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      Move quickly to detach: Strain rate–dependent myosin detachment and cardiac relaxation

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      The Journal of General Physiology
      Rockefeller University Press

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          Abstract

          Chung considers a new model that describes how a muscle responds to stretch and its implications on myosin detachment and physiology.

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          Most cited references19

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          Mechanisms of enhanced force production in lengthening (eccentric) muscle contractions.

          In contrast to isometric and shortening contractions, many observations made on actively lengthening muscles cannot be readily explained with the sliding filament and cross-bridge theory. Specifically, residual force enhancement, the persistent increase in force following active muscle lengthening, beyond what one would expect based on muscle length, has not been explained satisfactorily. Here, we summarize the experimental evidence on residual force enhancement, critically evaluate proposed mechanisms for the residual force enhancement, and propose a mechanism for residual force enhancement that explains all currently agreed upon experimental observations. The proposed mechanism is based on the engagement of the structural protein titin upon muscle activation and an increase in titin's resistance to active compared with passive stretching. This change in resistance from the passive to the active state is suggested to be based on 1) calcium binding by titin upon activation, 2) binding of titin to actin upon activation, and 3) as a consequence of titin-actin binding--a shift toward stiffer titin segments that are used in active compared with passive muscle elongation. Although there is some experimental evidence for the proposed mechanism, it must be stressed that much of the details proposed here remain unclear and should provide ample research opportunities for scientists in the future. Nevertheless, the proposed mechanism for residual force enhancement explains all basic findings in this area of research.
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            The contractile response during steady lengthening of stimulated frog muscle fibres.

            1. Steady lengthenings at different velocities (0.025-1.2 microns/s per half-sarcomere; temperature 2-5.5 degrees C) were imposed on isolated frog muscle fibres at the isometric tetanus plateau by means of a loudspeaker motor. The lengthening at the sarcomere level was measured by means of a striation follower either in fixed-end or in length-clamp mode. The force response was measured by a capacitance gauge transducer (resonance frequency 50 kHz). Preparations showing gross non-homogeneity during lengthening were excluded. 2. A steady tension was in all cases reached after about 20 nm per half-sarcomere of lengthening. Tension during this steady phase rose with speed of elongation up to 0.25-0.4 micron/s per half-sarcomere, when tension was 1.9-2 times isometric tetanic force (T0). Further increase in speed produced only very little increase in the steady tension. 3. During the transitory phase, before steady tension was reached, the tension rose monotonically if speed of lengthening was less than 0.25-0.3 micron/s per half-sarcomere; at higher speed the tension rose above the steady level, reaching a peak when extension was 10-14 nm per half-sarcomere, and then fell to the steady level. Tension at the peak continued to rise with speed of lengthening above 0.3 micron/s per half-sarcomere. 4. During the tension rise within the transitory phase of force response the segment elongated at a speed 15-20% lower than that imposed on the whole fibre, as a consequence of tendon compliance. 5. During the steady phase, non-homogeneity of lengthening speed began above a speed of lengthening which varied from fibre to fibre. At speeds below this value, segments elongated at the same speed as that imposed on the fibre. 6. Tension responses to large step stretches (up to 12 nm per half-sarcomere), applied at the plateau of isometric tetanus, showed that the instantaneous elasticity of contractile machinery is not responsible for the limit in force attained with high-speed lengthening. 7. Instantaneous stiffness was determined during the steady state of force response by superposing small steps (less than 1.5 nm per half-sarcomere) on steady lengthening at different velocities. Stiffness was 10-20% larger during lengthening than at the plateau of isometric tetanus and remained practically constant, independent of lengthening velocity, in the range of velocities used. 8. The results indicate that steady lengthening of a tetanized fibre induces a cross-bridge cycle characterized by fast detachment of the cross-bridge extended beyond a critical level.(ABSTRACT TRUNCATED AT 400 WORDS)
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              Relaxation kinetics following sudden Ca(2+) reduction in single myofibrils from skeletal muscle.

              To investigate the roles of cross-bridge dissociation and cross-bridge-induced thin filament activation in the time course of muscle relaxation, we initiated force relaxation in single myofibrils from skeletal muscles by rapidly (approximately 10 ms) switching from high to low [Ca(2+)] solutions. Full force decay from maximal activation occurs in two phases: a slow one followed by a rapid one. The latter is initiated by sarcomere "give" and dominated by inter-sarcomere dynamics (see the companion paper, Stehle, R., M. Krueger, and G. Pfitzer. 2002. Biophys. J. 83:2152-2161), while the former occurs under nearly isometric conditions and is sensitive to mechanical perturbations. Decreasing the Ca(2+)-activated force preceding the start of relaxation does not increase the rate of the slow isometric phase, suggesting that cycling force-generating cross-bridges do not significantly sustain activation during relaxation. This conclusion is strengthened by the finding that the rate of isometric relaxation from maximum force to any given Ca(2+)-activated force level is similar to that of Ca(2+)-activation from rest to that given force. It is likely, therefore, that the slow rate of force decay in full relaxation simply reflects the rate at which cross-bridges leave force-generating states. Because increasing [P(i)] accelerates relaxation while increasing [MgADP] slows relaxation, both forward and backward transitions of cross-bridges from force-generating to non-force-generating states contribute to muscle relaxation.
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                Author and article information

                Journal
                J Gen Physiol
                J. Gen. Physiol
                jgp
                The Journal of General Physiology
                Rockefeller University Press
                0022-1295
                1540-7748
                06 April 2020
                20 March 2020
                : 152
                : 4
                : e202012588
                Affiliations
                [1]Department of Physiology, Wayne State University, Detroit, MI
                Author notes
                Correspondence to Charles S Chung: cchung@ 123456med.wayne.edu
                Author information
                https://orcid.org/0000-0001-9180-3236
                Article
                jgp.202012588
                10.1085/jgp.202012588
                7141589
                32197272
                70be4d26-ccb8-4a33-859d-caebd95a0120
                © 2020 Chung

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

                History
                Page count
                Pages: 3
                Funding
                Funded by: American Heart Association, DOI http://dx.doi.org/10.13039/100000968;
                Award ID: 18TPA34170169
                Categories
                Commentary

                Anatomy & Physiology
                Anatomy & Physiology

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