Abstract
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.
