Muscle K+, Na+, and Cl- disturbances and Na+-K+ pump inactivation: implications for fatigue

Michael J McKenna, Jens Bangsbo, Jean-Marc Renaud

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    213 Citationer (Scopus)

    Abstract

    Membrane excitability is a critical regulatory step in skeletal muscle contraction and is modulated by local ionic concentrations, conductances, ion transporter activities, temperature, and humoral factors. Intense fatiguing contractions induce cellular K(+) efflux and Na(+) and Cl(-) influx, causing pronounced perturbations in extracellular (interstitial) and intracellular K(+) and Na(+) concentrations. Muscle interstitial K(+) concentration may increase 1- to 2-fold to 11-13 mM and intracellular K(+) concentration fall by 1.3- to 1.7-fold; interstitial Na(+) concentration may decline by 10 mM and intracellular Na(+) concentration rise by 1.5- to 2.0-fold. Muscle Cl(-) concentration changes reported with muscle contractions are less consistent, with reports of both unchanged and increased intracellular Cl(-) concentrations, depending on contraction type and the muscles studied. When considered together, these ionic changes depolarize sarcolemmal and t-tubular membranes to depress tetanic force and are thus likely to contribute to fatigue. Interestingly, less severe local ionic changes can also augment subtetanic force, suggesting that they may potentiate muscle contractility early in exercise. Increased Na(+)-K(+)-ATPase activity during exercise stabilizes Na(+) and K(+) concentration gradients and membrane excitability and thus protects against fatigue. However, during intense contraction some Na(+)-K(+) pumps are inactivated and together with further ionic disturbances, likely precipitate muscle fatigue.
    OriginalsprogEngelsk
    TidsskriftJournal of Applied Physiology
    Vol/bind104
    Udgave nummer1
    Sider (fra-til)288-295
    Antal sider8
    ISSN8750-7587
    DOI
    StatusUdgivet - 2008

    Bibliografisk note

    CURIS 2008 5200 005

    Citationsformater