EXCITATION-INDUCED FORCE RECOVERY IN POTASSIUM-INHIBITED RAT SOLEUS MUSCLE

1. Excitation markedly stimulates the Na+-K+ pump in skeletal muscle. The effect of this stimulation on contractility was examined in rat so leus muscles exposed to high extracellular K+ concentration ([K+](o)). 2. At a [K+](o) of 10 mM, tetanic force declined to 58% of the force in standard buffer with 5.9 mM K+. Subsequent direct stimulation of th e muscle at 1 min intervals with 30 Hz pulse trains of 2 s duration in duced a 97% recovery of force within 14 min. Force recovery could also be elicited by stimulation via the nerve. In muscles exposed to 12.5 mM K+, 30 Hz pulse trains of 2 s duration at 1 min intervals induced a recovery of force from 16 +/- 2 to 62 +/- 4% of the initial control f orce at a [K+](o) of 5.9 mM. 3. The recovery of force was associated w ith a decrease in intracellular Na+ and was blocked by ouabain. This i ndicates that the force recovery was secondary to activation of the Na +-K+ pump. 4. Excitation stimulates the release of calcitonin gene-rel ated peptide (CG;RP) from nerves in the muscle. Since CGRP stimulates the Na+-K+ pump, this may contribute to the excitation-induced force r ecovery. Indeed, reducing CGRP content by capsaicin pre-treatment or p rior denervation prevented both the excitation-induced force recovery and the drop in intracellular Na+. 5. The data suggest that activation of the Na+-K+ pump in contracting muscles counterbalances the depress ing effect of reductions in the chemical gradients for Na(+)and K(+)on excitability.