Introduction: Muscle production of lactate and hydrogen ions increase during exercise. Major attention has been directed at eluciding the consequences of the latter (e.g. acidity) on muscle function and especially excitability (Pedersen et al., 2004). Conversely, few attempts were made to look for possible effects of lactate ion on muscle excitability. Voltage-gated sodium channels (Nav) initiate and convey the action potential on fibre membrane, thereby fine-tuning muscle excitability. We hypothesized that lactate could modulate the electrophysiological properties of muscle Nav. Methods: The electrophysiological properties of muscle Nav were studied in the absence and in the presence of lactate by using the macro-patch-clamp method in dissociated fibres from rat Peroneus Longus (PL). Two different pipettes containing either a control or a lactate (10 mM) solution were sealed on the same area of PL fibers. Values are shown as means ± SEM. Results & Discussion: Compared with control condition, lactate increases the maximal sodium current (14.5 ± 1.2 vs. 10.1 ± 1.4 A.mm-2, n = 18 fibres, p = 0.022, Student’s paired t-test), while the voltage-dependence of activation (normalized conductance) is shifted at its midpoint by 12.4 mV toward the hyperpolarized potentials (p = 0.0029, Student’s paired t-test). This indicates a more rapid depolarization, allowing an earlier recruitment of the muscle fiber. The voltage-dependence of Nav fast inactivation is shifted by lactate in a hyperpolarizing direction compared with control condition (-63.1 ± 3.7 vs. -52.1 ± 2.4 mV, respectively, n = 18 fibres, p = 0.015, Student’s paired t-test). This implies a more rapid membrane repolarisation which is crucial for the elicitation of a novel action potential. Lactate induces a leftward shift in the relationship between the kinetic parameters and the imposed potentials, resulting in an acceleration of Nav activation. The slow inactivation process is decreased by lactate compared with control condition as shown by the greater residual current INa min/INa max (0.67 ± 0.06 vs. 0.48 ± 0.05, respectively, n = 15 fibres, p = 0.0099, Student’s paired t-test), corresponding to an enhancement in the number of excitable Nav. When lactate was only added in the Petri dish (and not in the pipette), the electrophysiological properties of Nav were unaffected. Thus, the modifications of sodium current properties are observed when the pipette contains lactate, indicating an extra-cellular pathway. Conclusion: Lactate ion modulates the electrophysiological properties of muscle Nav by an extra-cellular manner. These modifications of Nav characteristics are consistent with an increase in muscle excitability. This leads to preserve force production by reducing the muscle fatigability related to membrane excitability failure (Cairns et al., 2003; Karelis et al, 2004; Fitts, 1994).