Skeletal Muscle

Sandow, Alexander

doi:10.1146/annurev.ph.32.030170.000511

Cited by 185 publications

(68 citation statements)

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“…This observation has been used to suggest that the SREC cannot arise from a cross-bridge mechanism (Sandow, 1970). Experimental evidence shows that the SREC stiffness and tension actually peak in frog muscle fibres at a sarcomere length of around 3 ìm (Haugen & Sten-Knudsen, 1981) rather than around 2·2 ìm where maximal active tension is generated.…”

Section: Discussionmentioning

confidence: 99%

A cross‐bridge mechanism can explain the thixotropic short‐range elastic component of relaxed frog skeletal muscle

Campbell

Lakie

1998

The Journal of Physiology

122

130

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The precise control of posture and movement imposes severe constraints on the human neuromuscular system. In particular, to maintain stability, the motor control system must continually react to proprioceptive feedback as the body is perturbed by unpredictable external forces. In this type of control mechanism there is an inevitable time delay (due to e.g. nerve conduction and electromechanical coupling) between the sensing of the perturbation and the completion of the corrective movement. The delays in the feedback loop are destabilizing and may result in tremulous movement (McMahon, 1984). A small resistance to movement inherent in the muscle fibres themselves would provide Journal of Physiology (1998) 1. The passive tension and sarcomere length of relaxed frog skeletal muscle fibres were measured in response to imposed length stretches. The tension response to a constantvelocity stretch exhibited a clear discontinuity. Tension rose more rapidly during the initial • 0·4 % LÑ of the stretch than during the latter stages (where LÑ is the resting length of the fibre). This initial tension response is attributed to the short-range elastic component (SREC). 2. The use of paired triangular stretches revealed that the maximum tension produced during the SREC response of the second stretch was significantly reduced by the first stretch. This history-dependent behaviour of the SREC reflects thixotropic stiffness changes that have been previously described in relaxed muscle. 3. The biphasic nature of the SREC tension response to movement was most apparent during the first imposed length change after a period at a fixed length, irrespective of the direction of movement. 4. If a relaxed muscle was subjected to an imposed triangular length change so that the muscle was initially stretched and subsequently shortened back to its original fibre length, the resting tension at the end of the stretch was reduced relative to its initial pre-stretch value. Following the end of the stretch, tension slowly increased towards its initial value but the tension recovery was not accompanied by a contemporaneous increase in sarcomere length. This finding suggests that the resting tension of a relaxed muscle fibre is not entirely due to passive elasticity. The results are compatible with the suggestion that a portion of the resting tension -the filamentary resting tension (FRT) -is produced by a low level of active force generation. 5. If a second identical stretch was imposed on the muscle at a time when the resting tension was reduced by the previous stretch, the maximal tension produced during the second stretch was the same as that produced during the first, despite the second stretch commencing from a lower initial resting tension. 6. In experiments using paired triangular length changes, an inter-stretch interval of zero did not produce a substantially greater thixotropic reduction in the second stretch elastic limit force than an inter-stretch interval in the range 0·5-1 s. 7. A theoretical model was developed in which the SREC and ...

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Section: Discussionmentioning

confidence: 99%

A cross‐bridge mechanism can explain the thixotropic short‐range elastic component of relaxed frog skeletal muscle

Campbell

Lakie

1998

The Journal of Physiology

122

130

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“…If this assumption is valid, then a sustained increase in 45Ca efflux from the muscle reflects an increase in the amount of free intracellular calcium released from the sarcoplasmic reticulum. In the context of present ideas concerning the control of free myoplasmic calcium concentration (compare Sandow, 1970), it is possible that NEM causes release of calcium from the sarcoplasmic reticulum or blocks the active re-uptake of calcium; either effect would lead to a rise of free myoplasmic calcium above the threshold level required for contraction. Hasselbach (1966) found that NEM inhibits uptake of calcium by isolated vesicles of the sarcoplasmic reticulum and -SH groups located on the outer surface of these vesicles were implicated in active calcium transport (Hasselbach, 1966;Hasselbach & Seraydarian, 1966).…”

Section: Discussionmentioning

confidence: 99%

Effects of sulphydryl inhibitors on frog sartorius muscle: N‐ethylmaleimide

Kirsten

Kuperman

1970

British J Pharmacology

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Summary . The characteristic action of the –SH inhibitor, N‐ethylmaleimide (NEM), is muscle rigour. The dose‐response curve indicates a biphasic effect with maximum rigour tension produced by 10 mm NEM; beyond 1.0 mm there was an inverse relationship between dose and response. . NEM produces a membrane depolarization unrelated to rigour development. . NEM causes a sustained increase in 45Ca efflux from whole muscle. Pretreatment of a muscle with ethylenediamine tetra‐acetic acid (EDTA, 5 mm) to remove membrane calcium does not alter the NEM induced 45Ca efflux. . It is suggested that the primary site of NEM action is inhibition of calcium uptake by the sarcoplasmic reticulum thereby producing rigour. At concentrations above 1.0 mm, NEM may affect the myofilaments.

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“…It has been generally assumed that the contraction of striated muscle is caused by a release of calcium from sites on the terminal cisternae of the sarcoplasmic reticulum when local current passes across this membrane area (23)(24)(25)(26). Some drugs such as caffeine (27), urea and oleic acid (28), ADP (29) have been found to cause calcium re lease from sarcoplasmic reticulum.…”

Section: Incubation Experiments Rt'ith Chinoformmentioning

confidence: 99%

Actions of Chinoform and Oxine on the Isolated Phrenic Nerve-Diaphragm Preparation of the Rat: The Accumulation of Chinoform by Rat Diaphragm Strip

et al. 1974

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Abstract-Theactions of chinoform and oxine on isolated phrenic nerve-diaphragm preparation of the rat and the uptake of chinoform by rat diaphragm strip were in vestigated. Chinoform and oxine decreased both twitch responses to indirect and, to a lesser extent, to direct stimuli in the rat phrenic nerve-diaphragm preparation. The depressant action of oxine was reversible whereas that of chinoform was irrever sible and always accompanied by a marked rise in muscle tone. The neuromuscular block caused by these drugs was enhanced rather than antagonized by eserine and KCl. The depressant action and the rise in muscle tone caused by chinoform dis appeared in vitro by lowering muscle temp., by suspending the drug in dog serum and also by conjugating it with glucuronic acid. When rat diaphragm strips were incubated aerobically in Krebs-bicarbonate solution containing chinoform for 1 to 5 hr at 37°C, the drug was accumulated against a concentration gradient until con centration ratio (muscle/medium) of up to 36: 1 had been attained. These findings indicate that rat diaphragm strips accumulate chinoform largely by intracellular bind ing and that the drug can act intracellularly as a metabolic poison.Some years ago the usefulness of the amebicidal property of chinoform (5-chloro 7-iodo-8-hydroxy-quinoline) in the treatment of amebic dysentery was widely established (1, 2). Tsubaki et al. (3) were, however, the first to denominate a group of neuropathic symptoms SMON (Subacute Myelo-Optico-Neuro-pathy) which was once suspected as an endemic in Japan. Pathological, epidemiological and virological investigations have since been done in an attempt to determine the pathogenesis of this disease.Despite multidisciplinary studies, the etiology is still unknown. Takasu et al. (4) and Igata et al. (5) observed that the coated tongues and feces of SMON patients usually assumed a green color. Subsequently, this green substance was isolated from the urine of SMON patients and was identified as chinoform Fe(III) complex by Tamura (6). More over, when the drug was given in large doses to dogs, a close resemblance to the pathog nomonic symptoms seen in SMON patients was observed (7) . Now the relationship between chinoform and SMON is almost certain. On March, 1972, at the investigation conference on SMON sponsored by the Japanese Ministry of Public Welfare it was concluded that the disease was an untoward side-reaction of chino 1 Iodochlorhydroxyquin (USP) ; Clioquinol (BP).

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Skeletal Muscle

Cited by 185 publications

References 0 publications

A cross‐bridge mechanism can explain the thixotropic short‐range elastic component of relaxed frog skeletal muscle

A cross‐bridge mechanism can explain the thixotropic short‐range elastic component of relaxed frog skeletal muscle

Effects of sulphydryl inhibitors on frog sartorius muscle: N‐ethylmaleimide

Actions of Chinoform and Oxine on the Isolated Phrenic Nerve-Diaphragm Preparation of the Rat: The Accumulation of Chinoform by Rat Diaphragm Strip

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