Powers Scott K
Department of Applied Physiology and Kinesiology, University of Florida, PO Box 118205, Gainesville, FL, 32611, USA,
Sports Med. 2014 Nov;44 Suppl 2(Suppl 2):S155-65. doi: 10.1007/s40279-014-0255-x.
Long periods of skeletal muscle inactivity (e.g. prolonged bed rest or limb immobilization) results in a loss of muscle protein and fibre atrophy. This disuse-induced muscle atrophy is due to both a decrease in protein synthesis and increased protein breakdown. Although numerous factors contribute to the regulation of the rates of protein breakdown and synthesis in skeletal muscle, it has been established that prolonged muscle inactivity results in increased radical production in the inactive muscle fibres. Further, this increase in radical production plays an important role in the regulation of redox-sensitive signalling pathways that regulate both protein synthesis and proteolysis in skeletal muscle. Indeed, it was suggested over 20 years ago that antioxidant supplementation has the potential to protect skeletal muscles against inactivity-induced fibre atrophy. Since this original proposal, experimental evidence has implied that a few compounds with antioxidant properties are capable of delaying inactivity-induced muscle atrophy. The objective of this review is to discuss the role that radicals play in the regulation of inactivity-induced skeletal muscle atrophy and to provide an analysis of the recent literature indicating that specific antioxidants have the potential to defer disuse muscle atrophy.
长时间的骨骼肌不活动(例如长期卧床休息或肢体固定)会导致肌肉蛋白质流失和纤维萎缩。这种废用性肌肉萎缩是由于蛋白质合成减少和蛋白质分解增加所致。尽管有许多因素参与调节骨骼肌中蛋白质分解和合成的速率,但已经确定,长时间的肌肉不活动会导致不活动的肌纤维中自由基产生增加。此外,自由基产生的这种增加在调节氧化还原敏感信号通路中起重要作用,这些信号通路调节骨骼肌中的蛋白质合成和蛋白水解。事实上,20多年前就有人提出,补充抗氧化剂有可能保护骨骼肌免受废用性纤维萎缩的影响。自最初提出这一建议以来,实验证据表明,一些具有抗氧化特性的化合物能够延缓废用性肌肉萎缩。本综述的目的是讨论自由基在调节废用性骨骼肌萎缩中的作用,并对最近的文献进行分析,这些文献表明特定的抗氧化剂有可能延缓废用性肌肉萎缩。