Abstract

The purpose of this study was to examine the effects of aging and physical activityon heart mtDNA template availability. Young, mature and aged C57BL6 mice were used in this study with half of the animals having access to exercise wheels. Cardiac DNA was isolated and the mitochondrial DNA content was assessed by slot blots with a specific mtDNA probe. Mitochondrial DNA template availability increased in mouse cardiac tissue with senescence. This was reflected in increases in mitochondrial DNA content per milligram of cardiac tissue and mitochondrial DNA relative to nuclear DNA ratios. Oxidative capacity, as determined by citrate synthase activity, was not significantly decreased with aging. Compromises to the erLergy transducing pathway due to aging responses in cardiac tissue may have led to higher replicative rates of mtDNA to induce more mitochondrial specific proteins. The mature mice responded positively to the voluntary chronic physical activity displaying increased mitochondrial DNA to nuclear DNA ratios and elevated citrate synthase activities. Thus the increasing metabolic demand put on the mitochondrial system was associated with elevated mtDNA template levels in these animals. In contrast, the senescent animals’ mtDNA template content was unaffected by the physical activity. This lack of a relationship in the senescent animals is most likely due to low running velocities and therefore relative workloads in this age group, but this suggestion remains to be confirmed.

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