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Na+‐K+ Pump Stimulation Improves Contractility in Damaged Muscle Fibers

Abstract: Skeletal muscles have a high content of Na+‐K+‐ATPase, an enzyme that is identical to the Na+‐K+ pump, a transport system mediating active extrusion of Na+ from the cells and accumulation of K+ in the cells. The major function of the Na+‐K+ pumps is to maintain the concentration gradients for Na+ and K+ across the plasma membrane. This generates the resting membrane potential, allowing the propagation of action potentials, excitation‐contraction coupling and force development. Muscles exposed to (1) high extracellular K+ or (2) low extracellular Na+ show a considerable loss of force. A similar force decline is elicited by (3) increasing Na+ permeability or (4) decreasing K+ permeability. Under all of these four conditions, stimulation of the Na+‐K+ pumps can restore contractility. Following exposure to electroporation or fatiguing stimulation, muscle cell membranes develop leaks to Na+ and K+ and a partially reversible loss of force. The restoration of force is abolished by blocking the Na+‐K+ pumps and markedly improved by stimulating the Na+‐K+ pumps with β2‐agonists, calcitonin gene‐related peptide, or dbcAMP. These observations indicate that the Na+‐K+ pumps are important for the functional compensation of the commonly occurring loss of muscle cell integrity. Stimulation of the Na+‐K+ pumps with β2‐agonists or other agents may be of therapeutic value in the treatment of muscle cell damage induced by electrical shocks, prolonged exercise, burns, or bruises.