TY - JOUR
T1 - The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle
AU - Bori, Zoltan
AU - Zhao, Zhongfu
AU - Koltai, Erika
AU - Fatouros, Ioannis G.
AU - Jamurtas, Athanasios Z.
AU - Douroudos, Ioannis I.
AU - Terzis, Gerasimos
AU - Chatzinikolaou, Athanasios
AU - Sovatzidis, Apostolos
AU - Draganidis, Dimitrios
AU - Boldogh, Istvan
AU - Radak, Zsolt
N1 - Funding Information:
We are grateful to the support of Prof. A.W. Taylor in the preparation of this paper. The present work was supported by Hungarian grants from ETT 38388 , OTKA ( K75702 ) TAMOP/Magiszter awarded to Z. Radák.
PY - 2012/6
Y1 - 2012/6
N2 - 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.
AB - 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.
KW - Aging
KW - Exercise
KW - Fusion and fission
KW - Mitochondrial biogenesis
KW - Skeletal muscle
UR - https://www.scopus.com/pages/publications/84861183528
UR - https://www.scopus.com/pages/publications/84861183528#tab=citedBy
U2 - 10.1016/j.exger.2012.03.004
DO - 10.1016/j.exger.2012.03.004
M3 - Article
C2 - 22449457
AN - SCOPUS:84861183528
SN - 0531-5565
VL - 47
SP - 417
EP - 424
JO - Experimental Gerontology
JF - Experimental Gerontology
IS - 6
ER -