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1 Department of Pathobiology, Division of Anatomy and Physiology, Faculty of Veterinary Medicine, Utrecht University, P.O. Box 80.158, 3508 TD Utrecht, The Netherlands
2 Departments of Neurology and Neurophysiology, Leiden University Medical Centre, P.O. Box 9604, 2300 RC Leiden, The Netherlands
Exercise-induced loss of skeletal muscle K+ can seriously impede muscle performance through membrane depolarization. Thus far, it has been assumed that the negative equilibrium potential and large membrane conductance of Cl– attenuate the loss of force during hyperkalaemia. We questioned this idea because there is some evidence that Cl– itself can exert a depolarizing influence on membrane potential (Vm). With this study we tried to identify the possible roles played by Cl– during hyperkalaemia. Isolated rat soleus muscles were kept at 25 °C and twitch contractions were evoked by current pulses. Reducing [Cl–]o to 5 mM, prior to introducing 12.5 mM Ko, prevented the otherwise occurring loss of force. Reversing the order of introducing these two solutions revealed an additional effect, i.e. the ongoing hyperkalaemia-related loss of force was sped up tenfold after reducing [Cl–]o. However, hereafter twitch force recovered completely. The recovery of force was absent at [K+]o exceeding 14 mM. In addition, reducing [Cl–]o increased membrane excitability by 24%, as shown by a shift in the relationship between force and current level. Measurements of Vm indicated that the antagonistic effect of reducing [Cl–]o on hyperkalaemia-induced loss of force was due to low-Cl–-induced membrane hyperpolarization. The involvement of specific Cl– conductance was established with 9-anthracene carboxylic acid (9-AC). At 100 µM, 9-AC reduced the loss of force due to hyperkalaemia, while at 200 µM, 9-AC completely prevented loss of force. To study the role of the Na+–K+–2Cl– cotransporter (NKCC1) in this matter, we added 400 µM of the NKCC inhibitor bumetanide to the incubation medium. This did not affect the hyperkalaemia-induced loss of force. We conclude that Cl– exerts a permanent depolarizing influence on Vm. This influence of Cl– on Vm, in combination with a large membrane conductance, can apparently have two different effects on hyperkalaemia-induced loss of force. It might exert a stabilizing influence on force production during short periods of hyperkalaemia, but it can add to the loss of force during prolonged periods of hyperkalaemia.
(Received 8 July 2004;
accepted after revision 26 August 2004;
first published online 2 September 2004)
Corresponding author M. G. van Emst: Department of Pathobiology, Division of Anatomy and Physiology, Faculty of Veterinary Medicine, Utrecht University, P.O. Box 80.158, 3508 TD Utrecht, The Netherlands. Email: m.vanemst{at}vet.uu.nl
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