Relation between extracellular [K+], membrane potential and contraction in rat soleus muscle: modulation by the Na+-K+ pump
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An increased extracellular K+ concentration ([K+]0) is thought to cause muscle fatigue. We studied the effects of increasing [K+]0 from 4 mM to 8–14 mM on tetanic contractions in isolated bundles of fibres and whole soleus muscles from the rat. Whereas there was little depression of force at a [K+]0 of 8–9 mM, a further small increase in [K+]0 to 11–14 mM resulted in a large reduction of force. Tetanus depression at 11 mM [K+]o was increased when using weaker stimulation pulses and decreased with stronger pulses. Whereas the tetanic force/resting membrane potential (EM) relation showed only moderate force depression with depolarization from −74 to −62 mV, a large reduction of force occurred whenEM fell to −53 mV. The implications of these relations to fatigue are discussed. Partial inhibition of the Na+-K+ pump with ouabain (10−6 M) caused additional force loss at 11 mM [K+]0. Salbutamol, insulin, or calcitonin gene-related peptide all stimulated the Na+-K+ pump in muscles exposed to 11 mM [K+0] and induced an average 26–33% recovery of tetanic force. When using stimulation pulses of 0.1 ms, instead of the standard 1.0-ms pulses, force recovery with these agents was 41–44% which was significantly greater (P < 0.025). Only salbutamol caused any recovery ofEM (1.3 mV). The observations suggest that the increased Na+ concentration difference across the sarcolemma, following Na+-K+ pump stimulation, has an important role in restoring excitability and force.
Key wordsNa+-K+ pump Potassium Salbutamol Insulin Skeletal muscle Fatigue
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