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Regulation of Na+–K+ pump activity in contracting rat muscle

1 In rat soleus muscle, high frequency electrical stimulation produced a rapid increase in intra‐cellular 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 °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.