Sarcomere Length-tension Relation Research Articles

Maximal twitch tension in intact length-clamped ferret papillary muscles evoked by modified postextrasystolic potentiation.

A modified test of postextrasystolic potentiation achieved with a brief episode of rapid pacing followed by a 6-second pause (RPP maneuver) was used to evoke maximal force in isolated intact ferret right ventricular papillary muscles. Maximal RPP tensions were examined under length-clamped conditions and compared with the steady-state forces obtained when further increases in [Ca2+]o, did not further increase force and to the tensions recorded at the point of saturation of force when similarly length-clamped muscles were subjected to caffeine-induced tetanization. The results show that the calculated maximal twitch tension achieved with RPP is comparable to the 25-35 g/mm2 observed in intact single skeletal muscle fibers. The study also shows that the beat-to-beat decay of the potentiated contraction is exponential. While the amount of the constant fractional beat-to-beat decay is a function of [Ca2+]o, it is not influenced by length. During the decay of potentiation, the ratio of the potentiation of any beat divided by that of the previous beat is a constant, called (X). With certain assumptions, it is shown that (X) is a measure of the fraction of activator calcium taken up by the sarcoplasmic reticulum in each beat and, in the steady state, the fraction of activator calcium that comes from the sarcoplasmic reticulum. The (X) amounted to 33%, 50%, and 65% when [Ca2+]o was 1.25, 2.50, and 5.0 mM, respectively. Thus, at 1.25 mM [Ca2+]o, some two thirds of the total calcium required to activate the myofilaments comes from the extracellular compartment during excitation and only one third is contributed via release from the sarcoplasmic reticulum. In the region of optimal myofilament overlap, RPP force-length curves are remarkably shallow and almost indistinguishable from the sarcomere length-tension relation observed in skinned single cardiac cells. Tetanus plateau tensions are significantly smaller than RPP forces at any length, and the slope of the tetanus force-length curves is greater than that obtained with RPP. Thus, and by exclusion, we also suggest that caffeine may exert significant downstream inhibitory effects.

Absence of plateau of the sarcomere length-tension relation in frog muscle fibres.

Absence of plateau of the sarcomere length-tension relation in frog muscle fibres.

Effects of calcium on the sarcomere length-tension relation in rat cardiac muscle. Implications for the Frank-Starling mechanism.

HomeCirculation ResearchVol. 47, No. 4Effects of calcium on the sarcomere length-tension relation in rat cardiac muscle. Implications for the Frank-Starling mechanism. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessAbstractPDF/EPUBEffects of calcium on the sarcomere length-tension relation in rat cardiac muscle. Implications for the Frank-Starling mechanism. A M Gordon and G H Pollack A M GordonA M Gordon Search for more papers by this author and G H PollackG H Pollack Search for more papers by this author Originally published1 Oct 1980https://doi.org/10.1161/01.RES.47.4.610Circulation Research. 1980;47:610–619 Previous Back to top Next FiguresReferencesRelatedDetailsCited ByHancock W, Martyn D and Huntsman L (1993) Ca2+ and segment length dependence of isometric force kinetics in intact ferret cardiac muscle., Circulation Research, 73:4, (603-611), Online publication date: 1-Oct-1993.Walley K, Ford L and Wood L (1991) Effects of hypoxia and hypercapnia on the force-velocity relation of rabbit myocardium., Circulation Research, 69:6, (1616-1625), Online publication date: 1-Dec-1991.Schouten V, Bucx J, de Tombe P and ter Keurs H (1990) Sarcolemma, sarcoplasmic reticulum, and sarcomeres as limiting factors in force production in rat heart., Circulation Research, 67:4, (913-922), Online publication date: 1-Oct-1990.Gupta K, Bavaria J, Ratcliffe M, Edmunds L and Bogen D (1989) Measurement of end-systolic pressure-volume relations by intra-aortic balloon occlusion., Circulation, 80:4, (1016-1028), Online publication date: 1-Oct-1989.Urthaler F, Walker A, Reeves D and Hefner L (1988) Maximal twitch tension in intact length-clamped ferret papillary muscles evoked by modified postextrasystolic potentiation., Circulation Research, 62:1, (65-74), Online publication date: 1-Jan-1988.Lew W (1988) Time-dependent increase in left ventricular contractility following acute volume loading in the dog., Circulation Research, 63:3, (635-647), Online publication date: 1-Sep-1988.de Beer E, Schiereck P and van Kaam F (1986) Real-time kinetics of sarcomere relaxation by laser diffraction., Circulation Research, 58:6, (896-897), Online publication date: 1-Jun-1986.Pollack G (1986) Quantal mechanisms in cardiac contraction., Circulation Research, 59:1, (1-8), Online publication date: 1-Jul-1986.Lecarpentier Y, Martin J, Claes V, Chambaret J, Migus A, Antonetti A and Hatt P (1985) Real-time kinetics of sarcomere relaxation by laser diffraction., Circulation Research, 56:3, (331-339), Online publication date: 1-Mar-1985.Tucci P, Bregagnollo E, Spadaro J, Cicogna A and Ribeiro M (1984) Length dependence of activation studied in the isovolumic blood-perfused dog heart., Circulation Research, 55:1, (59-66), Online publication date: 1-Jul-1984. October 1, 1980Vol 47, Issue 4Article InformationMetrics Download: 250 Copyright © 1980 by American Heart Associationhttps://doi.org/10.1161/01.RES.47.4.610 Originally publishedOctober 1, 1980 PDF download

Sarcomere length‐tension relations of frog skinned muscle fibres at lengths above the optimum.

1. Single twitch fibres were dissected from anterior tibial muscles of the frog, Rana pipiens, and were then either chemically or mechanically skinned. Short segments of the skinned fibres were transferred to an experimental chamber and mounted between a force transducer and a stationary wire. 2. The average sarcomere length was determined from light photomicrographs of the segments obtained during activation and while relaxed. Activations were maximal, in solutions of pCa 5.49 and at 5 degrees C. Fibre segments having regions in which the striation pattern was highly non-uniform were rejected. 3. The relationship between tension and average sarcomere length was determined for sarcomere lengths between 2.1 and 3.8 micrometer. Tension always decreased when sarcomere length was increased above about 2.2 micrometer. Tension plotted against over-all average sarcomere length lay above data obtained from living fibres by Gordon, Huxley & Julian (1966a, b). 4. Good agreement with living fibre results was found when tension was plotted against the shortest average sarcomere length within a portion of the segment. 5. These findings indicate that sarcomere length non-uniformities greatly influence the shape of the sarcomere length-tension relation in skinned fibres at long lengths. In addition, no evidence was found for a length-dependent influence of calcium on tension development at long lengths during maximal activation.

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

The slope of the sarcomere length-tension relation in cardiac papillary muscle suggests length-dependent activation of the contractile system (1). However, there are no data on the effect of inotropic interventions on this curve. Only muscle length-tension curves are available, which give conflicting results (1,2,3). The purpose of the present study was to examine the effect of varied calcium concentrations on the sarcomere length-tension relationship, using laser diffraction techniques.

Sarcomere length‐tension relations of frog skinned muscle fibres during calcium activation at short lengths.

1. Single twitch fibres were isolated from anterior tibial muscles of the frog, Rana pipiens. The relationship between sarcomere length and steady tetanic tension at 5 degrees C was obtained from these living fibres in the range of sarcomere lengths between about 2.2 and 1.3 microns . These fibres were then either mechanically or chemically skinned. 2. Segments were cut from the skinned fibres and mounted in an experimental chamber using a technique designed to minimize segment compliance at the points of attachment. A piece approximately 1 mm in length remained exposed to the bathing solution. 3. The segments were photographed through a light microscope at magnifications of about 460 or 110 X during activation and relaxation, so that the sarcomere lengths could be determined from a part or the whole of the segment. Activations were done with solutions of pCa either 5.49 or 6.09 and at a temperature of 5 degrees C. Fibre segments which developed striation pattern irregularities during contraction were rejected. 4. The sarcomere length-tension relation obtained from these segments in the sarcomere length range 1.3-2.2 microns was similar to that obtained from the same fibres while still living. The results were similar at the two values of pCa used. 5. These results do not support the view that sarcomere length dependent variation in the amount of calcium which is released during tetanic stimulation is a major determinant of the form of the length-tension relation in living muscle fibres at sarcomere lengths less than about 2.0 microns.

Myofilament-generated tension oscillations during partial calcium activation and activation dependence of the sarcomere length-tension relation of skinned cardiac cells.

During partial Ca2+ activation, skinned cardiac cells with sarcoplasmic reticulum destroyed by detergent developed spontaneous tension oscillations consisting of cycles (0.1-1 Hz) of rapid decrease of tension corresponding to the yield of some sarcomeres and slow redevelopment of tension corresponding to the reshortening of these sarcomeres. Such myofilament-generated tension oscillations were never observed during the full activation induced by a saturating [free Ca2+] or during the rigor tension induced by decreasing [MgATP] in the absence of free Ca2+ or when the mean sarcomere length (SL) of the preparation was greater than 3.10 microm during partial Ca2+ activation. A stiff parallel elastic element borne by a structure that could be digested by elastase hindered the study of the SL--active tension diagram in 8-13-microm-wide skinned cells from the rat ventricle, but this study was possible in 2-7-microm-wide myofibril bundles from the frog or dog ventricle. During rigor the tension decreased linearly when SL was increased from 2.35 to 3.80 microm. During full Ca2+ activation the tension decreased by less than 20% when SL was increased from 2.35 to approximately 3.10 microm. During partial Ca2+ activation the tension increased when SL was increased from 2.35 to 3.00 microm. From this observation of an apparent increase in the sensitivity of the myofilaments to Ca2+ induced by increasing SL during partial Ca2+ activation, a model was proposed that describes the tension oscillations and permits the derivation of the maximal velocity of shortening (Vmax). Vmax was increased by increasing [free Ca2+] or decreasing [free Mg2+] but not by increasing SL.

The sarcomere length-tension relation in skeletal muscle.

Tension development during isometric tetani in single fibers of frog semitendinosus muscle occurs in three phases: (a) in initial fast-rise phase; (b) a slow-rise phase; and (c) a plateau, which lasts greater than 10 s. The slow-rise phase has previously been assumed to rise out of a progressive increase of sarcomere length dispersion along the fiber (Gordon et al. 1966. J. Physiol. [Lond.]. 184:143--169;184:170--192). Consequently, the "true" tetanic tension has been considered to be the one existing before the onset of the slow-rise phase; this is obtained by extrapolating the slowly rising tension back to the start of the tetanus. In the study by Gordon et al. (1966. J. Physiol. [Lond.] 184:170--192), as well as in the present study, the relation between this extrapolated tension and sarcomere length gave the familiar linear descending limb of the length-tension relation. We tested the assumption that the slow rise of tension was due to a progressive increase in sarcomere length dispersion. During the fast rise, the slow rise, and the plateau of tension, the sarcomere length dispersion at any area along the muscle was less than 4% of the average sarcomere length. Therefore, a progressive increase of sarcomere length dispersion during contraction appears unable to account for the slow rise of tetanic tension. A sarcomere length-tension relation was constructed from the levels of tension and sarcomere length measured during the plateau. Tension was independent of sarcomere length between 1.9 and 2.6 microgram, and declined to 50% maximal at 3.4 microgram. This result is difficult to reconcile with the cross-bridge model of force generation.

Sarcomere length non-uniformity in relation to tetanic responses of stretched skeletal muscle fibres.

At sarcomere lengths above the plateau region of the length-tension diagram, it has been found that isometric tetanic tension is proportional to the amount of thick and thin filament overlap. This finding has been questioned recently and is reinvestigated here. Central segments of single frog skeletal muscle fibres were held at constant length during contractions at various sarcomere lengths above those associated with the plateau region. Tension records showed little or no creep, and the tetanic tensions measured at 0 and 20°C were inversely proportional to sarcomere length. These results extend and substantiate earlier findings. In contrast, when a stretched fibre had only its ends fixed during a tetanus, a different tension response was observed. The tension rise was initially very rapid but soon slowed to a gradual upward creep as stimulation was continued. This was followed by a tension decline. These tension phases were correlated with large decreases in sarcomere length at the fibre ends, while sarcomeres in the middle were extended a small amount. This tetanic tension response can be explained using the sarcomere length-tension relation and the force-velocity properties of muscle. These results strongly support the sliding filament, cross-bridge theory of muscle contraction.

A reexamination of the influence of muscle length on myocardial performance.

HomeCirculation ResearchVol. 40, No. 3A reexamination of the influence of muscle length on myocardial performance. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessAbstractPDF/EPUBA reexamination of the influence of muscle length on myocardial performance. B R Jewell B R JewellB R Jewell Search for more papers by this author Originally published1 Mar 1977https://doi.org/10.1161/01.RES.40.3.221Circulation Research. 1977;40:221–230 Previous Back to top Next FiguresReferencesRelatedDetailsCited ByCooper M (1993) Postextrasystolic potentiation. Do we really know what it means and how to use it?, Circulation, 88:6, (2962-2971), Online publication date: 1-Dec-1993.de Tombe P and ter Keurs H (1991) Sarcomere dynamics in cat cardiac trabeculae., Circulation Research, 68:2, (588-596), Online publication date: 1-Feb-1991.Yasumura Y, Nozawa T, Futaki S, Tanaka N and Suga H (1989) Time-invariant oxygen cost of mechanical energy in dog left ventricle: consistency and inconsistency of time-varying elastance model with myocardial energetics., Circulation Research, 64:4, (764-778), Online publication date: 1-Apr-1989.Gupta K, Bavaria J, Ratcliffe M, Edmunds L and Bogen D (1989) Measurement of end-systolic pressure-volume relations by intra-aortic balloon occlusion., Circulation, 80:4, (1016-1028), Online publication date: 1-Oct-1989.Baan J and Van der Velde E (1988) Sensitivity of left ventricular end-systolic pressure-volume relation to type of loading intervention in dogs., Circulation Research, 62:6, (1247-1258), Online publication date: 1-Jun-1988.Zile M, Gaasch W, Wiegner A, Robinson K and Bing O (1987) Mechanical determinants of maximum isotonic lengthening rate in rat left ventricular myocardium., Circulation Research, 60:6, (815-823), Online publication date: 1-Jun-1987.Wisenbaugh T, Nissen S and DeMaria A (1986) Mechanics of postextrasystolic potentiation in normal subjects and patients with valvular heart disease., Circulation, 74:1, (10-20), Online publication date: 1-Jul-1986.Tucci P, Bregagnollo E, Spadaro J, Cicogna A and Ribeiro M (1984) Length dependence of activation studied in the isovolumic blood-perfused dog heart., Circulation Research, 55:1, (59-66), Online publication date: 1-Jul-1984.Miller W, Liedtke A and Nellis S (1984) Regional end-systolic pressure-length relationships using a volume-loading technique in the intact pig heart., Circulation Research, 55:3, (326-335), Online publication date: 1-Sep-1984.Hunter W, Janicki J, Weber K and Noordergraaf A (1983) Systolic mechanical properties of the left ventricle. Effects of volume and contractile state., Circulation Research, 52:3, (319-327), Online publication date: 1-Mar-1983.Lab M (1982) Contraction-excitation feedback in myocardium. Physiological basis and clinical relevance., Circulation Research, 50:6, (757-766), Online publication date: 1-Jun-1982.Tarr M, Trank J, Goertz K and Leiffer P (1981) Effect of initial sarcomere length on sarcomere kinetics and force development in single frog atrial cardiac cells., Circulation Research, 49:3, (767-774), Online publication date: 1-Sep-1981.Brutsaert D, Housmans P and Goethals M (1980) Dual control of relaxation. Its role in the ventricular function in the mammalian heart., Circulation Research, 47:5, (637-652), Online publication date: 1-Nov-1980.Levin K and Page E (1980) Quantitative studies on plasmalemmal folds and caveolae of rabbit ventricular myocardial cells., Circulation Research, 46:2, (244-255), Online publication date: 1-Feb-1980.ter Keurs H, Rijnsburger W, van Heuningen R and Nagelsmit M (1980) Tension development and sarcomere length in rat cardiac trabeculae. Evidence of length-dependent activation., Circulation Research, 46:5, (703-714), Online publication date: 1-May-1980.Gordon A and Pollack G (1980) Effects of calcium on the sarcomere length-tension relation in rat cardiac muscle. Implications for the Frank-Starling mechanism., Circulation Research, 47:4, (610-619), Online publication date: 1-Oct-1980.Chuck L and Parmley W (1980) Caffeine reversal of length-dependent changes in myocardial contractile state in the cat., Circulation Research, 47:4, (592-598), Online publication date: 1-Oct-1980.Suga H, Sagawa K and Demer L (1980) Determinants of instantaneous pressure in canine left ventricle. Time and volume specification., Circulation Research, 46:2, (256-263), Online publication date: 1-Feb-1980.Schwartz P and Stone H (1979) Effects of unilateral stellectomy upon cardiac performance during exercise in dogs., Circulation Research, 44:5, (637-645), Online publication date: 1-May-1979.Spotnitz W, Spotnitz H, Truccone N, Cottrell T, Gersony W, Malm J and Sonnenblick E (1979) Relation of ultrastructure and function. Sarcomere dimensions, pressure-volume curves, and geometry of the intact left ventricle of the immature canine heart., Circulation Research, 44:5, (679-691), Online publication date: 1-May-1979.Julian F, Moss R and Sollins M (1978) The mechanism for vertebrate striated muscle contraction., Circulation Research, 42:1, (2-14), Online publication date: 1-Jan-1978. March 1, 1977Vol 40, Issue 3Article InformationMetrics Download: 160 Copyright © 1977 by American Heart Associationhttps://doi.org/10.1161/01.RES.40.3.221 Originally publishedMarch 1, 1977 PDF download Advertisement

Resting sarcomere length-tension relation in living frog heart.

The sarcomere pattern and tension of isolated resting frog atrial trabeculae were continuously monitored. In the absence of any resting tension the sarcomere lengths varied with the diameter of the trabeculae. In over 75 % of the trabeculae the value exceeded 2.05 microm, the estimated in vivo length of the thin filaments, and it was never less than 1.89 microm. When the trabeculae were stretched the increase in length of the central undamaged portion could be completely accounted for by an increase in sarcomere length. The width of the A band was constant only at sarcomere lengths between 2.3 and 2.6 microm it decreased at smaller and increased at larger sarcomere lengths. A group of spontaneously active cells stretched the sarcomeres in cells in series to longer lengths than could be produced by passive tension applied to the ends of the trabeculae, but they did not influence the sarcomeres of adjacent cells. It is proposed that the connective tissue is a major factor in determining sarcomere length and that there are interactions between thick and thin filaments in resting muscles.