Muscle mitochondrial changes with aging and exercise

Muscle mitochondrial changes with aging and exercise
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DOI:
10.3945/ajcn.2008.26717d
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发表时间:
2009-01-01
影响因子:
7.1
通讯作者:
Nair, K. Sreekumaran
Nair, K. Sreekumaran
中科院分区:
医学1区
文献类型:
--
作者:
Lanza, Ian R.;Nair, K. Sreekumaran

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据报道,衰老伴随着线粒体功能和胰岛素敏感性的降低。这些有害影响是否是由实际年龄或生活方式相关因素(如肥胖和身体活动不足)造成的,仍有争议。运动对线粒体功能和胰岛素敏感性的有益影响已有充分的记录;然而,尚不清楚运动是否能有效预防、逆转或延迟这些与年龄相关的功能障碍的发生。其他研究人员和我们发现,耐力运动可以增强整个生命周期的线粒体功能,突出了运动在对抗年龄相关的线粒体功能障碍方面的有益作用。关于耐力运动使年龄相关的胰岛素抵抗正常化的能力,文献褒贬不一;然而,新出现的证据表明肥胖而不是年龄本身是年龄相关的胰岛素敏感性下降的主要决定因素。我们实验室最近的数据也揭示了线粒体功能和胰岛素敏感性之间有争议的关系。尽管一些研究人员声称线粒体功能障碍在胰岛素抵抗的病因中发挥着因果作用,但我们提供的证据表明,事实可能恰恰相反,因为胰岛素刺激健康对照受试者的线粒体功能,但不刺激2型糖尿病患者的线粒体功能。此外,我们发现,这两个变量在某些人群中是完全分离的,如亚洲印度人,尽管与欧洲裔美国人相比有显著的胰岛素抵抗,但他们表现出较高的线粒体容量。我们的数据不仅指出定期耐力运动是延迟年龄相关功能障碍发作的可行策略,而且还表明线粒体功能和胰岛素抵抗可能与其他因素有关,如体力活动。美国临床营养杂志2009(增刊);89:467 S-71 S。
Aging has been reported to be accompanied by reduced mitochondrial function and insulin sensitivity. Whether these deleterious effects result from chronological age or lifestyle-related factors such as adiposity and physical inactivity remains debatable. The beneficial effects of exercise on mitochondrial function and insulin sensitivity are well documented; however, it is unclear whether exercise can effectively prevent, reverse, or delay the onset of these age-related dysfunctions. Other investigators and we have found that endurance exercise enhances mitochondrial function across the life span, highlighting the beneficial role of exercise in combating age-related mitochondrial dysfunction. The literature is mixed concerning the ability of endurance exercise to normalize age-related insulin resistance; however, emerging evidence points to adiposity rather than age per se as a primary determinant of age-related declines in insulin sensitivity. Recent data from our laboratory also shed some light on the controversial relation between mitochondrial function and insulin sensitivity. Although some investigators purport a causal role of mitochondrial dysfunction in the etiology of insulin resistance, we provide evidence that the reverse may be true based on the fact that insulin stimulates mitochondrial function in healthy control subjects but not in patients with type 2 diabetes. Furthermore, we find that these 2 variables are completely dissociated in some populations, such as Asian Indians, who exhibit elevated mitochondrial capacity despite marked insulin resistance compared with European Americans. Our data not only point to regular endurance exercise as a viable strategy to delay the onset of age-related dysfunctions but they suggest that mitochondrial function and insulin resistance may be linked by additional factors such as physical activity. Am J Clin Nutr 2009(suppl);89:467S-71S.