期刊
EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY
卷 121, 期 3, 页码 721-748出版社
SPRINGER
DOI: 10.1007/s00421-020-04546-8
关键词
Skeletal muscle; Cardiac muscle; Hyperkalaemia; Hypokalaemia; Na+; K+-ATPase
This review integrates the current understanding of the role of skeletal muscle in whole-body potassium regulation, focusing on the regulation of skeletal muscle K+. It discusses how K+ transport proteins in skeletal muscle contribute to K+ disturbances during exercise and the implications on muscle and cardiac muscle contractile performance. The review also examines the implications of moderate plasma and interstitial K+ elevations during exercise and the dangerous health implications of chronic or acute changes in arterial plasma K+ levels.
This review integrates from the single muscle fibre to exercising human the current understanding of the role of skeletal muscle for whole-body potassium (K+) regulation, and specifically the regulation of skeletal muscle [K+]. We describe the K+ transport proteins in skeletal muscle and how they contribute to, or modulate, K+ disturbances during exercise. Muscle and plasma K+ balance are markedly altered during and after high-intensity dynamic exercise (including sports), static contractions and ischaemia, which have implications for skeletal and cardiac muscle contractile performance. Moderate elevations of plasma and interstitial [K+] during exercise have beneficial effects on multiple physiological systems. Severe reductions of the trans-sarcolemmal K+ gradient likely contributes to muscle and whole-body fatigue, i.e. impaired exercise performance. Chronic or acute changes of arterial plasma [K+] (hyperkalaemia or hypokalaemia) have dangerous health implications for cardiac function. The current mechanisms to explain how raised extracellular [K+] impairs cardiac and skeletal muscle function are discussed, along with the latest cell physiology research explaining how calcium, beta-adrenergic agonists, insulin or glucose act as clinical treatments for hyperkalaemia to protect the heart and skeletal muscle in vivo. Finally, whether these agents can also modulate K+-induced muscle fatigue are evaluated.
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