Glucose infusion attenuates muscle fatigue in rat plantaris muscle during prolonged indirect stimulation in situ.

Abstract

Carbohydrate ingestion increases both endurance time to exhaustion during prolonged exercise, and the ability to perform resistance exercise. The mechanism(s) underlying the increased performance following glucose ingestion remain(s) unclear. The purpose of the present study was to verify the hypothesis that glucose infusion could attenuate peripheral muscle fatigue in the anaesthetized rat during prolonged indirect electrical stimulation in situ. For this purpose the plantaris muscle was electrically stimulated (50 Hz for 200 ms every 2.7 s; 5 V; pulse width, 0.05 ms) in situ through the sciatic nerve to perform concentric contractions for 60 min while infusing intravenously either saline alone (7.25 ml kg(-1) h(-1)), or saline and glucose (1 g kg(-1) h(-1): plasma glucose 11 +/- 1.1, vs. 4.9 +/- 0.2 mm with infusion of saline) (8 rats per group). Glucose infusion attenuated the reduction in submaximal peak dynamic force (55% decrease vs. 70% decrease in rats infused with saline alone, P < 0.05). In a third group of rats (n = 8), infusion of glucose 30 min after the start of stimulation partially restored submaximal peak dynamic force (P < 0.05). Maximum dynamic and isometric forces at the end of the period of stimulation were also higher (P < 0.05) in rats infused with glucose (4.0 +/- 0.2 and 4.3 +/- 0.2 N, respectively) than saline alone (3.0 +/- 0.2 and 3.5 +/- 0.2 N, respectively). The beneficial effect of glucose infusion on peripheral muscle force during prolonged stimulation was not associated with a reduction in muscle glycogen utilisation, nor with a reduction of fatigue at the neuromuscular junction, as assessed through maximal direct muscle stimulation (200 Hz for 200 ms; 150 V; pulse width, 0.05 ms). However, changes in M-wave peak-to-peak amplitude, duration and total area suggest that glucose infusion, and/or the associated increase in plasma insulin concentration, may prevent the deterioration of electrical properties of the muscle fibre membrane.