期刊
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
卷 15, 期 1, 页码 58-63出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0b013e32834d19bc
关键词
anabolic resistance; mTOR signalling; protein synthesis; skeletal muscle
资金
- Research Councils UK
- Ajinomoto Inc.
- NIH-NIAMS [AR-054342]
- University of Nottingham
- BBSRC [BB/C516779/1]
- Biotechnology and Biological Sciences Research Council [BB/C516779/1] Funding Source: researchfish
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR054342] Funding Source: NIH RePORTER
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.
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