TY - JOUR
T1 - Muscle K+, Na+, and Cl- disturbances and Na+-K+ pump inactivation: implications for fatigue
AU - McKenna, Michael J
AU - Bangsbo, Jens
AU - Renaud, Jean-Marc
N1 - Keywords: Animals; Chlorides; Enzyme Activation; Exercise; Exercise Tolerance; Humans; Lactic Acid; Membrane Potentials; Muscle Contraction; Muscle Fatigue; Muscle Strength; Muscle, Skeletal; Potassium; Sodium; Sodium-Potassium-Exchanging ATPase; Time Factors
PY - 2008
Y1 - 2008
N2 - 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.
AB - 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.
U2 - 10.1152/japplphysiol.01037.2007
DO - 10.1152/japplphysiol.01037.2007
M3 - Journal article
C2 - 17962569
SN - 8750-7587
VL - 104
SP - 288
EP - 295
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 1
ER -