Abstract

There is some evidence that aged muscle does not increase mitochondrial protein content after exercise training, suggesting an improvement in mitochondrial quality rather than quantity. The purpose of this study was to determine if an improvement in oxidative capacity without an increase in mitochondrial content also occurs in a rat model, and to investigate one of the markers involved in mitochondrial biogenesis. Late middle aged (28 mo; 70% survival rate) Fisher 344-BN male rats performed treadmill running exercise 5 times/wk for 7 wk and were compared to an age-matched sedentary group. Muscle aerobic performance was assessed using a pump-perfused hindlimb model. Contralateral gastrocnemius and plantaris muscles were harvested for biochemical and molecular measurements. Endurance training increased muscle VO2 max (15%) and citrate synthase and complex IV activity (~25%) compared to the control group. CS protein content was not significantly different between training and sedentary groups, suggesting that mitochondrial content did not increase with training. PGC-1α protein but not mRNA was increased only in the plantaris muscle with training. These results show that endurance training of late middle aged rats increases oxidative enzyme activity without an increase in protein content. The training-induced improvement in mitochondrial function but not content may occur secondary to increased mitochondrial turnover. Supported by CIHR and the Alberta Provincial CIHR Training Program in Bone and Joint Health

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