Human Performance Laboratory, Ball State University, Muncie, IN 47306.
J Gerontol A Biol Sci Med Sci. 2014 Apr;69(4):371-8. doi: 10.1093/gerona/glt107. Epub 2013 Jul 20.
Perturbations in mitochondrial health may foster age-related losses of aerobic capacity (VO2peak) and skeletal muscle size. However, limited data exist regarding mitochondrial dynamics in aging human skeletal muscle and the influence of exercise. The purpose of this study was to examine proteins regulating mitochondrial biogenesis and dynamics, VO2peak, and skeletal muscle size before and after aerobic exercise training in young men (20 ± 1 y) and older men (74 ± 3 y). Exercise-induced skeletal muscle hypertrophy occurred independent of age, whereas the improvement in VO2peak was more pronounced in young men. Aerobic exercise training increased proteins involved with mitochondrial biogenesis, fusion, and fission, independent of age. This is the first study to examine pathways of mitochondrial quality control in aging human skeletal muscle with aerobic exercise training. These data indicate normal aging does not influence proteins associated with mitochondrial health or the ability to respond to aerobic exercise training at the mitochondrial and skeletal muscle levels.
线粒体健康的紊乱可能会促进与年龄相关的有氧能力（峰值摄氧量，VO2peak）和骨骼肌体积的丧失。然而，关于衰老过程中人类骨骼肌中线粒体动力学以及运动的影响的数据有限。本研究的目的是在年轻男性（20 ± 1 岁）和老年男性（74 ± 3 岁）进行有氧运动训练前后，检测调节线粒体生物发生和动力学、VO2peak 和骨骼肌体积的蛋白质。运动引起的骨骼肌肥大与年龄无关，而 VO2peak 的改善在年轻男性中更为明显。有氧运动训练增加了与线粒体生物发生、融合和分裂相关的蛋白质，与年龄无关。这是首次在衰老的人类骨骼肌中，用有氧运动训练来检测线粒体质量控制途径的研究。这些数据表明，正常衰老不会影响与线粒体健康或在线粒体和骨骼肌水平上对有氧运动训练做出反应的相关蛋白质。
