School of Graduate Entry Medicine and Health, City Hospital, University of Nottingham, Derby, UK.
Scand J Med Sci Sports. 2010 Feb;20(1):5-9. doi: 10.1111/j.1600-0838.2009.00967.x. Epub 2009 Jun 23.
Surprisingly little is known about the mechanisms of muscle atrophy with aging and disuse in human beings, in contrast to rodents, from which much has been extrapolated to explain the human condition. However, this extrapolation is likely unwarranted because the time course, extent of wasting, muscle fiber involvement and alterations of muscle protein turnover are all quite different in rodent and human muscle. Furthermore, there is little evidence that static indices of protein turnover represent dynamic changes and may be misleading. With disuse there are reductions in the rate of muscle protein synthesis (MPS) large enough to explain the atrophic loss of muscle protein without a concomitant increase in proteolysis. In aging, there is no evidence that there are marked alterations in basal muscle protein turnover in healthy individuals but instead the ability to maintain muscle after feeding is compromised. This anabolic resistance is evident with physical inactivity, which exacerbates the inability to maintain muscle mass with aging. The main conclusion of this review is that in uncomplicated, non-inflammatory disuse atrophy, the facilitative change causing loss of muscle mass is a depression of MPS, exacerbated by anabolic resistance during feeding, with possible adaptive depressions, rather than increases, of muscle proteolysis.
与啮齿动物相比，人们对人类衰老和废用导致的肌肉萎缩机制知之甚少，而从啮齿动物身上推断出了很多机制来解释人类的情况。然而，这种推断很可能没有依据，因为在啮齿动物和人类的肌肉中，萎缩的时间进程、程度、肌肉纤维的参与以及肌肉蛋白周转率的变化都有很大的不同。此外，几乎没有证据表明蛋白质周转率的静态指标代表了动态变化，并且可能具有误导性。在废用情况下，肌肉蛋白合成（MPS）的速率降低，足以解释肌肉蛋白质萎缩，而没有伴随的蛋白水解增加。在衰老过程中，没有证据表明健康个体的基础肌肉蛋白周转率有明显改变，相反，进食后维持肌肉的能力受损。这种合成代谢抵抗在身体不活动时很明显，这加剧了随着年龄增长无法维持肌肉质量的情况。本篇综述的主要结论是，在不复杂、非炎症性废用性萎缩中，导致肌肉质量损失的促进变化是 MPS 的降低，在进食期间，由于合成代谢抵抗，这种降低进一步加剧，可能是适应性的肌肉蛋白水解降低，而不是增加。
