作者: Supreeth S Rudrappa , Daniel J Wilkinson , Paul L Greenhaff , Kenneth Smith , Iskandar Idris
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摘要: The ever increasing burden of an ageing population and pandemic metabolic syndrome worldwide demands further understanding the modifiable risk factors in reducing disability morbidity associated with these conditions. Disuse skeletal muscle atrophy (sometimes referred to as “simple” atrophy) insulin resistance are ‘non-pathological’ events resulting from sedentary behaviour periods enforced immobilization e.g. due fractures or elective orthopaedic surgery. Yet, processes drivers regulating disuse molecular remain unclear – especially humans. aim this review is present current knowledge relationships between protein turnover, during disuse, principally Immobilisation lowers fasted state synthesis (MPS) induces fed-state ‘anabolic resistance’. While a lack dynamic measurements breakdown (MPB) precludes defining definitive role for MPB atrophy, some proteolytic “marker” studies (e.g. genes) suggest potential early elevation. also (IR). Moreover, trajectory appears be accelerated persistent IR states Type II diabetes), suggesting may contribute under Nonetheless, differences sensitivity across distinct groups its effects on rates remains unclear. Multifaceted time-course into collective turnover setting humans, needed facilitate development appropriate countermeasures efficacious rehabilitation protocols.