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 m m , tetanic force declined to 58 % of the force in standard buffer with 5.9 m m 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 m m 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 m m . 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.