Hood, David2015-08-282015-08-282014-04-232015-08-28http://hdl.handle.net/10315/29797Autophagy is a critical survival mechanism facilitating protein turnover and pathogen defense in post-mitotic cells. More recently, mitophagy has been identified for the selective recognition and targeting of mitochondria for degradation. Mitochondrial availability is the net result of organelle catabolism via mitophagy and mitochondrial biogenesis. Although the latter process has been well described, mitophagy in skeletal muscle is less understood, and it is unknown how these two opposing mechanisms converge during contractile activity. We employed an in vitro model of chronic contractile activity (CCA) of myotubes in cell culture in the presence of autophagy inhibitor Bafilomycin A1 (BafA) and assessed the implications of defective autophagy on the adaptations to contractile activity. BafA lead to severe deficits to mitochondrial respiration and enhanced reactive oxygen species. CCA ameliorated this defective phenotype, reverting levels back towards untreated controls. Thus, contractile activity normalizes mitophagy flux and maintains a healthier mitochondrial profile during autophagy deregulation.enAuthor owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.Cellular biologyKinesiologyElectronic Thesis or Dissertation2015-08-28AutophagyContractile activityMuscleCellsMitochondriaBiogenesisLC3-IIPINK1ParkinMitophagySkeletal MuscleExerciseReactive Oxygen SpeciesROSRespirationAntioxidantC2C12 cells