Prolonged exercise reduces Ca2+ release in rat skeletal muscle sarcoplasmic reticulum

Favero, Terence G.; Pessah, Isaac N.; Klug, G. A.

doi:10.1007/bf00375074

Cited by 63 publications

(58 citation statements)

References 8 publications

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“…The reductions in [Ca 2ϩ ] f could be due to a failure in coupling between the t-tubule and CRC (53) or to direct alterations in the CRC (1). Reductions in SR Ca 2ϩ -release, mediated by apparent structural alterations in the CRC, have been observed to occur in skeletal muscle with repetitive stimulation as assessed in vitro (17).…”

Section: Discussionmentioning

confidence: 99%

Muscle Na-K-pump and fatigue responses to progressive exercise in normoxia and hypoxia

Sandiford

Green

Duhamel

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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To investigate the effects of hypoxia and incremental exercise on muscle contractility, membrane excitability, and maximal Na+-K+-ATPase activity, 10 untrained volunteers (age = 20 ± 0.37 yr and weight = 80.0 ± 3.54 kg; ± SE) performed progressive cycle exercise to fatigue on two occasions: while breathing normal room air (Norm; FiO2 = 0.21) and while breathing a normobaric hypoxic gas mixture (Hypox; FiO2 = 0.14). Muscle samples extracted from the vastus lateralis before exercise and at fatigue were analyzed for maximal Na+-K+-ATPase (K+-stimulated 3-O-methylfluorescein phosphatase) activity in homogenates. A 32% reduction ( P < 0.05) in Na+-K+-ATPase activity was observed (90.9 ± 7.6 vs. 62.1 ± 6.4 nmol·mg protein−1·h−1) in Norm. At fatigue, the reductions in Hypox were not different (81 ± 5.6 vs. 57.2 ± 7.5 nmol·mg protein−1·h−1) from Norm. Measurement of quadriceps neuromuscular function, assessed before and after exercise, indicated a generalized reduction ( P < 0.05) in maximal voluntary contractile force (MVC) and in force elicited at all frequencies of stimulation (10, 20, 30, 50, and 100 Hz). In general, no differences were observed between Norm and Hypox. The properties of the compound action potential, amplitude, duration, and area, which represent the electomyographic response to a single, supramaximal stimulus, were not altered by exercise or oxygen condition when assessed both during and after the progressive cycle task. Progressive exercise, conducted in Hypox, results in an inhibition of Na+-K+-ATPase activity and reductions in MVC and force at different frequencies of stimulation; these results are not different from those observed with Norm. These changes occur in the absence of reductions in neuromuscular excitability.

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Section: Discussionmentioning

confidence: 99%

Muscle Na-K-pump and fatigue responses to progressive exercise in normoxia and hypoxia

Sandiford

Green

Duhamel

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…A number of studies have reported that Ca 2ϩ release from isolated SR is reduced by ϳ20 -40% following prolonged or intense exercise in humans (210,284,285) and rodents (161), although some studies found no change (111,396) or a reduction in slow-twitch but not fast-twitch muscle (161,221). It is unclear how long this effect persists after exercise, as this was only examined in one study to date, and the results were somewhat equivocal at the one recovery time examined (3.5 h) (210 ] i also greatly prolongs PCD in Xenopus fast-twitch fibers (69,70,269).…”

Section: Prolonged Reduction In Ca 2؉ Releasementioning

confidence: 99%

Skeletal Muscle Fatigue: Cellular Mechanisms

Allen¹,

Lamb²,

Westerblad³

2008

Physiological Reviews

1,806

1,820

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Repeated, intense use of muscles leads to a decline in performance known as muscle fatigue. Many muscle properties change during fatigue including the action potential, extracellular and intracellular ions, and many intracellular metabolites. A range of mechanisms have been identified that contribute to the decline of performance. The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals. Alternative explanations that will be considered are the effects of ionic changes on the action potential, failure of SR Ca2+ release by various mechanisms, and the effects of reactive oxygen species. Many different activities lead to fatigue, and an important challenge is to identify the various mechanisms that contribute under different circumstances. Most of the mechanistic studies of fatigue are on isolated animal tissues, and another major challenge is to use the knowledge generated in these studies to identify the mechanisms of fatigue in intact animals and particularly in human diseases.

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“…However, this technique may be self-limiting where macroscopic assays might provide more conclusive data. For example, it was previously determined that SR Ca 2ϩ release was reduced by 30% after a run to exhaustion in rats (46). It is believed that as few as one RYR channel exists per vesicle (some vesicles contain no channels), and if only 30% of the channels are dysfunctional, it is possible that 70% of the fusion events will contain unmodified RYR proteins.…”

Section: Sr Ca 2ϩ Release From An Experimental Perspectivementioning

confidence: 99%

“…Reductions in Ca 2ϩ release have been noted in single muscle fibers from mouse (6), single whole (136) and cut fibers from frog (64), and whole bullfrog muscle (10). Moreover, inhibition of SR Ca 2ϩ release was noted in the rat after it run to exhaustion (46). (For a more detailed account of the muscle preparations and fatigue protocols please see Refs.…”

mentioning

confidence: 99%

Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

Favero

1999

Journal of Applied Physiology

Self Cite

107

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Efforts to examine the relevant mechanisms involved in skeletal muscle fatigue are focusing on Ca2+ handling within the active muscle cell. It has been demonstrated time and again that reductions in sarcoplasmic reticulum (SR) Ca2+release resulting from increased or intense muscle contraction will compromise tension development. This review seeks to accomplish two related goals: 1) to provide an up-to-date molecular understanding of the Ca2+-release process, with considerable attention devoted to the SR Ca2+ channel, including its associated proteins and their regulation by endogenous compounds; and 2) to examine several putative mechanisms by which cellular alterations resulting from intense and/or prolonged contractile activity will modify SR Ca2+ release. The mechanisms that are likely candidates to explain the reductions in SR Ca2+ channel function following contractile activity include elevated Ca2+ concentrations, alterations in metabolic homeostasis within the “microcompartmentalized” triadic space, and modification by reactive oxygen species.

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Prolonged exercise reduces Ca2+ release in rat skeletal muscle sarcoplasmic reticulum

Cited by 63 publications

References 8 publications

Muscle Na-K-pump and fatigue responses to progressive exercise in normoxia and hypoxia

Muscle Na-K-pump and fatigue responses to progressive exercise in normoxia and hypoxia

Skeletal Muscle Fatigue: Cellular Mechanisms

Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

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Prolonged exercise reduces Ca2+ release in rat skeletal muscle sarcoplasmic reticulum

Cited by 63 publications

References 8 publications

Muscle Na-K-pump and fatigue responses to progressive exercise in normoxia and hypoxia

Muscle Na-K-pump and fatigue responses to progressive exercise in normoxia and hypoxia

Skeletal Muscle Fatigue: Cellular Mechanisms

Sarcoplasmic reticulum Ca2+release and muscle fatigue

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Resources

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Sarcoplasmic reticulum Ca²⁺release and muscle fatigue