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During exercise, skeletal muscle produces ROS via NOX2 while inducing some adaptations associated with contractile activity; the signals involved in this mechanism are debated. ATP is released from skeletal muscle during electrical stimulation and can signal autocrinely through purinergic receptors, we hypothesized that it may influence ROS production. The aim of this work was to measure ROS production induced by electrical stimulation and extracellular ATP. Electrical stimulation triggered a ROS transient increase in muscle fibers. The ROS production was mimicked by extracellular ATP and was prevented by CBX and suramin, antagonists of pannexin channel and purinergic receptors respectively. MRS2365, a P2Y1 receptor agonist induced a large signal while UTPyS (P2Y2 agonist) elicited a much smaller signal that was mimicked using ATP plus MRS2179, an antagonist of P2Y1. Inhibitors suggest that ROS production induced by ES or extracellular ATP was mediated by NOX2 via PKC. Extracellular ATP induced glutathionylation of RyR via NOX2. Electrical stimulation increase ROS production via P2Y1‐NOX2 and this effect appears to be involved in the regulation of RyR oxidation and thus in the regulation of calcium signaling in skeletal muscle fibers. Grant Funding Source: ACT 1111, Fondecyt 11090301