Intense exercise results in increases in intracellular Na⁺ and extracellular K⁺ concentrations, leading to depolarization and a loss of muscle excitability and contractility. Here, we use carbacholine to chronically activate the nicotinic acetylcholine (nACh) receptors to mimic the changes in membrane permeability, chemical Na⁺ and K⁺ gradients and membrane potential observed during intense exercise. Intact rat soleus muscles were mounted on force transducers and stimulated electrically to evoke short tetani at regular intervals. Carbacholine produced a 2.6‐fold increase in Na⁺ influx that was tetrodotoxin (TTX) insensitive, but abolished by tubocurarine, 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 much larger alterations than the more distal regions of the muscle, and showed a larger membrane depolarization from −73 ± 1 to −60 ± 1 mV compared with −64 ± 1 mV. Carbacholine (10⁻⁴m) significantly reduced tetanic force to 31 ± 3% of controls, which underwent significant recovery upon application of Na⁺–K⁺ pump stimulators: salbutamol (10⁻⁵m), adrenaline (10⁻⁵m) and calcitonin gene‐related peptide (CGRP; 10⁻⁷m). The force recovery with salbutamol was accompanied by a recovery of intracellular Na⁺ and K⁺ contents, and a small but significant 4–5 mV recovery of membrane potential. Similar results were obtained using succinylcholine (10⁻⁴m), indicating that Na⁺–K⁺ pump stimulation may prevent or restore succinylcholine‐induced hyperkalaemia. The stimulation of the Na⁺–K⁺ pump allows muscle to partially recover contractility by regaining excitability through electrogenically driven repolarization of the muscle membrane.