Christopher Lee, Philip C Woods, Amanda E Paluch, Mark S Miller
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When separated by sex, the few studies that examined females showed atrophy of MyHC II and IIA fibers with age, but no change in MyHC protein expression. Additional analyses by measurement technique, physical activity, and muscle biopsied provided important insights. In summary, age-related atrophy in fast-contracting fibers lead to more of the slow-contracting, lower force-producing isoform in older male muscles, which helps explain their age-related loss in whole muscle force, velocity, and power. Exercise or pharmacological interventions that shift MyHC expression towards faster isoforms and/or increase fast-contracting fiber size should decrease the prevalence of sarcopenia. Our findings also indicate that future studies need to include or focus solely on females, measure MyHC IIA and IIX isoforms separately, examine fiber type distribution, sample additional muscles to the vastus lateralis, and incorporate an objective measurement of physical activity.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. 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引用次数: 0
摘要
人类对肌肉疏松症(与年龄有关的骨骼肌质量和功能丧失)背后的细胞机制进行了研究,但结果并不一致。为了确定衰老对各种肌球蛋白重链(MyHC)异构体的蛋白质表达、大小和纤维分布的影响,我们进行了系统回顾和荟萃分析。研究资格包括对年轻人(18-49 岁)和老年人(≥ 60 岁)的 MyHC 进行比较,共确定了 27 项研究。随着年龄的增长,慢收缩 MyHC I 纤维的相对蛋白表达量较高,相应地,快收缩 MyHC II 和 IIA 值较低。随着年龄的增长,MyHC I 纤维的大小相似,而 MyHC II 和 IIA 纤维的大小较小。纤维分布与年龄相似。如果按性别区分,少数研究显示女性的肌强直素 II 和 IIA 纤维随着年龄的增长而萎缩,但肌强直素蛋白的表达没有变化。按测量技术、体力活动和肌肉活检进行的其他分析提供了重要的见解。总之,在老年男性肌肉中,与年龄相关的快速收缩纤维萎缩导致了更多的慢速收缩、低力异构体,这有助于解释与年龄相关的整块肌肉力、速度和力量的损失。通过运动或药物干预,将 MyHC 的表达转向较快的同工酶和/或增加快速收缩纤维的大小,应能降低肌肉疏松症的发病率。我们的研究结果还表明,未来的研究需要包括女性或仅关注女性,分别测量 MyHC IIA 和 IIX 同工酶,检查纤维类型分布,对阔筋膜外的其他肌肉进行抽样调查,并纳入体育锻炼的客观测量方法。
Effects of age on human skeletal muscle: A systematic review and meta-analysis of myosin heavy chain isoform protein expression, fiber size and distribution.
Human studies examining the cellular mechanisms behind sarcopenia, or age-related loss of skeletal muscle mass and function, have produced inconsistent results. A systematic review and meta-analysis were performed to determine the aging effects on protein expression, size and distribution of fibers with various myosin heavy chain (MyHC) isoforms. Study eligibility included MyHC comparisons between young (18-49 years) and older (≥ 60 years) adults, with 27 studies identified. Relative protein expression was higher with age for the slow-contracting MyHC I fibers, with correspondingly lower fast-contracting MyHC II and IIA values. Fiber sizes were similar with age for MyHC I, while smaller for MyHC II and IIA. Fiber distributions were similar with age. When separated by sex, the few studies that examined females showed atrophy of MyHC II and IIA fibers with age, but no change in MyHC protein expression. Additional analyses by measurement technique, physical activity, and muscle biopsied provided important insights. In summary, age-related atrophy in fast-contracting fibers lead to more of the slow-contracting, lower force-producing isoform in older male muscles, which helps explain their age-related loss in whole muscle force, velocity, and power. Exercise or pharmacological interventions that shift MyHC expression towards faster isoforms and/or increase fast-contracting fiber size should decrease the prevalence of sarcopenia. Our findings also indicate that future studies need to include or focus solely on females, measure MyHC IIA and IIX isoforms separately, examine fiber type distribution, sample additional muscles to the vastus lateralis, and incorporate an objective measurement of physical activity.
期刊介绍:
The American Journal of Physiology-Cell Physiology is dedicated to innovative approaches to the study of cell and molecular physiology. Contributions that use cellular and molecular approaches to shed light on mechanisms of physiological control at higher levels of organization also appear regularly. Manuscripts dealing with the structure and function of cell membranes, contractile systems, cellular organelles, and membrane channels, transporters, and pumps are encouraged. Studies dealing with integrated regulation of cellular function, including mechanisms of signal transduction, development, gene expression, cell-to-cell interactions, and the cell physiology of pathophysiological states, are also eagerly sought. Interdisciplinary studies that apply the approaches of biochemistry, biophysics, molecular biology, morphology, and immunology to the determination of new principles in cell physiology are especially welcome.