Disruption of excitation–contraction coupling and titin by endogenous Ca<sup>2+</sup>‐activated proteases in toad muscle fibres

Verburg, Esther; Murphy, Robyn M.; Stephenson, D. George; Lamb, Graham D.

doi:10.1113/jphysiol.2004.082180

Cited by 63 publications

(66 citation statements)

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“…In their review, Allen and Westerblad (3) propose elevated inorganic phosphate to be the key factor by leading to the precipitation of calcium phosphate. Alternatively excitation coupling may be disrupted by calciumactivated proteases (40). Our experimental findings provide some evidence for supporting the former because both the concentric and eccentric exercises can be expected to result in roughly similar profiles of activation (24) and calcium release (there is a moderate decrease of EMG activity in eccentric contractions) (21) but with very different use of metabolic energy.…”

Section: Discussionsupporting

confidence: 50%

“…The twitch response at 20 min after 20 contractions was 72 Ϯ 2.2%, and after 80 contractions it was 50 Ϯ 6.0% control (n ϭ 5). There was no significant difference between 40 A reduction in electrically induced EMG (M wave) following fatiguing electrical stimulation has been reported in both rats (23) and humans (25) with a maximum depression of ϳ50% after 60 min. Figure 3A shows that in the present experiments, there was also a decline in the M wave but that this was Ͻ20% for both concentric and eccentric contractions (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Fatigue and functional performance of human biceps muscle following concentric or eccentric contractions

Smith¹,

Newham²

2007

Journal of Applied Physiology

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Smith ICH, Newham DJ. Fatigue and functional performance of human biceps muscle following concentric or eccentric contractions. J Appl Physiol 102: 207-213, 2007. First published September 21, 2006; doi:10.1152/japplphysiol.00571.2006.-A long-lasting fatigue was measured in human biceps muscle, following 40 maximal isokinetic concentric or eccentric contractions of the forearm, as the response to single-shock stimuli every minute for 4 h. This protocol allowed new observations on the early time course of long-lasting fatigue. Concentric contractions induced a novel progressive decline to 30.2% (SE 7.8, n ϭ 7) of control at 23 min with complete recovery by 120 min. Eccentric contractions lead initially to a smaller force reduction of similar time course followed by a slower decline to 40.0% (SE 5.1, n ϭ 7) control at 120 min with recovery less than half complete at 4 h. A 50-Hz test stimuli overcame both fatigues, identifying low-frequency fatigue. EMG recordings from the biceps muscle showed moderate (Ͻ20%) changes during the fatigue. A visual-tracking task showed no decrement in performance at the time of maximal fatigue of the single-shock response. Because the eccentric contractions have a similar activation, a larger force, but much smaller metabolic usage than concentric contractions, it is concluded that the initial decline is related to the effects of metabolites, whereas the slower phase after eccentric contractions is associated with higher mechanical stress. skeletal muscle; motor control; skill PERIPHERAL MUSCLE FATIGUE can be both short term, with a simultaneous recovery of force and phosphocreatine largely complete within 1 min (36, 37), and long-lasting, remaining for at least 0.5 h after exercise (13). This later failure to develop tension is seen most clearly using low-frequency test stimuli, thus the nomenclature of low-frequency fatigue (19). It remains long after metabolic recovery and is associated with reduced calcium release per action potential (8, 9). In addition, it has long been recognized that high-intensity eccentric contractions give rise to further force reduction that lasts several days and is associated with muscle damage (30,29,35), although the mechanisms for the initial decline in force are still uncertain (2, 31). In this paper, which studies force reduction for up to 4 h after brief but intense fatiguing concentric or eccentric exercise, we refer to the force reduction by either protocol as fatigue. The time scale of the development of long-lasting fatigue remains unclear because it has been experimentally lost either by using a long period of fatiguing exercise or through infrequent test measurements of the degree of fatigue. Normally, the fatigue is shown as having developed by the first measurement point, leading to the assumption that it develops during the fatiguing exercise. However, it was recently found that, in response to short maximal isometric contractions, low-frequency fatigue developed between 3 and 9 min after the exercise (11). Thus, to achieve a faster time...

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Section: Discussionsupporting

confidence: 50%

Section: Resultsmentioning

confidence: 99%

Fatigue and functional performance of human biceps muscle following concentric or eccentric contractions

Smith¹,

Newham²

2007

Journal of Applied Physiology

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“…Much of the ubiquitous calpain is freely diffusible, but some is normally bound at triad junction (182), and raising [Ca 2ϩ ] within the physiological range increases calpain binding there (322,367). Ca 2ϩ -dependent uncoupling is prevented in toad skinned fiber by leupeptin, a calpain inhibitor, but only at low [Ca 2ϩ ] when the uncoupling proceeds slowly (254,451). Calpain inhibitors, however, were not found to prevent either long-duration fatigue in mouse fibers (89) or hypotonic-induced PCD in frog fibers (69).…”

Section: Prolonged Reduction In Ca 2؉ Releasementioning

confidence: 98%

“…Calpain inhibitors, however, were not found to prevent either long-duration fatigue in mouse fibers (89) or hypotonic-induced PCD in frog fibers (69). Calpain inhibitors such as leupeptin are quite poor at inhibiting in situ calpain-dependent proteolysis of structural proteins (141), unless used at very high concentration (241,322,451), so it still seems possible that they might play a role in the Ca 2ϩ -dependent uncoupling. It is known, however, that Ca 2ϩ -dependent uncoupling does not involve proteolysis of the DHPRs, RyRs, or another junctional protein, triadin (254).…”

Section: Prolonged Reduction In Ca 2؉ Releasementioning

confidence: 99%

Skeletal Muscle Fatigue: Cellular Mechanisms

Allen¹,

Lamb²,

Westerblad³

2008

Physiological Reviews

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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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“…Previous studies demonstrated that ischemiainduced stress increased [Ca 2ϩ ] i in skeletal muscle (32). The importance of prolonged elevation of resting [Ca 2ϩ ] i after contractions likely relates to the muscle weakness and/or activation of proteolytic pathways (12,55,56 homeostasis may be associated with the compromised SR function. In previous studies using cardiac muscle, decreased SR Ca 2ϩ transport and SR Ca 2ϩ content have been detected in animal diabetic models (13,19).…”

Section: Effects Of Muscle Contractions On [Ca 2ϩ ] I Accumulationmentioning

confidence: 99%

In vivo imaging of intracellular Ca²⁺ after muscle contractions and direct Ca²⁺ injection in rat skeletal muscle in diabetes

Eshima

Tanaka

Sonobe

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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([Ca 2ϩ ]i) accumulation in Type 1 diabetes are unclear. We tested the hypothesis that, following repeated bouts of muscle contractions, the rise in resting [Ca 2ϩ ]i evident in healthy rats would be increased in diabetic rats and that these changes would be associated with a decreased cytoplasmic Ca 2ϩ -buffering capacity. Adult male Wistar rats were divided randomly into diabetic (DIA; streptozotocin, ip) and healthy control (CONT) groups. Four weeks later, animals were anesthetized and spinotrapezius muscle contractions (10 sets of 50 contractions) were elicited by electrical stimulation (100 Hz). Ca 2ϩ imaging was achieved using Fura-2 AM in the spinotrapezius muscle in vivo (i.e., circulation intact). The ratio (340/380 nm) was determined from fluorescence images following each set of contractions for estimation of [Ca 2ϩ ]i. Also, muscle Ca 2ϩ buffering was studied in individual myocytes microinjected with 2 mM Ca 2ϩ solution. After muscle contractions, resting [Ca 2ϩ ]i in DIA increased earlier and more rapidly than in CONT (P Ͻ 0.05 vs. precontraction). Peak [Ca 2ϩ ]i in response to the Ca 2ϩ injection was significantly higher in CONT (25.8 Ϯ 6.0% above baseline) than DIA (10.2 Ϯ 1.1% above baseline). Subsequently, CONT [Ca 2ϩ ]i decreased rapidly (Ͻ15 s) to plateau 9 -10% above baseline, whereas DIA remained elevated throughout the 60-s measurement window. No differences in SERCA1 and SERCA2 (Ca 2ϩ uptake) protein levels were evident between CONT and DIA, whereas ryanodine receptor (Ca 2ϩ release) protein level and mitochondrial oxidative enzyme activity (succinate dehydrogenase) were decreased in DIA (P Ͻ 0.05). ] i evident in healthy rats would be magnified in muscles of diabetic rats and further that these changes would be associated with attenuation of the Ca 2ϩ -handling system within the in vivo environment. METHODS AnimalsMale Wistar rats (n ϭ 43, 10 wk of age; Japan SLC, Shizuoka, Japan) were used in this study. Rats were maintained on a 12:12-h light-dark cycle and received food and water ad libitum. Rats were divided into two groups: healthy control (CONT) and diabetic (DIA) rats. Rats were anesthetized using isoflurane and given intraperitoneal injection of 45 mg/kg body wt of streptozotocin (STZ; S0130, SigmaAldrich St. Louis, MO) prepared fresh in saline solution. CONT animals were injected with the saline solution. Urine glucose levels of rats were measured (New Uriesu Ga, Terumo, Japan) 2 days after STZ injection with the onset of diabetes raising glucose concentrations above 500 mg/dl. These measurements of urine glucose were continued each week for 4 wk. At experiment completion, blood was collected from a tail vein puncture to confirm that the blood glucose level exceeded 300 mg/dl. All experiments were conducted under the guidelines established by the Physiological Society of Japan and were approved by University of Electro-Communications Institutional Animal Care and Use Committee. The rats were anesthetized using pentobarbital sodium (60 mg/kg ip), and supplemental dose...

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Disruption of excitation–contraction coupling and titin by endogenous Ca²⁺‐activated proteases in toad muscle fibres

Cited by 63 publications

References 50 publications

Fatigue and functional performance of human biceps muscle following concentric or eccentric contractions

Fatigue and functional performance of human biceps muscle following concentric or eccentric contractions

Skeletal Muscle Fatigue: Cellular Mechanisms

In vivo imaging of intracellular Ca²⁺ after muscle contractions and direct Ca²⁺ injection in rat skeletal muscle in diabetes

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Disruption of excitation–contraction coupling and titin by endogenous Ca2+‐activated proteases in toad muscle fibres

Cited by 63 publications

References 50 publications

Fatigue and functional performance of human biceps muscle following concentric or eccentric contractions

Fatigue and functional performance of human biceps muscle following concentric or eccentric contractions

Skeletal Muscle Fatigue: Cellular Mechanisms

In vivo imaging of intracellular Ca2+ after muscle contractions and direct Ca2+ injection in rat skeletal muscle in diabetes

Contact Info

Product

Resources

About

Disruption of excitation–contraction coupling and titin by endogenous Ca²⁺‐activated proteases in toad muscle fibres

In vivo imaging of intracellular Ca²⁺ after muscle contractions and direct Ca²⁺ injection in rat skeletal muscle in diabetes