The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle.

The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle.
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DOI:
10.1016/j.exger.2012.03.004
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发表时间:
2012-06
影响因子:
3.9
通讯作者:
Radak Z
Radak Z
中科院分区:
医学2区
文献类型:
--
作者:
Bori Z;Zhao Z;Koltai E;Fatouros IG;Jamurtas AZ;Douroudos II;Terzis G;Chatzinikolaou A;Sovatzidis A;Draganidis D;Boldogh I;Radak Z

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衰老导致有氧能力显著下降,线粒体功能受损。我们测试了适度体力活动对有氧能力的影响和单次运动对人体骨骼肌线粒体生物发生和融合与分裂相关基因表达谱的影响。体力活动减轻了与年龄相关的最大摄氧量下降(p<0.05)。增龄增加,单次运动降低核呼吸因子-1(NRF1)的表达,而转录因子A(TFAM)的表达与最大摄氧量(VO2max)密切相关,在青年体力活动组显著增加。代表FIS1的线粒体分裂是由有规律的体育活动引起的,而一轮运动降低了融合相关基因的表达。多核苷酸磷酸化酶(PNPase)在青年组和老年组的表达呈相反变化,并随着年龄的增长而降低。在青年和老年受试者的骨骼肌样本中,单次运动均可诱导环磷酸腺苷活化蛋白激酶(AMPK)A2亚基的表达(p<0.05)。我们的数据表明,与老年受试者相比,年轻人中适度的定期体力活动增加了更多数量的线粒体生物发生相关基因的表达。线粒体分裂会因衰老而受损,这可能是与年龄相关的体力活动适应性反应下降的最敏感标志之一。
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 VO2max 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.