Effects of reduced muscle glycogen concentration on force, Ca2+ release and contractile protein function in intact mouse skeletal muscle.

Chin, Eva R.; Dg, Allen

doi:10.1113/jphysiol.1997.sp021838

Cited by 176 publications

(180 citation statements)

References 24 publications

(20 reference statements)

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“…In six experiments tension recovered to 93 ± 3 % and tetanic [Ca¥]é recovered to 100 ± 4 %. Note that the Ringer solution contains no glucose so this recovery in the absence of glucose is quite different from that seen in mouse fibres (Chin & Allen, 1997). We did not observe the failure of early recovery (post-contractile depression) described in Xenopus fibres (Westerblad & L annergren, 1986).…”

Section: Resultsmentioning

confidence: 99%

The role of calcium stores in fatigue of isolated single muscle fibres from the cane toad

Kabbara

Allen

1999

The Journal of Physiology

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Muscles which are used repeatedly at near their maximum tension output show a gradual reduction in tension production, in shortening velocity and a slowing of relaxation. These changes are collectively known as muscle fatigue and they represent an important limitation on exercise performance in athletes and on respiration and other activities in patients with muscle-wasting diseases. Current ideas on the mechanism of muscle fatigue are that it has several contributions (for review see Fitts, 1994; Allen et al. 1995). Intracellular accumulation of products of metabolism, such as inorganic phosphate (Pé), causes (i) reduced force production by the crossbridges and (ii) reduced Ca¥ sensitivity of the myofibrillar proteins (Dawson et al. 1978;Godt & Nosek, 1989;Millar & Homsher, 1990). In addition (iii) there is a reduction of sarcoplasmic reticulum (SR) Ca¥ release whose mechanism is unknown (Allen et al. 1989;Westerblad & Allen, 1991). In principle the reduction of Ca¥ release during fatigue could involve any of the components of excitation-contraction coupling such as (i) the action potential, (ii) the voltage sensor, (iii) the Ca¥ release channels in the SR, (iv) the store of Ca¥ available for release in the SR, (v) the SR Ca¥ pump. Of these factors, the SR Ca¥ store has received relatively little attention mainly because there was no simple and repeatable way to measure it. The total SR Ca¥ can be measured by electron probe microanalysis and Gonzalez-Serratos et al. (1978) showed that in a fatigued muscle the total Ca¥ in the store was substantially increased. This combination of increased store Ca¥ combined with reduced SR Ca¥ release led to the hypothesis that the SR release channels were failing to open normally during fatigue (Allen et al. 1995). Although Ca¥ stores have not been studied in detail in fatigued muscles, there are a number of suggestions that reduced Ca¥ release during fatigue might be a consequence of changes in the fraction of SR Ca¥ available for release. Fryer et al. (1995) demonstrated that in a skinned muscle fibre preparation with intact SR, a high myoplasmic Pé caused a reduced Ca¥ release. They suggested that this was because Ca¥ and Pé precipitated within the SR and that

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Section: Resultsmentioning

confidence: 99%

The role of calcium stores in fatigue of isolated single muscle fibres from the cane toad

Kabbara

Allen

1999

The Journal of Physiology

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“…33, 53). The mechanism responsible for peripheral fatigue below CT is obscure, but may be related to the depletion of muscle glycogen, since reduced Ca 2ϩ transients and hence lower force development have been observed in glycogendepleted single fibers (16) and whole muscle (27) in the mouse. At the end of these trials, the potentiated doublet torque was not different from trials performed above the CT (Table 1, Fig.…”

Section: Discussionmentioning

confidence: 99%

Distinct profiles of neuromuscular fatigue during muscle contractions below and above the critical torque in humans

Burnley

Vanhatalo

Jones

2012

Journal of Applied Physiology

173

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Burnley M, Vanhatalo A, Jones AM. Distinct profiles of neuromuscular fatigue during muscle contractions below and above the critical torque in humans. J Appl Physiol 113: 215-223, 2012. First published May 3, 2012 doi:10.1152/japplphysiol.00022.2012Whether the transition in fatigue processes between "low-intensity" and "high-intensity" contractions occurs gradually, as the torque requirements are increased, or whether this transition occurs more suddenly at some identifiable "threshold", is not known. We hypothesized that the critical torque (CT; the asymptote of the torqueduration relationship) would demarcate distinct profiles of central and peripheral fatigue during intermittent isometric quadriceps contractions (3-s contraction, 2-s rest). Nine healthy men performed seven experimental trials to task failure or for up to 60 min, with maximal voluntary contractions (MVCs) performed at the end of each minute. The first five trials were performed to determine CT [ϳ35-55% MVC, denoted severe 1 (S1) to severe 5 (S5) in ascending order], while the remaining two trials were performed 10 and 20% below the CT (denoted CT-10% and CT-20%). Dynamometer torque and the electromyogram of the right vastus lateralis were sampled continuously. Peripheral and central fatigue was determined from the fall in potentiated doublet torque and voluntary activation, respectively. Above CT, contractions progressed to task failure in ϳ3-18 min, at which point the MVC did not differ from the target torque (S1 target, 88.7 Ϯ 4.3 N·m vs. MVC, 89.3 Ϯ 8.8 N·m, P ϭ 0.94). The potentiated doublet fell significantly in all trials, and voluntary activation was reduced in trials S1-S3, but not trials S4 and S5. Below CT, contractions could be sustained for 60 min on 17 of 18 occasions. Both central and peripheral fatigue developed, but there was a substantial reserve in MVC torque at the end of the task. The rate of global and peripheral fatigue development was four to five times greater during S1 than during CT-10% (change in MVC/change in time S1 vs. CT-10%: Ϫ7.2 Ϯ 1.4 vs. Ϫ1.5 Ϯ 0.4 N·m·min Ϫ1 ). These results demonstrate that CT represents a critical threshold for neuromuscular fatigue development. central and peripheral fatigue; maximal voluntary contraction; muscle stimulation; exercise

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“…These results represent the strongest indication so far that the presence of non-washable glycogen in skeletal muscle fibres is a prerequisite for normal E-C coupling and that this protective role exerted by glycogen does not relate to its role of energy store in the fibre. Recently Chin & Allen (1997) reported that the mean values for myoplasmic [Ca¥] during tetanic stimulation in a mammalian skeletal muscle fibre was positively correlated with the relative glycogen concentration in the intact fibres and there is a large body of information, particularly for mammalian skeletal muscle, that associates the presence of glycogen above a critical level with the ability of the muscle to contract (Bergstr om et al 1967;Galbo et al 1979;Voellestad et al 1988;Fitts, 1994;Chin & Allen, 1997). Some have argued recently that glycogen depletion may lead to local shortages in ATP, which is locally needed for normal coupling processes (Chin & Allen, 1997).…”

Section: Discussionmentioning

confidence: 99%

Glycogen content and excitation‐contraction coupling in mechanically skinned muscle fibres of the cane toad

Stephenson

Nguyễn

Stephenson

1999

The Journal of Physiology

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There are consistent observations that depletion of intracellular glycogen stores in muscle is associated with reduced muscle performance (Bergstr om et al. 1967;Galbo et al. 1979;Voellestad et al. 1988;Fitts, 1994;Chin & Allen, 1997), but the cellular mechanisms responsible for the glycogen depletion-related impairment of muscle function are not understood (Fitts 1994;Chin & Allen, 1997). So far, all studies on the role of glycogen in muscle have involved the depletion of the muscle glycogen pool by inducing a state of muscle fatigue. Therefore, from these studies it is not possible to draw unequivocal conclusions concerning the nature of the relationship between glycogen content and muscle contractility because in addition to glycogen depletion, many other factors, known to affect excitation-contraction (E-C) coupling (Stephenson et al. 1998), would have been altered in the myoplasm of the fatigued muscle fibres. Further advances can be made if the relationship between glycogen and muscle contractility is investigated in single fibres containing different concentrations of glycogen under conditions where the ionic composition of the myoplasmic environment is kept constant and similar to that in a rested muscle. The mechanically skinned single muscle fibre preparation is particularly well suited for such a task

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Effects of reduced muscle glycogen concentration on force, Ca2+ release and contractile protein function in intact mouse skeletal muscle.

Cited by 176 publications

References 24 publications

The role of calcium stores in fatigue of isolated single muscle fibres from the cane toad

The role of calcium stores in fatigue of isolated single muscle fibres from the cane toad

Distinct profiles of neuromuscular fatigue during muscle contractions below and above the critical torque in humans

Glycogen content and excitation‐contraction coupling in mechanically skinned muscle fibres of the cane toad

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