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The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle
Authors
Z. Bori Zhao, Z. Koltai, E. Fatouros, I.G. Jamurtas, A.Z. Douroudos, I.I. Terzis, G. Chatzinikolaou, A. Sovatzidis, A. Draganidis, D. Boldogh, I. Radak, Z.
Publication date
1 January 2012
Publisher
Abstract
Aging results in a significant decline in aerobic capacity and impaired mitochondrial function. We have tested the effects of moderate physical activity on aerobic capacity and a single bout of exercise on the expression profile of mitochondrial biogenesis, and fusion and fission related genes in skeletal muscle of human subjects. Physical activity attenuated the aging-associated decline in VO2 max (p<0.05). Aging increased and a single exercise bout decreased the expression of nuclear respiratory factor-1 (NRF1), while the transcription factor A (TFAM) expression showed a strong relationship with VO 2max and increased significantly in the young physically active group. Mitochondrial fission representing FIS1 was induced by regular physical activity, while a bout of exercise decreased fusion-associated gene expression. The expression of polynucleotide phosphorylase (PNPase) changed inversely in young and old groups and decreased with aging. The A2 subunit of cyclic AMP-activated protein kinase (AMPK) was induced by a single bout of exercise in skeletal muscle samples of both young and old subjects (p<0.05). Our data suggest that moderate levels of regular physical activity increases a larger number of mitochondrial biogenesis-related gene expressions in young individuals than in aged subjects. Mitochondrial fission is impaired by aging and could be one of the most sensitive markers of the age-associated decline in the adaptive response to physical activity. © 2012 Elsevier Inc
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Last time updated on 10/02/2023