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 soleus 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 the muscle at 1 min intervals with 30 Hz pulse trains of 2 s duration induced 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 force at a [K+]o of 5.9 mM. 3. The recovery of force was associated with a decrease in intracellular Na+ and was blocked by ouabain. This indicates that the force recovery was secondary to activation of the Na+-K+ pump. 4. Excitation stimulates the release of calcitonin gene-related peptide (CGRP) from nerves in the muscle. Since CGRP stimulates the Na+-K+ pump, this may contribute to the excitation-induced force recovery. Indeed, reducing CGRP content by capsaicin pre-treatment or prior 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 depressing effect of reductions in the chemical gradients for Na+ and K+ on excitability.