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, β-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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http://dx.doi.org/10.1007/s00421-020-04546-8 | DOI Listing |
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