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Thomas, Melissa Michelle.
Changes in muscle calcium handling, oxidative stress and contractile function with aging and long-term exercise training in senescent rats.
Ph. D. -- University of Calgary, 2010
Ottawa : Library and Archives Canada = Bibliothèque et Archives Canada, [2011]
2 microfiches
Includes bibliographical references.
The age-related declines in skeletal muscle mass, skeletal muscle function and cardiac function can lead to impaired mobility and declines in quality of life. The loss of skeletal muscle mass, cardiomyocyte volume and skeletal and cardiac function is moderate up to late middle age and accelerates between late middle age and senescence and may be due to increased oxidative damage. In contrast, exercise training, which is protective against oxidative stress, may offer some benefits during this critical period of the lifespan. Sarcoplasmic reticulum (SR) calcium (Ca2+) handling plays an important role in muscle contraction and relaxation and has not been studied in rats that are experiencing significant muscle atrophy. We hypothesized that fast-twitch skeletal muscle and cardiac muscle of senescent rats would exhibit decreased Ca2+ release and uptake, due to decreased protein content and increased oxidative damage, and that this would be attenuated by exercise training. We initiated a treadmill training program at late middle age, where muscle functional declines are modest, and carried it out into senescence where muscle functional declines are severe. 'In situ' measures of skeletal muscle contractile properties were made to determine if exercise training could attenuate the loss in function. SR Ca2+ handling function was decreased in senescent fast-twitch skeletal muscle and cardiac muscle. Senescent skeletal muscle experienced significant increases in oxidative damage and antioxidant defense mechanisms while cardiac muscle only experienced mild increases in oxidative damage. Long-term exercise training had minor benefits on senescent skeletal muscle contractile properties and SR Ca2+ handling but significantly increased oxidative damage despite increased antioxidant defenses. Cardiac muscle showed no benefits in SR Ca2+ handling in response to exercise training and no change in oxidative damage. The age-related declines observed in both fast-twitch skeletal muscle and cardiac muscle Ca 2+ handling may explain some of the deficits seen in muscle function with aging. In conclusion, senescent skeletal and cardiac muscles exhibit an impaired ability to respond to exercise training which may due to the lack of decrease in oxidative stress.