Muscle Activation: Effects of Small Length Changes on Calcium Release in Single Fibers

Ridgeway, EB; Gordon, A. M.

doi:10.1126/science.1154025

Cited by 35 publications

(17 citation statements)

References 17 publications

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“…Activation of the contractile system thus seems to be the most likely explanation for the slow increase of DP. Lakatta and Jewell (1977) considered that the time-dependent increase in contraction reflects an accentuation of transsarcolemmal calcium influx secondary to reported (Dulhunty and Franzini-Armstrong, 1975;Ridgway and Gordon, 1975) changes in the cell membrane. Chuck and Parmley (1980), however, argue against the participation of extracellular calcium in the slow change of tension.…”

Section: Discussionmentioning

confidence: 99%

Length dependence of activation studied in the isovolumic blood-perfused dog heart.

Tucci¹,

Bregagnollo²,

Spadaro³

et al. 1984

Circulation Research

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SUMMARY. In studies utilizing the isolated isovolumic blood-perfused canine heart, left ventricular pressure was measured following a sudden expansion of ventricular volume. An increase in performance occurred in two phases: first, there was an instantaneous rise of developed pressure simultaneous with ventricular distension; in the second phase, developed pressure continued to increase for several minutes until a final steady state was reached. The immediate increase in developed pressure occurred with a prolongation of the time-to-peak pressure, and there was no further change of time-to-peak pressure during the time-dependent increase of developed pressure. In another series of experiments, systolic pressure was elevated without changing resting volume, and mechanical performance changed in a different manner: after an increase in systolic load, there was a modest and transient decrease of developed pressure; thereafter, ventricular pressure recovered only to original values. The influence of different degrees of ventricular expansion, calcium, and verapamil were studied. Under higher ventricular dilations the immediate as well as the slow increase of contraction were heightened and the time to reach half of the slow increase was shortened. When ventricular dilation was induced during an infusion of calcium chloride, higher values for the immediate pressure increase were observed, whereas the timedependent increase and the time to reach half of the slow increase did not change in comparison with control studies. Verapamil decreased the immediate and the time-dependent enhancement of contraction. The time-dependent increase in developed pressure occurs more slowly with verapamil. These findings in the intact heart are in accord with the hypothesis that myocardial stretch is followed by an increase in intracellular calcium stores, and with the concept that the Frank-Starling mechanism involves an activation of the contractile state. (Circ Res 55: 59-66, 1984)

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Section: Discussionmentioning

confidence: 99%

Length dependence of activation studied in the isovolumic blood-perfused dog heart.

Tucci¹,

Bregagnollo²,

Spadaro³

et al. 1984

Circulation Research

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“…Length dependence of calcium binding (England, 1976), calcium release (Ridgway and Gordon, 1975) or calcium storage, or modification of any of these by phosphorylation of the proteins involved, could underlie length dependence of activation. Evidence of changes of phosphorylation as a result of frequency potentiation or changes of Ca 2+ has not been found however (Ezrailson et al, 1977).…”

Section: Figurementioning

confidence: 99%

Tension development and sarcomere length in rat cardiac trabeculae. Evidence of length-dependent activation.

Keurs¹,

Rijnsburger²,

Heuningen³

et al. 1980

Circulation Research

328

100

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SUMMARY We studied the influence of inotropic factors on the shape of the relation between tension and sarcomere length. Tension measurements were performed on thin trabeculae dissected from the right ventricle of the rat heart. Sarcomere length was measured by laser diffraction techniques and controlled by a servomotor system. The relations between tension and sarcomere length were derived from contractions at various extracellular calcium concentrations [Ca 2+ ] o . The time course of tension development was dependent on both sarcomere length and [Ca 2+ ] o . At all [Ca 2+ ] o , the tension attained during contraction was zero at sarcomere lengths of 1.55-1.60 pm and maximal at a sarcomere length of 2.35 /im. Neither a summit nor a descending limb was found in the sarcomere length-tension relation. At [Ca 2+ ] o = 0.5 mM, tension increased linearly with sarcomere length, whereas at [Ca 2+ ] o = 2.5 mM, it approached maximal tension exponentially with sarcomere length. The relations between tension and sarcomere length derived from isometric contractions of the muscle and of sarcomeres were identical, and this suggests that shortening of sarcomeres does not contribute significantly to the effect of [Ca 2+ ] o . The relations between tension and sarcomere length obtained at [Ca 2+ ] o = 0.5 mM from contractions 30 seconds after a potentiating burst of stimuli (4 seconds at 4 Hz) were identical to the relation between tension and sarcomere length at [Ca 2+ ] o = 2.5 mm. Our results are consistent with the hypothesis that cardiac muscle length affects contractile performance by its influence on excitation contraction coupling. CircRes 46: [703][704][705][706][707][708][709][710][711][712][713][714] 1980 THE shape of the relation between tension and sarcomere length in cardiac papillary muscle suggests length-dependent activation of the contractile system (Jewell, 1977). However, there are no data on the effect of inotropic interventions on this curve. Only muscle length-tension curves are available, and these give conflicting results (Jewell, 1977;Huntsman and Stewart, 1977;Sonnenblick, 1962;Bodem et al., 1976). It is known that during isometric contractions there is considerable shortening of sarcomeres in the central region of papillary muscle. This happens at the expense of stretch of damaged regions near the clamps holding the ends of the specimen (Krueger and Pollack, 1975;Pollack and Krueger, 1976;Julian et al., 1976;Julian and Sollins, 1975). The damaged regions as well as the normal region may be influenced by inotropic factors. The interpretation of results of isometric contractions of the muscle is therefore ambiguous. The purpose of the present study was to examine the effect of different calcium concentrations on the relations Supported by Grants 74022 and 77086 from the Netherlands Heart Foundation.Dr. ter Keurs is an Established Investigator of the Netherlands Heart Foundation.Address for reprints: Henk E.D.J. ter Keurs, Department of Cardiology, Medical Faculty, State Un...

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“…Single fibers were stimulated under voltage-clamp conditions using a double-spiral electrode inserted along the length of the fiber. Voltage-clamp conditions are required to avoid the marked effect of changes in initial muscle length on calcium release from the sarcoplasmic reticulum (SR) (Ridgway and Gordon, 1975;Gordon and Ridgway, 1976). Changes in calcium binding to the activating sites are inferred by observing calcium dissociated from the binding sites in response to a step change in muscle length.…”

Section: Methodsmentioning

confidence: 99%

Extra calcium on shortening in barnacle muscle. Is the decrease in calcium binding related to decreased cross-bridge attachment, force, or length?

Gordon

Ridgway

1987

The Journal of General Physiology

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Barnacle single muscle fibers were microinjected with the calcium-specific photoprotein aequorin. We have previously shown (Ridgway, E.B., and A. M. Gordon, 1984, Journal of General Physiology, 83:75-104) that when barnacle fibers are stimulated under voltage clamp and length control and allowed to shorten during the declining phase of the calcium transient, extra myoplasmic calcium is observed. The time course of the extra calcium for shortening steps at different times during the calcium transient is intermediate between those of free calcium and muscle force. Furthermore, the amplitude increases with an increased stimulus, calcium transient, and force. Therefore, the extra calcium probably comes from the activating sites on the myofilaments, possibly as a result of changes in calcium binding by the activating sites. The change in calcium binding may be due, in turn, to the change in muscle length and/or muscle force and/or cross-bridge attachment per se. In the present article, we show that the amount of the extra calcium depends on the initial muscle length, declining at shorter lengths. This suggests lengthdependent calcium binding. The relation between initial length and extra calcium, however, parallels that between initial length and peak active force. The ratio of extra calcium to active force is therefore virtually independent of initial length. These data do not distinguish between a direct effect of length on calcium binding and an indirect effect owing to changes in cross-bridge attachment and force through some geometrical factor. The amount of extra calcium increases with the size of the shortening step, tending toward saturation for steps of >_10%. This experiment suggests that calcium binding depends on muscle force or cross-bridge attachment, not just length (if at all). There is much less extra calcium seen with shortening steps at high force when the high force results from stretch of the active muscle than when it results from on May 11, 2018 jgp.rupress.org Downloaded from http://doi.org/10.1085/jgp.90.3.321 Published Online: 1 September, 1987 | Supp Info: 322THE JOURNAL OF GENERAL PHYSIOLOGY 9 VOLUME 90 9 1987 increased stimulation of muscle. Thus, the number of attached cross-bridges appears to be more important than force itself. After a conditioning step decrease in length, force redevelops. A second test shortening step during force redevelopment produces less extra calcium than is seen in the absence of the conditioning step. Delaying the test step until more force has redeveloped increases the extra calcium seen with the test step, the increase paralleling the force redevelopment. This implies that calcium binding is increased by crossbridge reattachment. These experiments do not exclude the existence of lengthdependent calcium binding, but strongly suggest that there is increased calcium binding to the activating sites when cross-bridges attach.

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Muscle Activation: Effects of Small Length Changes on Calcium Release in Single Fibers

Cited by 35 publications

References 17 publications

Length dependence of activation studied in the isovolumic blood-perfused dog heart.

Length dependence of activation studied in the isovolumic blood-perfused dog heart.

Tension development and sarcomere length in rat cardiac trabeculae. Evidence of length-dependent activation.

Extra calcium on shortening in barnacle muscle. Is the decrease in calcium binding related to decreased cross-bridge attachment, force, or length?

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