TELOMERE DYNAMICS AND REGULATION: EFFECTS OF CHRONIC EXERCISE, ACUTE EXERCISE, AND OXIDATIVE STRESS

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dc.contributor.advisorRoth, Stephen Men_US
dc.contributor.authorLudlow, Andrew Todden_US
dc.contributor.departmentKinesiologyen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.date.accessioned2012-02-17T06:40:17Z
dc.date.available2012-02-17T06:40:17Z
dc.date.issued2011en_US
dc.description.abstractThis dissertation research is comprised of three studies each examining the effects of chronic exercise, acute exercise, or oxidative stress on telomere biology. Exercise training and physical activity have previously been associated with telomere maintenance, but the underlying mechanisms of this association are unclear. The majority of studies to date have been performed in immune cells; however, the findings from these cells may not reflect telomere biology in other tissues. Since exercise is a multi-organ stimulus we sought to describe the effect of exercise on telomere biology in multiple tissues, with a particular focus on skeletal muscle. Study #1 showed that the effect of chronic voluntary exercise on telomere length in CAST/Ei mice is tissue specific. Exercise was `telo-protective' (i.e., maintained telomere length) in cardiac and liver tissues, while telomere shortening was observed in skeletal muscle of exercised animals compared to sedentary and young mice. Study #2 was performed to elucidate the responses to acute exercise that could underlie the paradoxical response of telomere length in skeletal muscle to exercise training. This study revealed that the MAPK pathway appears to be related to the expression of telomere binding proteins in response to acute exercise. In skeletal muscle, p38 MAPK mediated a decrease in gene expression of telomere binding proteins, providing insight into a possible mechanism for eventual telomere shortening in response to chronic exercise. The results of study #2 indicate that the early cellular responses to exercise may accumulate (i.e., repeat bout effect) and underlie the shortened telomere length in skeletal muscle. Study #3 sought to determine if reactive oxygen species were a plausible mechanism of telomere shortening in adult skeletal muscle fibers, as no mechanism to date has been elucidated for telomere shortening in this tissue. Study #3 showed that oxidative stress is a potent telomere- shortening stimulus in skeletal muscle fibers of mice and that telomere binding protein expression was also significantly affected by oxidative stress. In total these results indicate that although chronic exercise attenuates telomere shortening in most tissues, skeletal muscle demonstrates a unique contradictory response likely due to its reaction to oxidative stress.en_US
dc.identifier.urihttp://hdl.handle.net/1903/12234
dc.subject.pqcontrolledKinesiologyen_US
dc.subject.pqcontrolledCellular biologyen_US
dc.subject.pqcontrolledPhysiologyen_US
dc.subject.pquncontrolledExerciseen_US
dc.subject.pquncontrolledshelterinen_US
dc.subject.pquncontrolledskeletal muscleen_US
dc.subject.pquncontrolledtelomeraseen_US
dc.subject.pquncontrolledtelomereen_US
dc.titleTELOMERE DYNAMICS AND REGULATION: EFFECTS OF CHRONIC EXERCISE, ACUTE EXERCISE, AND OXIDATIVE STRESSen_US
dc.typeDissertationen_US

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