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肌肉蛋白质合成在人体中的调节。

Regulation of muscle protein synthesis in humans.

机构信息

Division of Clinical Physiology, School of Graduate Entry Medicine and Health, University of Nottingham, Derby, UK.

出版信息

Curr Opin Clin Nutr Metab Care. 2012 Jan;15(1):58-63. doi: 10.1097/MCO.0b013e32834d19bc.

Abstract

PURPOSE OF REVIEW

Investigations into the regulation of muscle protein synthesis (MPS) are a cornerstone of understanding the control of muscle mass. Rates of MPS are finely tuned according to levels of activity, nutrient availability and health status. For instance, rates of MPS are positively regulated by exercise and nutrition, and negatively regulated by inactivity (e.g. disuse), ageing (i.e. sarcopenia) and in muscle-wasting related diseases (e.g. cancer).

RECENT FINDINGS

Skeletal muscles display a high degree of intrinsic regulation. Increases in MPS after exercise occur independently of the systemic milieu for example growth hormone/testosterone concentrations. In the absence of exercise, increases in MPS after feeding are of finite duration despite enduring precursor availability; that is muscles can sense they are 'full'. Intriguingly, exercise delays this 'muscle-full' response to allow for building and repair. In contrast, muscle-wasting conditions exhibit a premature 'muscle-full' response to nutrition and exercise (i.e. anabolic resistance), which may cause atrophy. Observations of 'dissociations' between MPS and anabolic signalling pathways have cast doubt on how much we understand of the molecular regulation of human MPS.

SUMMARY

Anabolic and anticatabolic interventions in health and disease should be aimed at manipulating the 'muscle-full' set point to maximize muscle maintenance/hypertrophy.

摘要

目的综述

肌肉蛋白质合成(MPS)调节的研究是理解肌肉质量控制的基石。MPS 的速率根据活动水平、营养供应和健康状况进行精细调节。例如,MPS 的速率受运动和营养的正调节,以及不活动(如废用)、衰老(即肌肉减少症)和肌肉消耗相关疾病(如癌症)的负调节。

最新发现

骨骼肌具有高度的内在调节能力。例如,运动后 MPS 的增加独立于生长激素/睾丸激素浓度等全身环境。在没有运动的情况下,尽管前体供应持续存在,进食后 MPS 的增加持续时间有限;也就是说,肌肉可以感觉到它们已经“饱了”。有趣的是,运动延迟了这种“肌肉饱足”的反应,以允许构建和修复。相比之下,肌肉消耗条件表现出对营养和运动的过早“肌肉饱足”反应(即合成代谢抵抗),这可能导致萎缩。MPS 和合成代谢信号通路之间“分离”的观察结果,使我们对人类 MPS 的分子调节有多少了解产生了怀疑。

总结

在健康和疾病中,合成代谢和抗分解代谢干预措施应旨在操纵“肌肉饱足”设定点,以最大程度地维持/增加肌肉。

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