbeau, Pierre-Andre
dc.date.accessioned 2017-09-12T19:06:16Z
dc.date.available 2018-08-29T05:00:20Z
dc.date.copyright 2017-08
dc.date.created 2017-08-29
dc.date.issued 2017-09-12
dc.identifier.uri http://hdl.handle.net/10214/11578
dc.description.abstract The transport of long chain fatty acids (LCFA) and ADP into the mitochondria are two major control points of oxidative phosphorylation that can be upregulated during exercise in order to maintain cellular ATP demand. The rate-limiting steps of LCFA and ADP transport are thought to be sensitive to redox modification, suggesting the importance of exercise-mediated mitochondrial ROS production. Therefore, we used MCAT mice, which have human catalase targeted to the mitochondria, to determine if decreasing mitochondrial ROS emission affects oxidative phosphorylation. Attenuating mitochondrial ROS significantly reduced exercise capacity in the absence of alterations in mitochondrial content. While an acute bout of exercise decreased ADP sensitivity by ~30% in WT mice, MCAT mice retained ADP sensitivity. In contrast, while exercise decreased MCoA-mediated inhibition of lipid-supported respiration, the responses within WT and MCAT mice were similar. Altogether, these findings demonstrate that exercise-mediated mitochondrial ROS emission regulates ADP sensitivity, but not lipid-supported respiration. en_US
dc.language.iso en en_US
dc.rights Attribution-NoDerivs 2.5 Canada *
dc.rights.uri http://creativecommons.org/licenses/by-nd/2.5/ca/ *
dc.subject Mitochondria en_US
dc.subject Mitochondrial ADP transport en_US
dc.subject Mitochondrial LCFA transport en_US
dc.subject Redox modification en_US
dc.subject Reactive oxygen species en_US
dc.subject MCAT mouse en_US
dc.subject Oxidative phosphorylation en_US
dc.subject Cellular respiration en_US
dc.title The Role of Exercise-Mediated Mitochondrial ROS Production in the Regulation of Oxidative Phosphorylation en_US
dc.type Thesis en_US
dc.degree.programme Human Health and Nutritional Sciences en_US
dc.degree.name Master of Science en_US
dc.degree.department Department of Human Health and Nutritional Sciences en_US


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Attribution-NoDerivs 2.5 Canada Except where otherwise noted, this item's license is described as Attribution-NoDerivs 2.5 Canada