The membrane capacity of mammalian skeletal muscle fibres

Dulhunty, Angela F.; Carter, Grant; Hinrichsen, Colin

doi:10.1007/bf00713110

Cited by 39 publications

(36 citation statements)

References 32 publications

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“…However, previous work has shown that the cross-sectional aspect ratios of transverse tubules are highly sensitive to osmolarity and the extracellular [NaCl] (Rapoport, 1969;Rapoport et al, 1969). This could explain the high variability of the observed aspect-ratios between independent EM studies (Rapoport, 1969;Franzini-Armstrong et al, 1975;Dulhunty et al, 1984) and would warrant a superresolution imaging approach in studying the triadic transverse tubules under controlled osmotic conditions. The cross-sectional aspect ratios of longitudinal tubules remain poorly documented and there are no reported association of these tubules with junctions.…”

Section: What Does a Tubule Look Like?mentioning

confidence: 98%

Three-dimensional reconstruction and analysis of the tubular system of vertebrate skeletal muscle

Jayasinghe

Launikonis

2013

Journal of Cell Science

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SummarySkeletal muscle fibres are very large and elongated. In response to excitation there must be a rapid and uniform release of Ca 2+ throughout for contraction. To ensure a uniform spread of excitation throughout the fibre to all the Ca 2+ release sites, the muscle internalizes the plasma membrane, to form the tubular (t-) system. Hence the t-system forms a complex and dense network throughout the fibre that is responsible for excitation-contraction coupling and other signalling mechanisms. However, we currently do not have a very detailed view of this membrane network because of limitations in previously used imaging techniques to visualize it. In this study we serially imaged fluorescent dye trapped in the t-system of fibres from rat and toad muscle using the confocal microscope, and deconvolved and reconstructed these images to produce the first three-dimensional reconstructions of large volumes of the vertebrate tsystem. These images showed complex arrangements of tubules that have not been described previously and also allowed the association of the t-system with cellular organelles to be visualized. There was a high density of tubules close to the nuclear envelope because of the close and parallel alignment of the long axes of the myofibrils and the nuclei. Furthermore local fluorescence intensity variations from sub-resolution tubules were converted to tubule diameters. Mean diameters of tubules were 85.966.6 and 91.268.2 nm, from rat and toad muscle under isotonic conditions, respectively. Under osmotic stress the distribution of tubular diameters shifted significantly in toad muscle only, with change specifically occurring in the transverse but not longitudinal tubules.

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Section: What Does a Tubule Look Like?mentioning

confidence: 98%

Three-dimensional reconstruction and analysis of the tubular system of vertebrate skeletal muscle

Jayasinghe

Launikonis

2013

Journal of Cell Science

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“…c, the specific capacitance of muscle cells, is around 4 mF kg-' wet weight muscle and varies little with cell size (Westgaard, 1975;Dulhunty, Carter & Hinrichsen, 1984).…”

Section: Methodsmentioning

confidence: 99%

Plasma potassium changes with high intensity exercise.

Medbø

Sejersted

1990

The Journal of Physiology

235

152

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SUMMARY1. Exercise seems to change the extracellular potassium concentration far beyond the narrow limits seen in resting subjects. To examine alterations in plasma potassium concentration during exercise, twenty healthy, well-trained men ran on the treadmill at 6 deg inclination with catheters inserted in the femoral vein and artery.2. During 1 min exhausting exercise plasma potassium concentration rose in parallel in the vein and artery, reaching peak post-exercise values of 8-34 + 023 mmol 1-and 817 +0-29 mmol 1-1. After 3 min recovery the potassium concentration was 0'50 + 0 05 mmol 1-1 below pre-exercise values. Both the rise of plasma potassium concentration during exercise and the decline during recovery followed exponential time courses with a half-time of 25 s.3. Exercise at reduced intensity showed that the peak post-exercise potassium concentration was linearly related to the exercise intensity. Individual resting, peak and nadir values were proportionally related.4. The increased potassium concentration during exercise can be explained in full by the electrical activity in the exercising muscles. Repeated 1 min exhausting exercise bouts revealed no relationship between potassium concentration and plasma pH nor glycogen break-down.5. All of the observations fit a simple model of potassium efflux from active muscle and elimination from blood with the following characteristics: the efflux increases (decreases) stepwise at the onset (end) of exercise, and the efflux rate during exercise increases with exercise intensity. Potassium is eliminated from blood by a proportional regulator which may be the Na+-K+ pump of the exercising muscle. Extracellular potassium is indirectly linked to the pump stimulus, and the rate of reuptake is proportional to the extracellular accumulation. Thus no limited maximal power for potassium uptake was found. The post-exercise undershoot of 0'5 mmol 1-1 can be explained by a higher gain of the pump after exercise.6. The large, rapid changes in the plasma potassium concentration during and after exercise is due to the first order kinetics of the reuptake mechanism rather than to a limited power to take up potassium.* To whom correspondence and reprint requests should be sent, to PO Box 8149 Dep., at the address above. MS 7602 J. I. MEDB0 AND 0. M. SEJERSTED

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“…However, local subsarcolemmal injections of free calcium induce highly circumscribed contractures, 14,25 which accords with the circumstance that skeletal muscle fibers are not possessed of a calcium-induced calcium release. 26 Our observation that the contractures are spatially confined (transversely and longitudinally) to the myofibrils that underlie MEPs suggests that the carbachol-induced MEP potential passed neither along the outer surface of the MEP to the muscle fiber nor into the T-tubules of the muscle fiber, because, otherwise, the contractures would have been more widespread and the stretching of neighboring sarcomeres would not have occurred, respectively. However, with an assumed space-constant of 20-40 lm for T-tubules, 26 even a low MEP potential could be propagated along those Ttubules of the MEP that open into the subsynaptic folds 27,28 and thereby into the deep regions of the myofibrils.…”

Section: Discussionmentioning

confidence: 78%

“…26 Our observation that the contractures are spatially confined (transversely and longitudinally) to the myofibrils that underlie MEPs suggests that the carbachol-induced MEP potential passed neither along the outer surface of the MEP to the muscle fiber nor into the T-tubules of the muscle fiber, because, otherwise, the contractures would have been more widespread and the stretching of neighboring sarcomeres would not have occurred, respectively. However, with an assumed space-constant of 20-40 lm for T-tubules, 26 even a low MEP potential could be propagated along those Ttubules of the MEP that open into the subsynaptic folds 27,28 and thereby into the deep regions of the myofibrils. Here the depolarization could induce an inward calcium current across the membrane of the T-system 29,30 and calcium release through the sarcoplasmic reticulum by dihydropyridine receptor charge movements, which depend on the luminal calcium concentration.…”

Section: Discussionmentioning

confidence: 78%

Early effects of carbachol on the morphology of motor endplates of mammalian skeletal muscle fibers

Voigt

2009

Muscle and Nerve

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Long-term disturbance of the calcium homeostasis of motor endplates (MEPs) causes necrosis of muscle fibers. The onset of morphological changes in response to this disturbance, particularly in relation to the fiber type, is presently unknown. Omohyoid muscles of mice were incubated for 1-30 minutes in 0.1 mM carbachol, an acetylcholine agonist that causes an inward calcium current. In these muscles, the structural changes of the sarcomeres and the MEP sarcoplasm were evaluated at the light-and electron-microscopic level. Predominantly in type I fibers, carbachol incubation resulted in strong contractures of the sarcomeres underlying the MEPs. Owing to these contractures, the usual beret-like form of the MEP-associated sarcoplasm was deformed into a mushroom-like body. Consequently, the squeezed MEPs partially overlapped the adjacent muscle fiber segments. There are no signs of contractures below the MEPs if muscles were incubated in carbachol in calcium-free Tyrode's solution. Carbachol induced inward calcium current and produced fiber-type-specific contractures. This finding points to differences in the handling of calcium in MEPs. Possible mechanisms for these fiber-type-specific differences caused by carbachol-induced calcium entry are assessed.Carbachol is an acetylcholine agonist. When applied chronically, it causes a profound destruction of the myofibrils underlying the motor endplate (MEP). This effect is attributable to dissolution of the Z-line.1,2 The pathological changes are reputed to be calcium-dependent 1,2 and are comparable with those manifested in patients with slow-channel syndrome.3 Similar calcium-dependent destruction of the myofibrils beneath the MEP can be elicited by daily application of an acetylcholinesterase inhibitor. 4,5 The effect is brought on by prolonged opening of the acetylcholine receptors (AChRs) and ensuing entry of calcium in the area of the MEP. A genetic manipulation of the AChRs that prolongs the opening time of the receptor channels causes a slow-channel-syndrome-like pathology in mice.6 However, not all skeletal muscle fibers are affected.6 This selectivity accords with observations relating to the effects of carbachol. 1,2According to earlier data, carbachol affects preferentially type I fibers. This, combined with the observation that type I fibers are predominantly damaged by ACh esterase inhibitors, 4 suggests a greater vulnerability to calcium homeostasis in these fibers.Little is known of the early morphological changes associated with short-term carbachol stimulation. To improve our understanding of the disturbances in MEP calcium homeostasis that are elicited by the entry of calcium through activated AChRs, it would be beneficial to temporally and topographically pinpoint the first visible signs of damage and to ascertain whether the changes are fiber-specific. To address these questions, the omohyoid muscle of mice was stimulated with carbachol under isometric conditions for 1-30 minutes. The treated muscles were evaluated at the light-and transmissi...

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The membrane capacity of mammalian skeletal muscle fibres

Cited by 39 publications

References 32 publications

Three-dimensional reconstruction and analysis of the tubular system of vertebrate skeletal muscle

Three-dimensional reconstruction and analysis of the tubular system of vertebrate skeletal muscle

Plasma potassium changes with high intensity exercise.

Early effects of carbachol on the morphology of motor endplates of mammalian skeletal muscle fibers

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