• G Gutierrez, R Kiiski, E Fernandez, and D H Lee.
• Department of Internal Medicine, University of Texas Houston Health Science Center 77030, USA.
• J Crit Care. 1996 Dec 1; 11 (4): 197-205.

PurposeSkeletal muscle fatigue has been associated with potassium efflux from the myocytes, resulting in endogenous increases in blood potassium concentration ([K+]). Conversely, exogenous increases in extracellular [K+] potentiates contraction in isolated muscle preparations. The mechanisms responsible for these contradictory effects of [K+] on skeletal muscle function are unknown. Moreover, little is known about the effect of exogenous increases in [K+] on force generation by intact animals, given potassium's deleterious effect on cardiac function.MethodsWe compared the response to exogenous increases in blood [K+] in rabbits given an infusion of potassium chloride (KCl) intravenously (IV) (0.2 mol/L; KCl group; n = 7) to a group given 0.9% sodium chloride (NaCl) (control; n = 7). The rabbits underwent low-frequency, isometric twitch stimulation of the left hindlimb (square wave pulses 100 microseconds, 40V, 0.25 Hz) throughout the experiment. Both groups received 0.9% NaCl (25 mL/h) during the first hour of twitch stimulation and experienced similar decreases in hindlimb forces to 70% of initial force. A continuous infusion of KCl or of saline (60 mL/h) was started, and hindlimb stimulation continued for 2 hours.ResultsThere were no changes in [K+] in the control group, and twitch forces progressively declined during the next 2 hours (369 +/- 47 g to 279 +/- 34 g, P < .01). Arterial [K+] increased in the KCl group from 2.6 +/- 0.1 to 10.1 +/- 0.5 mmol/L (P < .01), and hindlimb twitch forces almost doubled (418 +/- 49 g to 756 +/- 55 g, P < .01). Force frequency curves showed improved contractility in the KCl group at stimulation frequencies below 30 Hz.ConclusionsExogenous increases in blood [K+] potentiate skeletal muscle contraction in intact animals and reverse low-frequency twitch fatigue. A possible mechanism may be the maintenance of intracellular [K+] by hindering K+ efflux from skeletal muscle cells.

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