Mechano‐sensitive linkage in excitation‐contraction coupling in frog skeletal muscle.

Bruton, Joseph D.; Lännergren, Jan; Westerblad, Håkan

doi:10.1113/jphysiol.1995.sp020699

Cited by 24 publications

(32 citation statements)

References 23 publications

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“…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). 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.…”

Section: Prolonged Reduction In Ca 2؉ Releasementioning

confidence: 97%

“…PCD is caused by inhibition of SR Ca 2ϩ release despite normal membrane potential and AP properties (219,266,283,471,475). The exact mechanism underlying PCD has not been revealed, but it seems to involve impaired mechanical coupling between the t-tubular voltage sensors (DHPR) and the SR Ca 2ϩ release channels (RyR) (69,72).…”

Section: A Delayed Recovery From Fatiguementioning

confidence: 99%

“…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). On the other hand, in a recent study fatigue was induced by repeated tetani in isolated mouse fibers exposed to N-benzyl-p-toluene sulfonamide (BTS), which inhibits cross-bridge force production (66).…”

Section: Prolonged Reduction In Ca 2؉ Releasementioning

confidence: 99%

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Skeletal Muscle Fatigue: Cellular Mechanisms

Allen¹,

Lamb²,

Westerblad³

2008

Physiological Reviews

1,867

1,876

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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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Section: Prolonged Reduction In Ca 2؉ Releasementioning

confidence: 97%

Section: A Delayed Recovery From Fatiguementioning

confidence: 99%

Section: Prolonged Reduction In Ca 2؉ Releasementioning

confidence: 99%

See 1 more Smart Citation

Skeletal Muscle Fatigue: Cellular Mechanisms

Allen¹,

Lamb²,

Westerblad³

2008

Physiological Reviews

1,867

1,876

View full text Add to dashboard Cite

show abstract

“…The mouse mammary gland has a mechanism similar to the thyroid iodide pump that is inhibited by perchlorate (Rillema and Rowady, 1997); however, it is unclear whether this has any significance for human health. At high (millimolar) concentrations, perchlorate is known to potentiate excitation-contraction (E-C) coupling and charge movement in muscle cells (Bruton et al, 1995;Gonzalez and Rios, 1993;Jong et al, 1997;Khammari et al, 1996;Ma et al, 1993;Pereon et al, 1996). At this level, part of the E-C effect is due to activation of calcium ion release from the sarcoplasmic reticulum (Fruen et al, 1994;Percival et al, 1994;Yano et al, 1995).…”

Section: Physiological and Health Effectsmentioning

confidence: 99%

Perchlorate Chemistry: Implications for Analysis and Remediation

Urbansky

1998

Bioremediation Journal

473

387

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Abstract:Since the discovery of perchlorate in the ground and surface waters of several western states, there has been increasing interest in the health effects resulting from chronic exposure to low (parts per billion [ppb]) levels. With this concern has come a need to investigate technologies that might be used to remediate contaminated sites or to treat contaminated water to make it safe for drinking. Possible technologies include physical separation (precipitation, anion exchange, reverse osmosis, and electrodialysis), chemical and electrochemical reduction, and biological or biochemical reduction. A fairly unique combination of chemical and physical properties of perchlorate poses challenges to its analysis and reduction in the environment or in drinking water. The implications of these properties are discussed in terms of remediative or treatment strategies. Recent developments are also covered.

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“…During the period of depressed force, electirical stimulation results in normal action potentials and application of a high concentration of caffeine (12 mai) gives high force contractures. We therefore concluded that the long-lasting loss of force production, induced by fibre swelling and subsequent slhrinkage due to the hypotonic treatment, reflects a weakening of a mechano-sensitive link involved in E-C coupling (Bruton et al 1995 (Lee, Wl'esterblad & Allen, 1991 to both A and B.…”

mentioning

confidence: 99%