Aerobic power declines with aging in rat skeletal muscles perfused at matched convective O 2 delivery

Although it is well established that maximal O 2 uptake (V˙o 2 max ) declines from adulthood to old age, the role played by alterations in skeletal muscle is unclear. Specifically, because during whole body exercise reductions in convective O 2 delivery to the working muscles from adulthood to old age compromise aerobic performance, this obscures the influence of alterations within the skeletal muscles. We sought to overcome this limitation by using an in situ pump-perfused hindlimb preparation to permit matching of muscle convective O 2 delivery in young adult (8 mo; muscle convective O 2 delivery = 569 ± 42 μmol O 2 · min −1 · 100 g −1 ) and late middle-aged (28–30 mo; 539 ± 62 μmol O 2 · min −1 · 100 g −1 ) Fischer 344 × Brown Norway F1 hybrid rats. The distal hindlimb muscles were electrically stimulated for 4 min (60 tetani/min), and V˙o 2 max was determined.V˙o 2 max normalized to the contracting muscle mass was 22% lower in the 28- to 30-mo-old (344 ± 17 μmol O 2 · min −1 · 100 g −1 ) than the 8-mo-old (441 ± 20 μmol O 2 · min −1 · 100 g −1 ; P < 0.05) rats. The flux through the electron transport chain complexes I–III was 45% lower in homogenates prepared from the plantaris muscles of the older animals. Coincident with these alterations, the tension atV˙o 2 max and lactate efflux were reduced in the 28- to 30-mo-old animals, whereas the percent decline in tension was greater in the 28- to 30-mo-old vs. 8-mo-old animals. Collectively, these results demonstrate that alterations within the skeletal muscles, such as a reduced mitochondrial oxidative capacity, contribute to the reduction in V˙o 2 max with aging.