Clock-related regulation of mitochondrial physiology in skeletal muscle

dc.contributor.advisorHood, David
dc.creatorPastore, Stephen Francesco
dc.date.accessioned2016-09-13T13:14:24Z
dc.date.available2016-09-13T13:14:24Z
dc.date.copyright2012-12
dc.degree.disciplineKinesiology & Health Science
dc.degree.levelMaster's
dc.degree.nameMSc - Master of Science
dc.description.abstractBiological rhythms regulate numerous functional processes within organisms, including the expression of peroxisome proliferator-activated receptor-y coactivator 1-a (PGC-1a), a potent regulator of mitochondrial biogenesis. Homozygous Clock mutant mice are characterized by arrhythmic and suppressed expression of circadian genes within skeletal muscle, including PGC-1a. The present study sought to investigate mitochondrial physiology within these mutant animals, and to assess their adaptability to a chronic voluntary endurance training protocol. Our results indicate that Clock mutant mice exhibit decreased mitochondrial content, and this contributes to exercise intolerance in these mutant animals. Interestingly, endurance training ameliorates the decrement in mitochondrial content, as well as restores exercise capacity to levels evident in the wildtype mice. Thus, a functional CLOCK protein is necessary for optimal mitochondrial physiology, however Clock mutant mice retain the ability to adapt to chronic exercise.
dc.identifier.urihttp://hdl.handle.net/10315/31961
dc.rightsAuthor owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.
dc.subject.keywordsMitochondrial physiology
dc.subject.keywordsSkeletal muscle
dc.subject.keywordsEndurance training protocol.
dc.subject.keywordsExercise
dc.titleClock-related regulation of mitochondrial physiology in skeletal muscle
dc.typeElectronic Thesis or Dissertation

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