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1 Institute of Physiology and Biophysics, University of Aarhus, Århus, Denmark
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 (10–4 M) significantly reduced tetanic force to 31 ± 3% of controls, which underwent significant recovery upon application of Na+–K+ pump stimulators: salbutamol (10–5 M), adrenaline (10–5 M) and calcitonin gene-related peptide (CGRP; 10–7 M). 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 (10–4 M), 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.
(Received 2 December 2004;
accepted after revision 6 January 2005;
first published online 13 January 2005)
Corresponding author W.A. Macdonald: Institute of Physiology and Biophysics, University of Aarhus, DK-8000, Århus C, Denmark. Email: wmd{at}fi.au.dk
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