Fulle Stefania, Protasi Feliciano, Di Tano Guglielmo, Pietrangelo Tiziana, Beltramin Andrea, Boncompagni Simona, Vecchiet Leonardo, Fanò Giorgio
Istituto Interuniversitario di Miologia, Università Degli Studi G. d'Annunzio, Nuovo Polo Didattico Pal. B, Via dei Vestini 29, Chieti I-66013, Italy.
Exp Gerontol. 2004 Jan;39(1):17-24. doi: 10.1016/j.exger.2003.09.012.
Ageing is a complex process that in muscle in usually associated with a decrease in mass, strength, and velocity of contraction. One of the most striking effects of ageing on muscle is known as sarcopenia, a process that is the result of many cellular changes, such as a reduction in the number of motor units coupled with an increase in motor unit size, progressive denervation, decreased synthesis of myofibrillar components, atrophy due to disuse, accumulation of connective tissue, etc. It has been suggested that sarcopenia may be triggered by reactive oxygen species (ROS) that have accumulated throughout one's lifetime. ROS, which are generated by the addition of a single electron to the oxygen molecule, are formed in all tissues including muscle fibres and, especially, in the mitochondrial respiratory chain. Such reactive elements are usually quite harmful and result in oxidative stress that can damage other cellular components such as DNA, proteins, lipids, etc. resulting in further damage to the cells and tissues. As a consequence, the intra and intercellular membranes of the muscle fibers, in particular those of the Sarcoplasmic reticulum, may be modified and the Ca(2+) transport mechanism altered. During the ageing process ROS production may drastically increase because of an altered function of the respiratory chain and an insufficient functioning of the antioxidant cellular defences. How such an oxidative insult plays a role in the age-related decrease of muscle performance and mass has yet to be defined. What does have a clear role in the progression of sarcopenia is the significant reduction of the regenerative potential of muscle fibres. This reduction is due to a reduced pool of satellite cells that are usually recruited to replace damaged fibres and promote their regeneration. Exercise as a method to prevent or at least delay sarcopenia has been discussed in many scientific reports. While on the one hand, it seems clear that exercise is effective in reducing the loss of muscle mass, on the other it appears that physical activity increases both the mechanical damage and the accumulation of free radicals as a result of an increase in the aerobic metabolism of the muscles involved.
衰老 是一个复杂的过程,在肌肉中通常与质量、力量和收缩速度的下降有关。衰老对肌肉最显著的影响之一被称为肌肉减少症,这一过程是许多细胞变化的结果,比如运动单位数量减少,同时运动单位大小增加、进行性失神经支配、肌原纤维成分合成减少、废用性萎缩、结缔组织积累等。有人认为,肌肉减少症可能是由一生中积累的活性氧(ROS)引发的。ROS是通过向氧分子添加单个电子而产生的,在包括肌纤维在内的所有组织中形成,尤其是在线粒体呼吸链中。这些活性元素通常非常有害,会导致氧化应激,从而损害其他细胞成分,如DNA、蛋白质、脂质等,进而对细胞和组织造成进一步损害。因此,肌纤维的细胞内膜和细胞间膜,尤其是肌浆网的膜,可能会发生改变,钙(Ca2+)转运机制也会改变。在衰老过程中,由于呼吸链功能改变和细胞抗氧化防御功能不足,ROS的产生可能会急剧增加。这种氧化损伤如何在与年龄相关的肌肉性能和质量下降中发挥作用,还有待确定。在肌肉减少症的进展中,明确起作用的是肌纤维再生潜力的显著降低。这种降低是由于卫星细胞池减少,而卫星细胞通常被募集来替代受损纤维并促进其再生。许多科学报告都讨论了运动作为预防或至少延缓肌肉减少症的一种方法。一方面,运动似乎确实能有效减少肌肉质量的损失,另一方面,体育活动似乎会因所涉及肌肉有氧代谢的增加而增加机械损伤和自由基的积累。