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J Appl Physiol 94: 744-751, 2003. First published October 4, 2002; doi:10.1152/japplphysiol.00737.2002
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Vol. 94, Issue 2, 744-751, February 2003

Aerobic power declines with aging in rat skeletal muscles perfused at matched convective O2 delivery

Russell T. Hepple1,2, Jason L. Hagen1, Daniel J. Krause2, and Cory C. Jackson1

1 Faculty of Kinesiology and 2 Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 1N4

Although it is well established that maximal O2 uptake (VO2 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 O2 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 O2 delivery in young adult (8 mo; muscle convective O2 delivery = 569 ± 42 µmol O2 · min-1 · 100 g-1) and late middle-aged (28-30 mo; 539 ± 62 µmol O2 · 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 VO2 max was determined. VO2 max normalized to the contracting muscle mass was 22% lower in the 28- to 30-mo-old (344 ± 17 µmol O2 · min-1 · 100 g-1) than the 8-mo-old (441 ± 20 µmol O2 · 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 at VO2 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 VO2 max with aging.

sarcopenia; Fischer 344 × Brown Norway F1 hybrid rat; muscle blood flow; rat hindlimb; mitochondria


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