Regulation of muscle potassium: exercise performance, fatigue and health implications
| Autor: | Michael I. Lindinger, Simeon P. Cairns |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Cell physiology
Cardiac function curve medicine.medical_specialty Physiology medicine.medical_treatment chemistry.chemical_element Calcium 03 medical and health sciences 0302 clinical medicine Physiology (medical) Internal medicine medicine Orthopedics and Sports Medicine Na+/K+-ATPase Muscle fatigue business.industry Insulin Public Health Environmental and Occupational Health Cardiac muscle Skeletal muscle 030229 sport sciences General Medicine Endocrinology medicine.anatomical_structure chemistry business 030217 neurology & neurosurgery |
| Zdroj: | European Journal of Applied Physiology. 121:721-748 |
| ISSN: | 1439-6327 1439-6319 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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