The Na+,K+pump and muscle excitability

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Abstract
In most types of mammalian skeletal muscles the total concentration of Na+,K+ pumps is 0.2–0.8 nmol g wet wt−1. At rest, only around 5% of these Na+,K+ pumps are active, but during high-frequency stimulation, virtually all Na+,K+ pumps may be called into action within a few seconds. Despite this large capacity for active Na+,K+ transport, excitation often induces a net loss of K+, a net gain of Na+, depolarization and ensuing loss of excitability. In muscles exposed to high [K+]o or low [Na+]o, alone or combined, excitability is reduced. Under these conditions, hormonal or excitation-induced stimulation of the Na+,K+ pump leads to considerable force recovery. This recovery can be blocked by ouabain and seems to be the result of Na+,K+ pump induced hyperpolarization and restoration of Na+,K+ gradients. In muscles where the capacity of the Na+,K+ pump is reduced, the decline in the force developing during continuous electrical stimulation (30–90 Hz) is accelerated and the subsequent force recovery considerably delayed. The loss of endurance is significant within a few seconds after the onset of stimulation. Increased concentration of Na+ channels or open-time of Na+ channels is also associated with reduced endurance and impairment of force recovery. This indicates that during contractile activity, excitability is acutely dependent on the ratio between Na+ entry and Na+,K+ pump capacity. Contrary to previous assumptions, the Na+,K+ pump, due to rapid activation of its large transport capacity seems to play a dynamic role in the from second to second ongoing restoration and maintenance of excitability in working skeletal muscle.