Résumé :
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During muscle contraction, lactate production and translocation across the membrane increase. Less is known regarding a potential effect of lactate on the voltage-gated sodium channel (Nav) of skeletal muscle. The electrophysiological properties of muscle Nav were studied in the absence and in the presence of lactate (10 mM) by using the macro-patch-clamp method in dissociated fibers from rat Peroneus Longus (PL). Lactate in the external medium (Petri dish + pipette) increases the maximal sodium current, while the voltage-dependence of activation and fast inactivation are shifted toward the hyperpolarized potentials. Lactate induces a leftward shift in the relationship between the kinetic parameters and the imposed potentials, resulting in an earlier recruitment of muscle Nav. The slow inactivation process is decreased by lactate, corresponding to an enhancement in the number of excitable Nav. In an additional series of experiments, lactate (10 mM) was only added to the Petri dish, while the pipette remained sealed on the membrane area. In this approach, the Nav properties were unaffected by lactate compared with control condition, indicating an extracellular pathway. These effects are consistent with an enhancement in excitability, providing new insights into the role of lactate in muscle physiology and suggesting new hypothesis in the pathophysiology of glycolysis defects (Journal of Applied Physiology, 2012).
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