1. In rat soleus muscle, high frequency electrical stimulation produced a rapid increase in intracellular Na+(Na+ i) content. This was considerably larger in muscles contracting without developing tension than in muscles contracting isometrically. During subsequent rest a net extrusion of Na+ took place at rates which, depending on the frequency and duration of stimulation, approached the maximum transport capacity of the Na (+)-K+ pumps present in the muscle. 2. In isometrically contracting muscles, the net extrusion of Na+ continued for up to 10 min after stimulation, reducing Na+ i to values 30% below the resting level (P< 0.001). This undershoot in Na+ i, seen in both soleus and extensor digitorum longus muscles, could be maintained for up to 30 min and was blocked by ouabain or cooling to 0 degree C. 3. The undershoot in Na+ i could be elicited by direct stimulation as well as by tubocurarine-suppressible stimulation via the motor endplate. It could not be attributed to a decrease in Na+ influx, to effects of noradrenaline or calcitonin gene-related peptide released from nerve endings, to an increase in extracellular K+ or the formation of nitric oxide. 4. The results indicate that excitation rapidly activates the Na (+)-K+ pump, partly via a change in its transport characteristics and partly via an increase in intracellular Na+ concentration. This activation allows an approximately 20-fold increase in the rate of Na+ efflux to take place within 10 s. 5. The excitation-induced activation of the Na (+)-K+ pump may represent a feed-forward mechanism that protects the Na (+)-K+ gradients and the membrane potential in working muscle. Contrary to previous assumptions, the Na (+)-K+ pump seems to play a dynamic role in maintenance of excitability during contractile activity.