Impact of N-2-mercaptopropionylglycine (MPG) and simvastatin on exercise-induced cardiac adaptations

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dc.contributor.advisorStarnes, Joseph W.en
dc.creatorNelson, Matthew Jayen
dc.date.accessioned2012-09-20T18:02:18Zen
dc.date.accessioned2017-05-11T22:27:26Z
dc.date.available2012-09-20T18:02:18Zen
dc.date.available2017-05-11T22:27:26Z
dc.date.issued2008-08en
dc.descriptiontexten
dc.description.abstractExperiments were conducted to investigate the role of free radicals in exercise induced cardiac adaptations and to determine if statin administration would adversely affect cardiac adaptations to exercise. In the first experiment myocardial antioxidant enzymes, cardiac function and cardiac hypertrophy were assessed following a chronic exercise protocol previously used by our lab. MPG effectively reduced myocardial oxidative stress and activation of the signaling proteins Akt and S6 following an exercise bout. Skeletal muscle mitochondria content increased to similar levels in E and E+MPG. Similar increases (P<0.05) in both exercised groups were observed for heart wt and heart wt to body wt ratio. Cardiac function at the high workload improved in E vs S as indicated by higher (P<0.05) peak systolic pressure (SP), cardiac output (CO), coronary flow, COxSP and mechanical efficiency (COxSP/VO2). MPG prevented these exercise-induced functional improvements. This study provides evidence that free radicals do not play a role in the development of exercise-induced cardiac hypertrophy, however, they are involved in functional cardiac adaptations, which may be mediated through the PI3K/Akt pathway. In the second experiment a similar exercise protocol was used to determine if statins which have been shown to prevent pathological forms of cardiac hypertrophy, would be detrimental to exercise induced cardiac adaptations. In addition to the sedentary and exercise groups sedentary+statin and exercise+statin groups were assessed. Hearts were isolated and perfused and assessed for function at low and high workloads. Exercise treatment resulted in cardiac hypertrophy in absolute and relative terms to a similar extent in statin-treated and untreated exercised rats. Additionally it resulted in significant functional increases for SP, CO, COxSP, VO₂, and EFF in both exercised groups. In conclusion, these studies provide evidence that exercise in the cold is a valid model for physiological cardiac hypertrophy and that pathological and physiological cardiac hypertrophy signal through different pathways due to the fact that two well established treatments (mpg and statins) that prevent pathological cardiac hypertrophy did not affect exercise induced cardiac hypertrophy.en
dc.description.departmentKinesiology and Health Educationen
dc.format.mediumelectronicen
dc.identifier.urihttp://hdl.handle.net/2152/17945en
dc.language.isoengen
dc.rightsCopyright is held by the author. Presentation of this material on the Libraries' web site by University Libraries, The University of Texas at Austin was made possible under a limited license grant from the author who has retained all copyrights in the works.en
dc.subject.lcshHeart--Hypertrophyen
dc.subject.lcshExercise--Physiological aspectsen
dc.subject.lcshOxidative stressen
dc.subject.lcshFree radicals (Chemistry)--Physiological effecten
dc.subject.lcshFree radicals (Chemistry)--Pathophysiologyen
dc.subject.lcshAntioxidants--Therapeutic useen
dc.subject.lcshStatins (Cardiovascular agents)en
dc.subject.lcshHeart--Effect of cold onen
dc.titleImpact of N-2-mercaptopropionylglycine (MPG) and simvastatin on exercise-induced cardiac adaptationsen

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