The purpose of this study was to examine the effects of aging and phys
ical activity on heart mtDNA template availability, Young, mature and
aged C57BL6 mice were used in this study with half of the animals havi
ng access to exercise wheels, Cardiac DNA was isolated and the mitocho
ndrial DNA content was assessed by slot blots with a specific mtDNA pr
obe, Mitochondrial DNA template availability increased in mouse cardia
c tissue with senescence. This was reflected in increases in mitochond
rial 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 energy 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 responde
d positively to the voluntary chronic physical activity displaying inc
reased mitochondrial DNA to nuclear DNA ratios and elevated citrate sy
nthase activities, Thus the increasing metabolic demand put on the mit
ochondrial system was associated with elevated mtDNA template levels i
n these animals, In contrast, the senescent animals' mtDNA template co
ntent was unaffected by the physical activity, This lack of a relation
ship in the senescent animals is most likely due to low running veloci
ties and therefore relative workloads in this age group, but this sugg
estion remains to be confirmed.