Intracellular acidosis enhances the excitability of working muscle.
Intracellular acidification of skeletal muscles is commonly thought to contribute to muscle fatigue. However, intracellular acidosis also acts to preserve muscle excitability when muscles become depolarized, which occurs with working muscles. Here, we show that this process may be mediated by decreased chloride permeability, which enables action potentials to still be propagated along the internal network of tubules in a muscle fiber (the T system) despite muscle depolarization. These results implicate chloride ion channels in muscle function and emphasize that intracellular acidosis of muscle has protective effects during muscle fatigue.
Department of Physiology, University of Aarhus, DK-8000, Denmark.
Thomas H
TH
Pedersen
Ole B
OB
Nielsen
Graham D
GD
Lamb
D George
DG
Stephenson
D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000378:metabolism; D018118:Chloride Channels / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism; D004558:Electric Stimulation; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000378:metabolism; D008564:Membrane Potentials; D009119:Muscle Contraction; D018763:Muscle Fatigue; D018485:Muscle Fibers, Skeletal / Q000378:metabolism / Q000502:physiology*; D018482:Muscle, Skeletal / Q000378:metabolism / Q000502:physiology*; D010539:Permeability; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
D018118:Chloride Channels; D002712:Chlorides; D019344:Lactic Acid; D011188:Potassium; D002118:Calcium