Peripheral mechanisms of fatigue in muscles of normal and dystrophic mice

Pagala, Murali; Venkatachari, S. A. T.; Nandakumar, Namrata; Ravindran, K.; Kerstein, Joshua; Namba, Tatsuji; Grob, David

doi:10.1016/0960-8966(91)90103-y

Cited by 11 publications

(16 citation statements)

References 37 publications

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“…28,35 While such a change in the fiber type composition can account for the slight increase in resistance to fatigue in old EDL, it may not account for the marked increase in resistance to fatigue in old soleus as observed in the present study. A similar increase in resistance to fatigue, without a comparable increase in slow-twitch oxidative fibers, was observed in muscles of the dystrophic mice, 46 especially in the soleus of the dystrophic mice, 42 and in denervated soleus of normal mice. 41 Though loss of muscle mass is a common factor in dystrophic, denervated, and aged muscles, smaller size of the muscle is not a cause of their increased resistance to fatigue, because thin bundles of EDL and soleus muscles from normal young mice showed a similar time course of fatigue as whole muscles.…”

Section: Discussionsupporting

confidence: 72%

“…11,22,27,33 Much of the fatigue in normal skeletal muscles is caused by impairment in peripheral physiological processes like neuromuscular transmission, 18,24,51 muscle membrane excitation, 14,32 excitationcontraction coupling and contractility, 3,31 or a combination of these processes. 13,39,42,43 Only in certain neuropathological conditions such as multiple sclerosis, 45 amyotrophic lateral sclerosis, 22 postpolio syndrome, 50 and chronic fatigue syndrome 21 is an impairment in central physiological process known to be involved in the development of muscle fatigue.…”

Section: Discussionmentioning

confidence: 98%

“…41 Though loss of muscle mass is a common factor in dystrophic, denervated, and aged muscles, smaller size of the muscle is not a cause of their increased resistance to fatigue, because thin bundles of EDL and soleus muscles from normal young mice showed a similar time course of fatigue as whole muscles. 42 In isolated muscles, diffusion of oxygen and nutrients to the core decreases with increase in size and cross-sectional area of the muscle, leading to decrease in their responses with time. 48 In the present study, the weight of the young EDL was 19.5% greater than old EDL, and of the young soleus was 24.2% greater than old soleus (Table 1).…”

Section: Discussionmentioning

confidence: 99%

“…Isometric tension responses evoked by a 0.5-s train of muscle stimuli at 30 Hz and 100 Hz were then recorded. The tension measured in grams was converted into specific force, given as Newtons/cm 2 , by using the following formula 42,48 Fatigue was induced by stimulating the muscles at 30 Hz for 0.5 s every 2.5 s until the original tension of the slowly fatiguing muscle declined by about 50% or until a maximum period of 10 min had elapsed. A frequency of 30 Hz was selected for stimulating both EDL and soleus muscles because this frequency is close to the physiological firing frequency of motor units, 20 and it evoked fused tetanic tension responses of similar magnitude in both of these muscles at 20°C.…”

Section: Monitoring the Fatigue Of Isolated Skeletal Mus-mentioning

confidence: 99%

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Skeletal muscle fatigue and physical endurance of young and old mice

et al. 1998

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Monitoring the Fatigue Of Isolated Skeletal Mus-mentioning

confidence: 99%

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Skeletal muscle fatigue and physical endurance of young and old mice

et al. 1998

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“…43 The area analysis showed that in normal intercostal muscle, after 30 min of fatigue stimulation, nerve-evoked tension decreased by 58%, while muscle-evoked tension decreased by 35% ( Table 1). The difference of 23% between these two decreases represents the part of fatigue attributable to impairment of nerve conduction and neuromuscular transmission.…”

Section: Resultsmentioning

confidence: 97%

Mechanisms of fatigue in normal intercostal muscle and muscle from patients with myasthenia gravis

et al. 1993

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Fatigue mechanisms in normal intercostal muscle and muscle from patients with myasthenia gravis (MG) were evaluated by monitoring the compound muscle action potential (CMAP) and tetanic tension responses to repetitive nerve or muscle stimulation in vitro. When fatigue was induced by nerve stimulation at 30 Hz for 0.5 s every 2.5 s, about half of the original tension decreased after 30 min in normal muscle and 5 min in MG muscle. Analysis of the changes in area of CMAPs and tension indicated that impairment of neuromuscular transmission, muscle membrane excitation, and excitation-contraction (E-C) coupling and contractility accounted for 40%, 29%, and 31% of fatigue in normal muscle, and 83%, 0%, and 17% of fatigue in MG muscle. When fatigue was induced by muscle stimulation at 30 Hz, tension declined by a quarter after 30 min in normal muscle, but by a half after 17 min in MG muscle. Impairment of muscle membrane excitation and E-C coupling and contractility accounted for 58% and 42% of fatigue in normal muscle, and 22% and 78% of fatigue in MG muscle. Thus, fatigue of normal muscle is caused by impairment of at least four processes, and enhanced fatigue of MG muscle is caused by greater impairment of neuromuscular transmission, E-C coupling, and contractility.

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Potassium and caffeine contractures of mouse muscles before and after fatiguing stimulation

et al. 1994

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To assess the impairment of muscle membrane excitation, excitationcontraction (E-C) coupling, and contractility during muscle fatigue, we monitored the contracture responses of resting and fatigued muscles on exposure to high potassium and caffeine. On exposure to 140 mmol/L potassium, mouse extensor digitorum longus (EDL) developed a contracture which was 15.7% of tetanic tension before fatigue and 31.7% after fatigue, while soleus developed 59.4% contracture before and 68.8% after fatigue. Potassium causes contractures by depolarizing the muscle fiber membrane. Hence, membrane excitation is reduced in fatigued EDL and soleus. On exposure to 32 mmol/L caffeine, the contracture was 7.1% in resting EDL, 8.5% in fatigued EDL, 50.1% in resting soleus, and 43.7% in fatigued soleus. On exposure to 1 mmol/L caffeine followed by rapid cooling, the contracture was 3.0% in resting EDL, 3.2% in fatigued EDL, 21.5% in resting soleus, and 10.3% in fatigued soleus. Caffeine causes contracture by releasing Ca+ + from the sarcoplasmic reticulum. Our results indicate reduced E-C coupling attributable to reduced membrane excitation in fatigued EDL, and reduced contractility in fatigued soleus. 0 1994 John Wiley & Sons, Inc.

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Peripheral mechanisms of fatigue in muscles of normal and dystrophic mice

Cited by 11 publications

References 37 publications

Skeletal muscle fatigue and physical endurance of young and old mice

Skeletal muscle fatigue and physical endurance of young and old mice

Mechanisms of fatigue in normal intercostal muscle and muscle from patients with myasthenia gravis

Potassium and caffeine contractures of mouse muscles before and after fatiguing stimulation

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