Mechanisms regulating muscle mass during disuse atrophy and rehabilitation in humans.

Mechanisms regulating muscle mass during disuse atrophy and rehabilitation in humans.
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人类废用性萎缩和康复期间肌肉质量的调节机制。

DOI:
10.1152/japplphysiol.00962.2010
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发表时间:
2011
期刊:
1985)
影响因子:
--
通讯作者:
Marimuthu K
Marimuthu K
中科院分区:
--
文献类型:
--
作者:
Marimuthu K

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人类的肌肉质量损失伴随着卧床休息和肢体固定的时期,需要康复锻炼以有效恢复质量和功能。尽管最近的证据表明肌肉蛋白质分解的早期和短暂增加导致了肌肉质量的下降,但驱动因素似乎是肌肉蛋白质合成的减少,尤其是由于对氨基酸供应的合成代谢抵抗的发展。尽管 AKT 信号通路在小动物中已被确定为调节肌肉蛋白质合成的核心,但目前的几项人类研究表明,在进食、运动和固定过程中 AKT 信号传导与肌肉蛋白质合成之间存在分离,这表明调节人类骨骼肌中蛋白质合成的机制比最初想象的更为复杂(至少在非炎症状态下)。在康复过程中,运动诱发的肌生成可能部分负责肌肉质量的恢复。运动引起的肌肉生长抑制素 mRNA 表达的快速和持续抑制,先于肌肉质量的增加,表明它与其他生肌蛋白一起,是人类运动康复过程中肌肉再生的潜在调节剂。
Muscle mass loss accompanies periods of bedrest and limb immobilization in humans and requires rehabilitation exercise to effectively restore mass and function. Although recent evidence points to an early and transient rise in muscle protein breakdown contributing to this decline in muscle mass, the driving factor seems to be a reduction in muscle protein synthesis, not least in part due to the development of anabolic resistance to amino acid provision. Although the AKT signaling pathway has been identified in small animals as central to the regulation of muscle protein synthesis, several studies in humans have now demonstrated a disassociation between AKT signaling and muscle protein synthesis during feeding, exercise, and immobilization, suggesting that the mechanisms regulating protein synthesis in human skeletal muscle are more complex than initially thought (at least in non-inflammatory states). During rehabilitation, exercise-induced myogenesis may in part be responsible for the recovery of muscle mass. Rapid and sustained exercise-induced suppression of myostatin mRNA expression, that precedes any gain in muscle mass, points to this, along with other myogenic proteins, as being potential regulators of muscle regeneration during exercise rehabilitation in humans.
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