Intense exercise results in increases in intracellular Na⁺ and extracellular K⁺ concentrations, leading to depolarisation and a loss of muscle excitability and contractility. Here, we use carbacholine to chronically activate the nicotinic acetylcholine (nACh) receptors, mimicking the changes in membrane permeability, chemical Na⁺ and K⁺ gradients and membrane potential, observed during intense exercise. Intact soleus muscles obtained from humanely killed rats were mounted on force transducers and stimulated electrically to evoke short tetani of 60 Hz, 12 V, 2 s, every 10 min, at 30°C. Carbacholine (10^-4 M) produced a 2.6-fold increase in Na⁺ influx, that was tetrodotoxin (TTX, 10^-6 M) insensitive but abolished by tubocurarine (10^-5 M), resulting in a significant 36% increase in intracellular Na⁺ and 8% decrease in intracellular K⁺ content. The mid region, near the motor end plate, had larger changes in Na⁺ and K⁺ contents than did more distal regions of the muscle, and was associated with a greater membrane depolarisation of 13 mV compared to 9 mV. Carbacholine significantly reduced tetanic force to ~30% of controls, which was significantly recovered by Na⁺-K⁺ pump stimulation with salbutamol (10^-5 M), adrenaline (10^-5 M) and calcitonin gene related peptide (CGRP, 10^-7 M). The salbutamol induced force recovery was accompanied by a restoration of intracellular Na⁺ and K⁺ contents and a small 4-5 mV recovery of membrane potential. Similar results were obtained using succinylcholine (10^-4 M), indicating that Na⁺-K⁺ pump stimulation may prevent or restore depression of muscle finction caused by succinylcholine-induced hyperkalemia. Stimulation of the Na⁺-K⁺ pump allows muscle to partially recover contractility, by regaining excitability through electrogenically driven repolarisation of the muscle membrane.