Accumulating evidence suggests that reactive oxygen species (ROS) generated in skeletal muscles during normal functioning, are implicated in various types of intra- and intercellular signalling.

In order to investigate the possible effects of ROS on the electrical membrane properties of developing muscle cells in vitro, electrophysiological recordings were performed in mouse skeletal myotubes using perforated and whole-cell patch-clamp techniques. Under current clamp conditions, hydrogen peroxide (H₂O₂) facilitated the anode break Na⁺ spike elicited following a large hyperpolarizing current pulse, decreasing the time of onset for action potential initiation, while the antioxidant N-acetyl cysteine induced the opposite effect, increasing the delay for the spike appearance. The kinetics of Na⁺ channel were not affected by H₂O₂, thereby excluding a modulation of these parameters as a target for ROS action. However, the fast inward rectifier K⁺ currents were reduced by H₂O₂. The consequent block of the small outward current normally contributed by inward rectifier de-activation following a large negative current pulse, could most likely explain the observed shift in anode break spike latency in the presence of H₂O₂. Our data would thus suggest that ROS, produced either during muscle activity or under action of various trophic factors, could be involved in control of muscle cell excitability.