Muscle membrane excitation and impulse propagation velocity are reduced during muscle fatigue

Abstract

In order to determine whether or not impulse propagation was impaired during muscle fatigue, evoked muscle compound potentials (MCP) and twitches were recorded, both before and after fatigue, from the first dorsal interosseus (FDI), adductor pollicis (AP), and anterior tibialis (AT) muscles following supramaximal ulnar and peroneal nerve stimulation, respectively. The muscles were fatigued by maintaining maximum voluntary isometric, index finger abduction, thumb adduction, or ankle dorsiflexion for 1-5 minutes. FDI was most markedly altered, with reduced MCP amplitude (mean 32%) and increased MCP duration (mean 47%) after only 1 minute. After fatigue of longer duration (3-5 minutes), there were corresponding reductions in both the MCP amplitudes and the twitch tensions recorded from both the FDI and ankle dorsiflexors. We conclude that (1) a reduction in both the level of excitation and impulse propagation velocity of muscle membranes occurs during muscle fatigue, and (2) the magnitude of this reduced membrane function and its contribution to the mechanisms underlying fatigue depend both on the duration and degree of fatigue, as well as on the intrinsic properties of the particular muscle.

Alterações hidroeletrolíticas agudas ocorridas no Triatlon Ironman Brasil

“…Porém, ao cessar a atividade de contração muscular no exercício de alta intensidade ocorre um rápido decréscimo do K+ plasmático a valores próximos de 2mmol/ l (22,26) . Há relatos de que exercícios submáxi-mos prolongados promovem perdas contínuas de K+ do músculo esquelético em contração (28)(29) e levam à mudanças no potencial de membrana de repouso implicando menos freqüentemente em fadiga muscular (30)(31) . As reservas intracelulares contêm cerca de 3000 a 4200mmol de K+ para mobilização.…”

Behaviour of short and long latency reflexes in fatigued human muscles.

“…J. DUCHATEAU AND K. HAINAUT Enoka & Stuart, 1992). Changes in EMG activity do not result mainly from neuromuscular junction failure in fatigue of short duration at the physiological frequency of motor unit activation, but from modifications to ionic muscle membrane processes (Merton, 1954;Bigland-Ritchie, Kukulka, Lippold & Woods, 1982;Duchateau & Hainaut, 1985;Milner-Brown & Miller, 1986). It has also been suggested that the excitability of the a-motoneurone (MN) pool is depressed during fatigue (Kukulka, Moore & Russell, 1986;Garland & McComas, 1990) and thus contributes to the decline in the motor unit firing frequency recorded during sustained MVC (Bigland-Ritchie, Johansson, Lippold, Smith & Woods, 1983;Marsden, Meadows & Merton, 1983).…”

31P nuclear magnetic resonance studies of high energy phosphates and pH in human muscle fatigue. Comparison of aerobic and anaerobic exercise.

“…Several factors have been proposed including alteration of muscle membrane function (1,2), reduction of high energy phosphates (3)(4)(5), accumulation of H+ (6-10), and impairment of excitation-contraction coupling (11-13). Evidence for each of these has been found using in vitro animal preparations, but the relative importance ofthese mechanisms in human fatigue (defined as a decline of mnaximum forcegenerating capacity) remains uncertain.…”