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¹ Department of Physiology and Biophysics, University of Aarhus, Århus, Denmark

During contractile activity, skeletal muscles undergo a net loss of cytoplasmic K⁺ to the interstitial space. During intense exercise, plasma K⁺ in human arterial blood may reach 8 mM, and interstitial K⁺ 10–12 mM. This leads to depolarization, loss of excitability and contractile force. However, little is known about the effects of these physiological increases in extracellular K⁺ ([K⁺]_o) on contractile endurance. Soleus muscles from 4-week-old rats were mounted on transducers for isometric contractions in Krebs–Ringer bicarbonate buffer containing 4–10 mM K⁺, and endurance assessed by recording the rate of force decline during continuous stimulation at 60 Hz. Increasing [K⁺]_o from 4 to 8 or 10 mM and equilibrating the muscles for 40 or 20 min augmented the rate of force decline 2.4-fold and 7.2-fold, respectively (P < 0.001). The marked loss of endurance elicited by exposure to 8 or 10 mM K⁺ was alleviated or significantly reduced by stimulating the Na⁺,K⁺-pumps by intracellular Na⁺ loading, the ₂-agonist salbutamol, adrenaline, calcitonin gene related peptide, insulin or repeated excitation. In conclusion, excitation-induced increase in [K⁺]_o is an important cause of high-frequency fatigue, and the Na⁺,K⁺-pumps are essential for the maintenance of contractile force in the physiological range of [K⁺]_o. Recordings of contractile force during continuous stimulation at 8–10 mM K⁺ may be used to analyse the effects of agents or conditions influencing the excitability of working isolated muscles.

(Received 14 May 2007; accepted after revision 30 July 2007; first published online 2 August 2007)
Corresponding author T. Clausen: Institute of Physiology and Biophysics, University of Aarhus, Ole Worms Allé 1160, DK-8000 Århus C, Denmark. Email: tc{at}fi.au.dk

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