Статті в журналах: "Sarcomere mechanics"

1

Crocini, Claudia, and Michael Gotthardt. "Cardiac sarcomere mechanics in health and disease." Biophysical Reviews 13, no. 5 (October 2021): 637–52. http://dx.doi.org/10.1007/s12551-021-00840-7.

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AbstractThe sarcomere is the fundamental structural and functional unit of striated muscle and is directly responsible for most of its mechanical properties. The sarcomere generates active or contractile forces and determines the passive or elastic properties of striated muscle. In the heart, mutations in sarcomeric proteins are responsible for the majority of genetically inherited cardiomyopathies. Here, we review the major determinants of cardiac sarcomere mechanics including the key structural components that contribute to active and passive tension. We dissect the molecular and structural basis of active force generation, including sarcomere composition, structure, activation, and relaxation. We then explore the giant sarcomere-resident protein titin, the major contributor to cardiac passive tension. We discuss sarcomere dynamics exemplified by the regulation of titin-based stiffness and the titin life cycle. Finally, we provide an overview of therapeutic strategies that target the sarcomere to improve cardiac contraction and filling.

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Rassier, Dilson E. "Sarcomere mechanics in striated muscles: from molecules to sarcomeres to cells." American Journal of Physiology-Cell Physiology 313, no. 2 (August 1, 2017): C134—C145. http://dx.doi.org/10.1152/ajpcell.00050.2017.

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Muscle contraction is commonly associated with the cross-bridge and sliding filament theories, which have received strong support from experiments conducted over the years in different laboratories. However, there are studies that cannot be readily explained by the theories, showing 1) a plateau of the force-length relation extended beyond optimal filament overlap, and forces produced at long sarcomere lengths that are higher than those predicted by the sliding filament theory; 2) passive forces at long sarcomere lengths that can be modulated by activation and Ca2+, which changes the force-length relation; and 3) an unexplained high force produced during and after stretch of activated muscle fibers. Some of these studies even propose “new theories of contraction.” While some of these observations deserve evaluation, many of these studies present data that lack a rigorous control and experiments that cannot be repeated in other laboratories. This article reviews these issues, looking into studies that have used intact and permeabilized fibers, myofibrils, isolated sarcomeres, and half-sarcomeres. A common mechanism associated with sarcomere and half-sarcomere length nonuniformities and a Ca2+-induced increase in the stiffness of titin is proposed to explain observations that derive from these studies.

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3

Lieber, R. L. "659 SARCOMERE MECHANICS." Medicine & Science in Sports & Exercise 26, Supplement (May 1994): S118. http://dx.doi.org/10.1249/00005768-199405001-00661.

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4

Müller, Dominik, Thorben Klamt, Lara Gentemann, Alexander Heisterkamp, and Stefan Michael Klaus Kalies. "Evaluation of laser induced sarcomere micro-damage: Role of damage extent and location in cardiomyocytes." PLOS ONE 16, no. 6 (June 4, 2021): e0252346. http://dx.doi.org/10.1371/journal.pone.0252346.

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Whereas it is evident that a well aligned and regular sarcomeric structure in cardiomyocytes is vital for heart function, considerably less is known about the contribution of individual elements to the mechanics of the entire cell. For instance, it is unclear whether altered Z-disc elements are the reason or the outcome of related cardiomyopathies. Therefore, it is crucial to gain more insight into this cellular organization. This study utilizes femtosecond laser-based nanosurgery to better understand sarcomeres and their repair upon damage. We investigated the influence of the extent and the location of the Z-disc damage. A single, three, five or ten Z-disc ablations were performed in neonatal rat cardiomyocytes. We employed image-based analysis using a self-written software together with different already published algorithms. We observed that cardiomyocyte survival associated with the damage extent, but not with the cell area or the total number of Z-discs per cell. The cell survival is independent of the damage position and can be compensated. However, the sarcomere alignment/orientation is changing over time after ablation. The contraction time is also independent of the extent of damage for the tested parameters. Additionally, we observed shortening rates between 6–7% of the initial sarcomere length in laser treated cardiomyocytes. This rate is an important indicator for force generation in myocytes. In conclusion, femtosecond laser-based nanosurgery together with image-based sarcomere tracking is a powerful tool to better understand the Z-disc complex and its force propagation function and role in cellular mechanisms.

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5

de Tombe, Pieter P., and Henk E. D. J. ter Keurs. "Cardiac muscle mechanics: Sarcomere length matters." Journal of Molecular and Cellular Cardiology 91 (February 2016): 148–50. http://dx.doi.org/10.1016/j.yjmcc.2015.12.006.

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6

Russell, Robert J., Shen-Ling Xia, Richard B. Dickinson, and Tanmay P. Lele. "Sarcomere Mechanics in Capillary Endothelial Cells." Biophysical Journal 97, no. 6 (September 2009): 1578–85. http://dx.doi.org/10.1016/j.bpj.2009.07.017.

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7

Russell, Robert J., Richard B. Dickinson, and Tanmay P. Lele. "Sarcomere Mechanics in the Stress Fiber." Biophysical Journal 96, no. 3 (February 2009): 626a. http://dx.doi.org/10.1016/j.bpj.2008.12.3310.

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8

NAGORNYAK, EKATERINA, and GERALD H. POLLACK. "Connecting filament mechanics in the relaxed sarcomere." Journal of Muscle Research and Cell Motility 26, no. 6-8 (February 2, 2006): 303–6. http://dx.doi.org/10.1007/s10974-005-9036-3.

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9

Kollár, Veronika, Dávid Szatmári, László Grama, and Miklós S. Z. Kellermayer. "Dynamic Strength of Titin's Z-Disk End." Journal of Biomedicine and Biotechnology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/838530.

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Titin is a giant filamentous protein traversing the half sarcomere of striated muscle with putative functions as diverse as providing structural template, generating elastic response, and sensing and relaying mechanical information. The Z-disk region of titin, which corresponds to the N-terminal end of the molecule, has been thought to be a hot spot for mechanosensing while also serving as anchorage for its sarcomeric attachment. Understanding the mechanics of titin's Z-disk region, particularly under the effect of binding proteins, is of great interest. Here we briefly review recent findings on the structure, molecular associations, and mechanics of titin's Z-disk region. In addition, we report experimental results on the dynamic strength of titin's Z1Z2 domains measured by nanomechanical manipulation of the chemical dimer of a recombinant protein fragment.

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10

Ter Keurs, Henk E. D. J., Tsuyoshi Shinozaki, Ying Ming Zhang, Yuji Wakayama, Yoshinao Sugai, Yutaka Kagaya, Masahito Miura, Penelope A. Boyden, Bruno D. M. Stuyvers, and Amir Landesberg. "Sarcomere Mechanics in Uniform and Nonuniform Cardiac Muscle." Annals of the New York Academy of Sciences 1123, no. 1 (March 19, 2008): 79–95. http://dx.doi.org/10.1196/annals.1420.010.

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11

Koch, T. J., and W. Herzog. "Sarcomere number plays an important role in joint mechanics." Journal of Biomechanics 27, no. 6 (January 1994): 643. http://dx.doi.org/10.1016/0021-9290(94)90915-6.

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12

Lyon, Aurore, Lauren J. Dupuis, Theo Arts, Harry J. G. M. Crijns, Frits W. Prinzen, Tammo Delhaas, Jordi Heijman та Joost Lumens. "Differentiating the effects of β-adrenergic stimulation and stretch on calcium and force dynamics using a novel electromechanical cardiomyocyte model". American Journal of Physiology-Heart and Circulatory Physiology 319, № 3 (1 вересня 2020): H519—H530. http://dx.doi.org/10.1152/ajpheart.00275.2020.

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This work identifies the contribution of electrical and mechanical alterations to regulation of calcium and force under exercise-like conditions using a novel human electromechanical model integrating ventricular electrophysiology and sarcomere mechanics. By better understanding their individual and combined effects, this can uncover arrhythmogenic mechanisms in exercise-like situations. This publicly available model is a crucial step toward understanding the complex interplay between cardiac electrophysiology and mechanics to improve arrhythmia risk prediction and treatment.

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13

Guccione, J. M., L. K. Waldman, and A. D. McCulloch. "Mechanics of Active Contraction in Cardiac Muscle: Part II—Cylindrical Models of the Systolic Left Ventricle." Journal of Biomechanical Engineering 115, no. 1 (February 1, 1993): 82–90. http://dx.doi.org/10.1115/1.2895474.

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Models of contracting ventricular myocardium were used to study the effects of different assumptions concerning active tension development on the distributions of stress and strain in the equatorial region of the intact left ventricle during systole. Three models of cardiac muscle contraction were incorporated in a cylindrical model for passive left ventricular mechanics developed previously [Guccione et al. ASME Journal of Biomechanical Engineering, Vol. 113, pp. 42-55 (1991)]. Systolic sarcomere length and fiber stresses predicted by a general “deactivation” model of cardiac contraction [Guccione and McCulloch, ASME Journal of Biomechanical Engineering, Vol. 115, pp. 72-81 (1993)] were compared with those computed using two less complex models of active fiber stress: In a time-varying “elastance” model, isometric tension development was computed from a function of peak intracellular calcium concentration, time after contraction onset and sarcomere length; a “Hill” model was formulated by scaling this isometric tension using the force-velocity relation derived from the deactivation model. For the same calcium ion concentration, the sarcomeres in the deactivation model shortened approximately 0.1 μm less throughout the wall at end-systole than those in the other models. Thus, muscle fibers in the intact ventricle are subjected to rapid length changes that cause deactivation during the ejection phase of a normal cardiac cycle. The deactivation model predicted rather uniform transmural profiles of fiber stress and cross-fiber stress distributions that were almost identical to those of the radial component. These three components were indistinguishable from the principal stresses. Transmural strain distributions predicted at end-systole by the deactivation model agreed closely with experimental measurements from the anterior free wall of the canine left ventricle.

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14

EINARSSON, F., T. HULTGREN, B. O. LJUNG, E. RUNESSON, and J. FRIDÉN. "Subscapularis Muscle Mechanics in Children with Obstetric Brachial Plexus Palsy." Journal of Hand Surgery (European Volume) 33, no. 4 (August 2008): 507–12. http://dx.doi.org/10.1177/1753193408090764.

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This study investigates the passive mechanical properties of the subscapularis muscle in children with a contracture as a result of obstetrical brachial plexus palsy. Muscle biopsies were harvested from nine children undergoing open surgery for shoulder contracture. Passive mechanical testing of single cells and muscle bundles was performed. Corresponding comparisons were made using muscle biopsies from seven healthy controls. Single muscle fibres from patients with obstetric brachial plexus palsy displayed a shorter slack sarcomere length, linear deformation of the fibre within a wider zone of sarcomere length and a greater relative increase in stiffness compared with muscle bundles. We conclude that secondary changes in muscle fibre properties will occur as a result of a longstanding lack of sufficient passive stretch, leading to compensatory changes in the extracellular matrix. These results suggest the presence of a dynamic feedback system constituting a muscle-to-extracellular matrix communication interface.

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15

Ottenheijm, C. "Sarcomere structure and mechanics in nemaline myopathy: A developing story." Neuromuscular Disorders 26 (October 2016): S88. http://dx.doi.org/10.1016/j.nmd.2016.06.013.

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16

Zacharchenko, Thomas, Eleonore von Castelmur, Daniel J. Rigden, and Olga Mayans. "Structural advances on titin: towards an atomic understanding of multi-domain functions in myofilament mechanics and scaffolding." Biochemical Society Transactions 43, no. 5 (October 1, 2015): 850–55. http://dx.doi.org/10.1042/bst20150084.

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Titin is a gigantic filamentous protein of the muscle sarcomere that plays roles in myofibril mechanics and homoeostasis. 3D-structures of multi-domain fragments of titin are now available that start revealing the molecular mechanisms governing its mechanical and scaffolding functions. This knowledge is now being translated into the fabrication of self-assembling biopolymers. Here we review the structural advances on titin, the novel concepts derived from these and the emerging translational avenues.

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17

Piroddi, Nicoletta, E. Rosalie Witjas-Paalberends, Claudia Ferrara, Cecilia Ferrantini, Giulia Vitale, Beatrice Scellini, Paul J. M. Wijnker, et al. "The homozygous K280N troponin T mutation alters cross-bridge kinetics and energetics in human HCM." Journal of General Physiology 151, no. 1 (December 21, 2018): 18–29. http://dx.doi.org/10.1085/jgp.201812160.

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Hypertrophic cardiomyopathy (HCM) is a genetic form of left ventricular hypertrophy, primarily caused by mutations in sarcomere proteins. The cardiac remodeling that occurs as the disease develops can mask the pathogenic impact of the mutation. Here, to discriminate between mutation-induced and disease-related changes in myofilament function, we investigate the pathogenic mechanisms underlying HCM in a patient carrying a homozygous mutation (K280N) in the cardiac troponin T gene (TNNT2), which results in 100% mutant cardiac troponin T. We examine sarcomere mechanics and energetics in K280N-isolated myofibrils and demembranated muscle strips, before and after replacement of the endogenous troponin. We also compare these data to those of control preparations from donor hearts, aortic stenosis patients (LVHao), and HCM patients negative for sarcomeric protein mutations (HCMsmn). The rate constant of tension generation following maximal Ca2+ activation (kACT) and the rate constant of isometric relaxation (slow kREL) are markedly faster in K280N myofibrils than in all control groups. Simultaneous measurements of maximal isometric ATPase activity and Ca2+-activated tension in demembranated muscle strips also demonstrate that the energy cost of tension generation is higher in the K280N than in all controls. Replacement of mutant protein by exchange with wild-type troponin in the K280N preparations reduces kACT, slow kREL, and tension cost close to control values. In donor myofibrils and HCMsmn demembranated strips, replacement of endogenous troponin with troponin containing the K280N mutant increases kACT, slow kREL, and tension cost. The K280N TNNT2 mutation directly alters the apparent cross-bridge kinetics and impairs sarcomere energetics. This result supports the hypothesis that inefficient ATP utilization by myofilaments plays a central role in the pathogenesis of the disease.

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18

Caremani, Marco, and Massimo Reconditi. "Anisotropic Elasticity of the Myosin Motor in Muscle." International Journal of Molecular Sciences 23, no. 5 (February 25, 2022): 2566. http://dx.doi.org/10.3390/ijms23052566.

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To define the mechanics and energetics of the myosin motor action in muscles, it is mandatory to know fundamental parameters such as the stiffness and the force of the single myosin motor, and the fraction of motors attached during contraction. These parameters can be defined in situ using sarcomere−level mechanics in single muscle fibers under the assumption that the stiffness of a myosin dimer with both motors attached (as occurs in rigor, when all motors are attached) is twice that of a single motor (as occurs in the isometric contraction). We use a mechanical/structural model to identify the constraints that underpin the stiffness of the myosin dimer with both motors attached to actin. By comparing the results of the model with the data in the literature, we conclude that the two-fold axial stiffness of the dimers with both motors attached is justified by a stiffness of the myosin motor that is anisotropic and higher along the axis of the myofilaments. A lower azimuthal stiffness of the motor plays an important role in the complex architecture of the sarcomere by allowing the motors to attach to actin filaments at different azimuthal angles relative to the thick filament.

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19

Hassoun, Roua, Heidi Budde, Andreas Mügge, and Nazha Hamdani. "Cardiomyocyte Dysfunction in Inherited Cardiomyopathies." International Journal of Molecular Sciences 22, no. 20 (October 15, 2021): 11154. http://dx.doi.org/10.3390/ijms222011154.

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Inherited cardiomyopathies form a heterogenous group of disorders that affect the structure and function of the heart. Defects in the genes encoding sarcomeric proteins are associated with various perturbations that induce contractile dysfunction and promote disease development. In this review we aimed to outline the functional consequences of the major inherited cardiomyopathies in terms of myocardial contraction and kinetics, and to highlight the structural and functional alterations in some sarcomeric variants that have been demonstrated to be involved in the pathogenesis of the inherited cardiomyopathies. A particular focus was made on mutation-induced alterations in cardiomyocyte mechanics. Since no disease-specific treatments for familial cardiomyopathies exist, several novel agents have been developed to modulate sarcomere contractility. Understanding the molecular basis of the disease opens new avenues for the development of new therapies. Furthermore, the earlier the awareness of the genetic defect, the better the clinical prognostication would be for patients and the better the prevention of development of the disease.

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20

Caremani, Marco, Francesca Pinzauti, Massimo Reconditi, Gabriella Piazzesi, Ger J. M. Stienen, Vincenzo Lombardi, and Marco Linari. "Size and speed of the working stroke of cardiac myosin in situ." Proceedings of the National Academy of Sciences 113, no. 13 (March 16, 2016): 3675–80. http://dx.doi.org/10.1073/pnas.1525057113.

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The power in the myocardium sarcomere is generated by two bipolar arrays of the motor protein cardiac myosin II extending from the thick filament and pulling the thin, actin-containing filaments from the opposite sides of the sarcomere. Despite the interest in the definition of myosin-based cardiomyopathies, no study has yet been able to determine the mechanokinetic properties of this motor protein in situ. Sarcomere-level mechanics recorded by a striation follower is used in electrically stimulated intact ventricular trabeculae from the rat heart to determine the isotonic velocity transient following a stepwise reduction in force from the isometric peak force TP to a value T (0.8–0.2 TP). The size and the speed of the early rapid shortening (the isotonic working stroke) increase by reducing T from ∼3 nm per half-sarcomere (hs) and 1,000 s−1 at high load to ∼8 nm⋅hs−1 and 6,000 s−1 at low load. Increases in sarcomere length (1.9–2.2 μm) and external [Ca2+]o (1–2.5 mM), which produce an increase of TP, do not affect the dependence on T, normalized for TP, of the size and speed of the working stroke. Thus, length- and Ca2+-dependent increase of TP and power in the heart can solely be explained by modulation of the number of myosin motors, an emergent property of their array arrangement. The motor working stroke is similar to that of skeletal muscle myosin, whereas its speed is about three times slower. A new powerful tool for investigations and therapies of myosin-based cardiomyopathies is now within our reach.

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21

Longobardi, Stefano, Anna Sher, and Steven A. Niederer. "In silico identification of potential calcium dynamics and sarcomere targets for recovering left ventricular function in rat heart failure with preserved ejection fraction." PLOS Computational Biology 17, no. 12 (December 6, 2021): e1009646. http://dx.doi.org/10.1371/journal.pcbi.1009646.

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Heart failure with preserved ejection fraction (HFpEF) is a complex disease associated with multiple co-morbidities, where impaired cardiac mechanics are often the end effect. At the cellular level, cardiac mechanics can be pharmacologically manipulated by altering calcium signalling and the sarcomere. However, the link between cellular level modulations and whole organ pump function is incompletely understood. Our goal is to develop and use a multi-scale computational cardiac mechanics model of the obese ZSF1 HFpEF rat to identify important biomechanical mechanisms that underpin impaired cardiac function and to predict how whole-heart mechanical function can be recovered through altering cellular calcium dynamics and/or cellular contraction. The rat heart was modelled using a 3D biventricular biomechanics model. Biomechanics were described by 16 parameters, corresponding to intracellular calcium transient, sarcomere dynamics, cardiac tissue and hemodynamics properties. The model simulated left ventricular (LV) pressure-volume loops that were described by 14 scalar features. We trained a Gaussian process emulator to map the 16 input parameters to each of the 14 outputs. A global sensitivity analysis was performed, and identified calcium dynamics and thin and thick filament kinetics as key determinants of the organ scale pump function. We employed Bayesian history matching to build a model of the ZSF1 rat heart. Next, we recovered the LV function, described by ejection fraction, peak pressure, maximum rate of pressure rise and isovolumetric relaxation time constant. We found that by manipulating calcium, thin and thick filament properties we can recover 34%, 28% and 24% of the LV function in the ZSF1 rat heart, respectively, and 39% if we manipulate all of them together. We demonstrated how a combination of biophysically based models and their derived emulators can be used to identify potential pharmacological targets. We predicted that cardiac function can be best recovered in ZSF1 rats by desensitising the myofilament and reducing the affinity to intracellular calcium concentration and overall prolonging the sarcomere staying in the active force generating state.

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22

MacKenna, D. A., J. H. Omens, A. D. McCulloch, and J. W. Covell. "Contribution of collagen matrix to passive left ventricular mechanics in isolated rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 3 (March 1, 1994): H1007—H1018. http://dx.doi.org/10.1152/ajpheart.1994.266.3.h1007.

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Although it makes up only 2-6% of left ventricular dry weight, collagen is thought to be the major structural protein determining passive ventricular stiffness. However, the relationship between structure of the extracellular matrix and passive mechanics is not understood. Hence, to deplete the collagen matrix, 16 rat hearts were perfused with bacterial collagenase for 60 min. Quantitative morphology using picrosirius red revealed a 36% decrease in collagen area fraction predominantly in the medium-sized fibers. Scanning electron microscopy revealed damage to the endomysial struts. Passive pressure-volume curves showed increases in left ventricular volume at all pressures (from 0.203 +/- 0.061 to 0.265 +/- 0.061 ml at 5 mmHg, P < 0.0001). Strain during loading, calculated from lengths obtained from a triplet of piezoelectric crystals, was unchanged with collagen depletion. However, remodeling strain computed from the collagenase-treated state referred to the Krebs solution-treated state at the same ventricular pressure showed both circumferential (0.145 +/- 0.166 to 0.170 +/- 0.158) and longitudinal (0.070 +/- 0.120 to 0.068 +/- 0.069) stretching. Sarcomere lengths increased at all depths (5.2% at midwall). Thus alterations in the extracellular matrix lead to increased ventricular volume and sarcomere lengths without altering ventricular compliance.

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23

Lu, Li, Ya Xu, Peili Zhu, Clifford Greyson, and Gregory G. Schwartz. "A common mechanism for concurrent changes of diastolic muscle length and systolic function in intact hearts." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 4 (April 1, 2001): H1513—H1518. http://dx.doi.org/10.1152/ajpheart.2001.280.4.h1513.

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Mechanical properties of the myocardium at end diastole have been thought to be dominated by passive material properties rather than by active sarcomere cross-bridge interactions. This study tested the hypothesis that residual cross-bridges significantly contribute to end-diastolic mechanics in vivo and that changes in end-diastolic cross-bridge interaction parallel concurrent changes in systolic cross-bridge interaction. Open-chest anesthetized pigs were treated with intracoronary verapamil ( n = 7) or 2,3-butanedione monoxime (BDM; n = 8). Regional left ventricular external work and end-diastolic pressure (EDP) versus end-diastolic segment length (EDL) relations were determined in the treated and untreated regions of each heart. Both agents reduced external work of treated regions to 31–38% of baseline and concurrently shifted EDP versus EDL relations to the right (i.e., greater EDL at a given EDP) by an average of 5% ( P < 0.05). During washout of the drugs, EDP versus EDL returned to baseline in parallel with recovery of external work. Sarcomere length, measured by transmission electron microscopy in BDM-treated and untreated regions of the same hearts after diastolic arrest and perfusion fixation, was 8% greater in BDM-treated regions ( P < 0.01). We concluded that residual diastolic cross-bridges significantly and reversibly influence end-diastolic mechanics in vivo. Alterations of end-diastolic and systolic cross-bridge interactions occur in parallel.

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Ma, Weikang, Marcus Henze, Robert L. Anderson, Henry Gong, Fiona L. Wong, Carlos L. del Rio, and Thomas Irving. "The Super-Relaxed State and Length Dependent Activation in Porcine Myocardium." Circulation Research 129, no. 6 (September 3, 2021): 617–30. http://dx.doi.org/10.1161/circresaha.120.318647.

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Rationale: Myofilament length-dependent activation (LDA) is the key underlying mechanism of cardiac heterometric autoregulation, commonly referred as the Frank-Starling Law of the heart. Although alterations in LDA are common in cardiomyopathic states, the precise structural and biochemical mechanisms underlying LDA remain unknown. Objective: Here, we examine the role of structural changes in the thick filament during diastole, in particular changes in the availability of myosin heads, in determining both calcium sensitivity and maximum contractile force during systole in permeabilized porcine cardiac fibers. Methods and Results: Permeabilized porcine fibers from ventricular myocardium were studied under relaxing conditions at short and long sarcomere length using muscle mechanics, biochemical measurements, and X-ray diffraction. Upon stretch, the porcine myocardium showed the increased calcium sensitivity and maximum calcium-activated force characteristic of LDA. Stretch increased diastolic ATP turnover, recruiting reserve myosin heads from the super-relaxed state at longer sarcomere length. Structurally, X-ray diffraction studies in the relaxed-muscle confirmed a departure from the helical ordering of the thick filament upon stretch which occurred concomitantly with a displacement of myosin heads towards actin, facilitating cross-bridge formation upon systolic activation. Mavacamten, a selective myosin-motor inhibitor known to weaken the transition to actin-bound power-generating states and to enrich the ordered super-relaxed state myosin population, reversed the structural effects of stretch on the thick filament, blunting the mechanical consequences of stretch; mavacamten did not, however, prevent other structural changes associated with LDA in the sarcomere, such as decreased lattice spacing or troponin-displacement. Conclusions: Our findings strongly indicate that in ventricular muscle, LDA and its systolic consequences are dependent on the population of myosin heads competent to form cross bridges and involves the recruitment of myosin heads from the reserve super-relaxed state pool during diastole.

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25

de Souza Leite, Felipe, Fabio C. Minozzo, David Altman, and Dilson E. Rassier. "Microfluidic perfusion shows intersarcomere dynamics within single skeletal muscle myofibrils." Proceedings of the National Academy of Sciences 114, no. 33 (August 1, 2017): 8794–99. http://dx.doi.org/10.1073/pnas.1700615114.

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The sarcomere is the smallest functional unit of myofibrils in striated muscles. Sarcomeres are connected in series through a network of elastic and structural proteins. During myofibril activation, sarcomeres develop forces that are regulated through complex dynamics among their structures. The mechanisms that regulate intersarcomere dynamics are unclear, which limits our understanding of fundamental muscle features. Such dynamics are associated with the loss in forces caused by mechanical instability encountered in muscle diseases and cardiomyopathy and may underlie potential target treatments for such conditions. In this study, we developed a microfluidic perfusion system to control one sarcomere within a myofibril, while measuring the individual behavior of all sarcomeres. We found that the force from one sarcomere leads to adjustments of adjacent sarcomeres in a mechanism that is dependent on the sarcomere length and the myofibril stiffness. We concluded that the cooperative work of the contractile and the elastic elements within a myofibril rules the intersarcomere dynamics, with important consequences for muscle contraction.

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26

Usyk, T. P., J. H. Omens, and A. D. McCulloch. "Regional septal dysfunction in a three-dimensional computational model of focal myofiber disarray." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 2 (August 1, 2001): H506—H514. http://dx.doi.org/10.1152/ajpheart.2001.281.2.h506.

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MLC2v/ ras transgenic mice display a phenotype characteristic of hypertrophic cardiomyopathy, with septal hypertrophy and focal myocyte disarray. Experimental measurements of septal wall mechanics in ras transgenic mice have previously shown that regions of myocyte disarray have reduced principal systolic shortening, torsional systolic shear, and sarcomere length. To investigate the mechanisms of this regional dysfunction, a three-dimensional prolate spheroidal finite-element model was used to simulate filling and ejection in the hypertrophied mouse left ventricle with septal disarray. Focally disarrayed septal myocardium was modeled by randomly distributed three-dimensional regions of altered material properties based on measured statistical distributions of muscle fiber angular dispersion. Material properties in disarrayed regions were modeled by decreased systolic anisotropy derived from increased fiber angle dispersion and decreased systolic tension development associated with reduced sarcomere lengths. Compared with measurements in ras transgenic mice, the model showed similar heterogeneity of septal systolic strain with the largest reductions in principal shortening and torsional shear in regions of greatest disarray. Average systolic principal shortening on the right ventricular septal surface of the model was −0.114 for normal regions and −0.065 for disarrayed regions; for torsional shear, these values were 0.047 and 0.019, respectively. These model results suggest that regional dysfunction in ras transgenic mice may be explained in part by the observed structural defects, including myofiber dispersion and reduced sarcomere length, which contributed about equally to predicted dysfunction in the disarrayed myocardium.

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27

da Silva Lopes, Katharina, Agnieszka Pietas, Michael H. Radke, and Michael Gotthardt. "Titin visualization in real time reveals an unexpected level of mobility within and between sarcomeres." Journal of Cell Biology 193, no. 4 (May 9, 2011): 785–98. http://dx.doi.org/10.1083/jcb.201010099.

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The giant muscle protein titin is an essential structural component of the sarcomere. It forms a continuous periodic backbone along the myofiber that provides resistance to mechanical strain. Thus, the titin filament has been regarded as a blueprint for sarcomere assembly and a prerequisite for stability. Here, a novel titin-eGFP knockin mouse provided evidence that sarcomeric titin is more dynamic than previously suggested. To study the mobility of titin in embryonic and neonatal cardiomyocytes, we used fluorescence recovery after photobleaching and investigated the contribution of protein synthesis, contractility, and calcium load to titin motility. Overall, the kinetics of lateral and longitudinal movement of titin-eGFP were similar. Whereas protein synthesis and developmental stage did not alter titin dynamics, there was a strong, inhibitory effect of calcium on titin mobility. Our results suggest a model in which the largely unrestricted movement of titin within and between sarcomeres primarily depends on calcium, suggesting that fortification of the titin filament system is activity dependent.

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28

Nakamachi, Eiji, Jun Tsukamoto, and Youjiro Tamura. "Skeletal Muscle Contraction Analyses Based on Molecular Potential Theory. Contraction of Sarcomere." Transactions of the Japan Society of Mechanical Engineers Series A 60, no. 578 (1994): 2464–70. http://dx.doi.org/10.1299/kikaia.60.2464.

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29

Knupp and Squire. "Myosin Cross-Bridge Behaviour in Contracting Muscle—The T1 Curve of Huxley and Simmons (1971) Revisited." International Journal of Molecular Sciences 20, no. 19 (October 2, 2019): 4892. http://dx.doi.org/10.3390/ijms20194892.

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The stiffness of the myosin cross-bridges is a key factor in analysing possible scenarios to explain myosin head changes during force generation in active muscles. The seminal study of Huxley and Simmons (1971: Nature 233: 533) suggested that most of the observed half-sarcomere instantaneous compliance (=1/stiffness) resides in the myosin heads. They showed with a so-called T1 plot that, after a very fast release, the half-sarcomere tension reduced to zero after a step size of about 60Å (later with improved experiments reduced to 40Å). However, later X-ray diffraction studies showed that myosin and actin filaments themselves stretch slightly under tension, which means that most (at least two-thirds) of the half sarcomere compliance comes from the filaments and not from cross-bridges. Here we have used a different approach, namely to model the compliances in a virtual half sarcomere structure in silico. We confirm that the T1 curve comes almost entirely from length changes in the myosin and actin filaments, because the calculated cross-bridge stiffness (probably greater than 0.4 pN/Å) is higher than previous studies have suggested. Our model demonstrates that the formulations produced by previous authors give very similar results to our model if the same starting parameters are used. However, we find that it is necessary to model the X-ray diffraction data as well as mechanics data to get a reliable estimate of the cross-bridge stiffness. In the light of the high cross-bridge stiffness found in the present study, we present a plausible modified scenario to describe aspects of the myosin cross-bridge cycle in active muscle. In particular, we suggest that, apart from the filament compliances, most of the cross-bridge contribution to the instantaneous T1 response may come from weakly-bound myosin heads, not myosin heads in strongly attached states. The strongly attached heads would still contribute to the T1 curve, but only in a very minor way, with a stiffness that we postulate could be around 0.1 pN/Å, a value which would generate a working stroke close to 100 Å from the hydrolysis of one ATP molecule. The new model can serve as a tool to calculate sarcomere elastic properties for any vertebrate striated muscle once various parameters have been determined (e.g., tension, T1 intercept, temperature, X-ray diffraction spacing results).

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30

Ishibashi, Yuji, Judith C. Rembert, Blase A. Carabello, Shintaro Nemoto, Masayoshi Hamawaki, Michael R. Zile, Joseph C. Greenfield, and George Cooper. "Normal myocardial function in severe right ventricular volume overload hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 1 (January 1, 2001): H11—H16. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h11.

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Severe left ventricular volume overloading causes myocardial and cellular contractile dysfunction. Whether this is also true for severe right ventricular volume overloading was unknown. We therefore created severe tricuspid regurgitation percutaneously in seven dogs and then observed them for 3.5–4.0 yr. All five surviving operated dogs had severe tricuspid regurgitation and right heart failure, including massive ascites, but they did not have left heart failure. Right ventricular cardiocytes were isolated from these and from normal dogs, and sarcomere mechanics were assessed via laser diffraction. Right ventricular cardiocytes from the tricuspid regurgitation dogs were 20% longer than control cells, but neither the extent (0.171 ± 0.005 μm) nor the velocity (2.92 ± 0.12 μm/s) of sarcomere shortening differed from controls (0.179 ± 0.005 μm and 3.09 ± 0.11 μm/s, respectively). Thus, despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function was normal. This finding for the severely volume-overloaded right ventricle stands in distinct contrast to our finding for the left ventricle severely volume overloaded by mitral regurgitation, wherein intrinsic contractile function is depressed.

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31

Sweeney, H. L., S. A. Corteselli, and M. J. Kushmerick. "Measurements on permeabilized skeletal muscle fibers during continuous activation." American Journal of Physiology-Cell Physiology 252, no. 5 (May 1, 1987): C575—C580. http://dx.doi.org/10.1152/ajpcell.1987.252.5.c575.

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A mechanical stabilization technique involving the cycling of calcium activated rabbit psoas fibers between states of isometric force development and isovelocity shortenings at near maximal velocity (Vmax) was evaluated. This protocol succeeded in stabilizing both the sarcomere striation pattern and mechanical performance (isometric force and velocity of unloaded shortening) of the fibers for up to 10 min of continuous maximal calcium activation at 12 degrees C and for greater than 15 min at half-maximal activation. Between these cycling events, a variety of mechanical measurements can be made. A description of the strategies involved in the measurements and specific illustrations are presented. A general description of a computerized fiber mechanics system, which utilizes separate microprocessors for experimental control and data collection, is given. The techniques should be of general applicability to muscle physiologists studying permeabilized preparations and offer the great advantage of providing reproducibility of measurement in a stable preparation.

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32

Shabarchin, A. A., and Andrey K. Tsaturyan. "Proposed role of the M-band in sarcomere mechanics and mechano-sensing: a model study." Biomechanics and Modeling in Mechanobiology 9, no. 2 (August 8, 2009): 163–75. http://dx.doi.org/10.1007/s10237-009-0167-0.

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33

Salick, Max R., Brett N. Napiwocki, Jin Sha, Gavin T. Knight, Shahzad A. Chindhy, Timothy J. Kamp, Randolph S. Ashton, and Wendy C. Crone. "Micropattern width dependent sarcomere development in human ESC-derived cardiomyocytes." Biomaterials 35, no. 15 (May 2014): 4454–64. http://dx.doi.org/10.1016/j.biomaterials.2014.02.001.

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34

Pavlov, Ivan, Rowan Novinger, and Dilson E. Rassier. "The mechanical behavior of individual sarcomeres of myofibrils isolated from rabbit psoas muscle." American Journal of Physiology-Cell Physiology 297, no. 5 (November 2009): C1211—C1219. http://dx.doi.org/10.1152/ajpcell.00233.2009.

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The goal of this study was to develop a system to experiment with sarcomeres mechanically isolated from skeletal muscles. Single myofibrils from rabbit psoas were transferred into a temperature-controlled (22°C or 15°C) experimental chamber, and sarcomeres were isolated using precalibrated glass microneedles that were pierced externally, adjacent to the Z-lines. The force produced during activation was measured by tracking the displacement of the microneedles, and the sarcomere and half-sarcomere changes were measured by continuously tracking the Z-lines and A-bands position during the experiments. Sarcomeres produced a stress (force/cross-sectional area) of 112.75 ± 4.96 nN/μm2 (15°C) and 128.47 ± 5.58 nN/μm2 (22°C) at lengths between 2.0 μm and 2.4 μm. The descending limb was fitted with linear regression for length between 2.4 μm and 3.5 μm, which provided an abscissa extrapolating to 3.87 μm. The force-length relation was remarkably similar to a theoretical curve based on the degree of filament overlap. During sarcomere activation, we tracked the distance between the center of the A-band and the Z-lines. At lengths below 1.6 μm, movements of A-band were not detected. A-band movements increased with length to achieve a maximum displacement of 59.40 ± 10.1 nm from the center at 2.0 μm–2.4 μm. A-band displacement decreased linearly in sarcomere lengths between 2.6 μm and 3.6 μm. A technique for monitoring force and length in single sarcomeres isolated from myofibrils represents a reliable technique to evaluate contractile mechanisms at the most basic, intact level of muscle organization, opening the possibility to clarify long-standing issues in the field of muscle contraction.

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35

TER KEURS, H. E. D. J., Y. WAKAYAMA, Y. SUGAI, G. PRICE, Y. KAGAYA, P. A. BOYDEN, M. MIURA, and B. D. M. STUYVERS. "Role of Sarcomere Mechanics and Ca2+ Overload in Ca2+ Waves and Arrhythmias in Rat Cardiac Muscle." Annals of the New York Academy of Sciences 1080, no. 1 (October 1, 2006): 248–67. http://dx.doi.org/10.1196/annals.1380.020.

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36

ter Keurs, Henk E. D. J., Tsuyoshi Shinozaki, Ying Ming Zhang, Mei Luo Zhang, Yuji Wakayama, Yoshinao Sugai, Yutaka Kagaya, et al. "Sarcomere mechanics in uniform and non-uniform cardiac muscle: A link between pump function and arrhythmias." Progress in Biophysics and Molecular Biology 97, no. 2-3 (June 2008): 312–31. http://dx.doi.org/10.1016/j.pbiomolbio.2008.02.013.

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37

Thomas, A. J., J. S. Arnold, B. Simhai, and S. G. Kelsen. "Structure of abdominal muscles in the hamster: effect of elastase-induced emphysema." Journal of Applied Physiology 63, no. 4 (October 1, 1987): 1665–70. http://dx.doi.org/10.1152/jappl.1987.63.4.1665.

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The present study examined the effects of elastase-induced emphysema on the structure of the external oblique and transverse abdominis muscles and a non-respiratory muscle, the extensor digitorum longus. Muscle structure was assessed from the cross-sectional area (CSA) and percent of individual fiber types in histochemically stained sections and from the number of sarcomeres arranged in series along the length of individual fibers. Data were obtained in eight hamsters with emphysema and nine saline-injected controls. In the normal (control) animals the external oblique was thicker but contained fewer sarcomeres than the transverse abdominis. Fiber size was similar in the two muscles. In the transverse abdominis the percents of fast-glycolytic and fast-oxidative fibers were greater and smaller, respectively, than in the external oblique. Lung volume of emphysematous hamsters was 168% of control values (P less than 0.001). In emphysematous compared with control animals, the CSA of fast-twitch fibers in the external oblique and transverse abdominis was significantly reduced. Fiber length and sarcomere number were significantly decreased in the transverse abdominis but not in the external oblique in emphysematous hamsters. In contrast, fiber size and composition of the extensor digitorum longus was similar in emphysematous and control animals. These data indicate that cellular responses of the ventilatory muscles to chronic hyperinflation and altered thoracic geometry induced by emphysema are not present in limb skeletal muscle. We speculate that changes in fiber length and CSA of fast fibers in the abdominal expiratory muscles reflect responses to chronic alterations in the mechanics of breathing that may affect muscle load, length, or the pattern of activity.

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38

Linke, Wolfgang A., Diane E. Rudy, Thomas Centner, Mathias Gautel, Christian Witt, Siegfried Labeit, and Carol C. Gregorio. "I-Band Titin in Cardiac Muscle Is a Three-Element Molecular Spring and Is Critical for Maintaining Thin Filament Structure." Journal of Cell Biology 146, no. 3 (August 9, 1999): 631–44. http://dx.doi.org/10.1083/jcb.146.3.631.

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In cardiac muscle, the giant protein titin exists in different length isoforms expressed in the molecule's I-band region. Both isoforms, termed N2-A and N2-B, comprise stretches of Ig-like modules separated by the PEVK domain. Central I-band titin also contains isoform-specific Ig-motifs and nonmodular sequences, notably a longer insertion in N2-B. We investigated the elastic behavior of the I-band isoforms by using single-myofibril mechanics, immunofluorescence microscopy, and immunoelectron microscopy of rabbit cardiac sarcomeres stained with sequence-assigned antibodies. Moreover, we overexpressed constructs from the N2-B region in chick cardiac cells to search for possible structural properties of this cardiac-specific segment. We found that cardiac titin contains three distinct elastic elements: poly-Ig regions, the PEVK domain, and the N2-B sequence insertion, which extends ∼60 nm at high physiological stretch. Recruitment of all three elements allows cardiac titin to extend fully reversibly at physiological sarcomere lengths, without the need to unfold Ig domains. Overexpressing the entire N2-B region or its NH2 terminus in cardiac myocytes greatly disrupted thin filament, but not thick filament structure. Our results strongly suggest that the NH2-terminal N2-B domains are necessary to stabilize thin filament integrity. N2-B–titin emerges as a unique region critical for both reversible extensibility and structural maintenance of cardiac myofibrils.

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39

Kirn, Borut. "Visualization of Myocardial Strain Pattern Uniqueness with Respect to Activation Time and Contractility: A Computational Study." Data 4, no. 2 (May 24, 2019): 79. http://dx.doi.org/10.3390/data4020079.

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Speckle tracking echography is used to measure myocardial strain patterns in order to assess the state of myocardial tissue. Because electro-mechanical coupling in myocardial tissue is complex and nonlinear, and because of the measurement errors the uniqueness of strain patterns is questionable. In this study, the uniqueness of strain patterns was visualized in order to revel characteristics that may improve their interpretation. A computational model of sarcomere mechanics was used to generate a database of 1681 strain patterns, each simulated with a different set of sarcomere parameters: time of activation (TA) and contractility (Con). TA and Con ranged from −100 ms to 100 ms and 2% to 202% in 41 steps respectively, thus forming a two-dimensional 41 × 41 parameter space. Uniqueness of the strain pattern was assessed by using a cohort of similar strain patterns defined by a measurement error. The cohort members were then visualized in the parameter space. Each cohort formed one connected component (or blob) in the parameter space; however, large differences in the shape, size, and eccentricity of the blobs were found for different regions in the parameter space. The blobs were elongated along the TA direction (±50 ms) when contractility was low, and along the Con direction (±50%) when contractility was high. The uniqueness of the strain patterns can be assessed and visualized in the parameter space. The strain patterns in the studied database are not degenerated because a cohort of similar strain patterns forms only one connected blob in the parameter space. However, the elongation of the blobs means that estimations of TA when contractility is low and of Con when contractility is high have high uncertainty.

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40

Luo, Y., R. Cooke, and E. Pate. "A model of stress relaxation in cross-bridge systems: effect of a series elastic element." American Journal of Physiology-Cell Physiology 265, no. 1 (July 1, 1993): C279—C288. http://dx.doi.org/10.1152/ajpcell.1993.265.1.c279.

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Many experimental protocols employed in the study of muscle mechanics use tension transients as a probe of the magnitudes of the kinetic rates in the underlying cross-bridge dynamics. These transients could potentially be modified by the elastic elements that exist both within the fiber and at the points of attachment to the experimental apparatus. To better understand the magnitude of such modifications, we have used computer simulation to investigate the transients that would be expected for cross bridges acting on an actin filament attached to an elastic element. The original model of cross-bridge mechanics by A.F. Huxley was used (Prog. Biophys. 7: 255-318, 1957). After an isometric equilibrium is achieved, a tension transient is produced by changing the dissociation rate constant, g1, while holding the attachment rate constant, f1, fixed. This decreases the number of attached, force-producing cross bridges. We find that the tension transients are markedly slowed by the presence of even a few (> or = 2) nanometers of series elastic strain per half-sarcomere. Thus some rate constants inferred from mechanical transients (e.g., those induced by caged ligands) may underestimate the actual kinetic rates of the cross-bridge processes.

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41

van de Locht, Martijn, Tamara C. Borsboom, Josine M. Winter, and Coen A. C. Ottenheijm. "Troponin Variants in Congenital Myopathies: How They Affect Skeletal Muscle Mechanics." International Journal of Molecular Sciences 22, no. 17 (August 25, 2021): 9187. http://dx.doi.org/10.3390/ijms22179187.

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The troponin complex is a key regulator of muscle contraction. Multiple variants in skeletal troponin encoding genes result in congenital myopathies. TNNC2 has been implicated in a novel congenital myopathy, TNNI2 and TNNT3 in distal arthrogryposis (DA), and TNNT1 and TNNT3 in nemaline myopathy (NEM). Variants in skeletal troponin encoding genes compromise sarcomere function, e.g., by altering the Ca2+ sensitivity of force or by inducing atrophy. Several potential therapeutic strategies are available to counter the effects of variants, such as troponin activators, introduction of wild-type protein through AAV gene therapy, and myosin modulation to improve muscle contraction. The mechanisms underlying the pathophysiological effects of the variants in skeletal troponin encoding genes are incompletely understood. Furthermore, limited knowledge is available on the structure of skeletal troponin. This review focusses on the physiology of slow and fast skeletal troponin and the pathophysiology of reported variants in skeletal troponin encoding genes. A better understanding of the pathophysiological effects of these variants, together with enhanced knowledge regarding the structure of slow and fast skeletal troponin, will direct the development of treatment strategies.

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42

Campbell, Kenneth S., and Richard L. Moss. "SLControl: PC-based data acquisition and analysis for muscle mechanics." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 6 (December 2003): H2857—H2864. http://dx.doi.org/10.1152/ajpheart.00295.2003.

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SLControl is a computerized data acquisition and analysis system that was developed in our laboratory to help perform mechanical experiments using striated muscle preparations. It consists of a computer program (Windows 2000 or later) and a commercially available data acquisition board (16-bit resolution, DAP5216a, Microstar Laboratories, Bellevue, WA). Signals from the user's existing equipment representing force, fiber length (FL), and (if desired) sarcomere length (SL) are connected to the system through standard Bayonet Neill Concelman cables and saved to data files for later analysis. Output signals from the board control FL and trigger additional equipment, e.g., flash lamps. Windows dialogs drive several different experimental protocols, including slack tests and rate of tension recovery measurements. Precise measurements of muscle stiffness and force velocity/power characteristics can also be accomplished using SL and tension control, respectively. In these situations, the FL command signal is updated in real time (at rates ≥2.5 kHz) in response to changes in the measured SL or force signals. Data files can be exported as raw text or analyzed within SLControl with the use of built-in tools for cursor analysis, digital filtering, curve fitting, etc. The software is available for free download at http://www.slcontrol.com .

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Rome, L. C., I. H. Choi, G. Lutz, and A. Sosnicki. "The influence of temperature on muscle function in the fast swimming scup. I. Shortening velocity and muscle recruitment during swimming." Journal of Experimental Biology 163, no. 1 (February 1, 1992): 259–79. http://dx.doi.org/10.1242/jeb.163.1.259.

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In this study, electromyography showed that scup can swim to a maximum speed of 80 cm s-1 with their red muscle whereas previous results showed that carp can swim to only 45 cm s-1. Our aim was to evaluate the adaptations that enable scup to swim nearly twice as fast as carp. Although we anticipated that, at their respective maximum speeds, the red muscle of scup would be shortening at twice the velocity (V) of carp muscle, we found that the values of V were the same (2.04 muscle lengths s-1). At any given swimming speed, V was higher in carp than in scup because carp had a larger sarcomere length excursion and higher tail-beat frequency. The smaller sarcomere excursion in scup is primarily associated with using a less undulatory style of swimming (i.e. with a smaller backbone curvature). This less undulatory style of swimming may be an important adaptation that not only reduces V but may also reduce drag. At their respective maximum speeds, however, the 28% lower sarcomere length excursion in scup is balanced by a 26% higher tail-beat frequency, giving an equal V to that of carp. Although the scup in this study were somewhat longer than the carp in the previous one (19.7 vs 13.4 cm), we believe that many of the observed differences are species-related rather than size-related. We also found that scup swam in a kinematically similar fashion at 10 degrees C and 20 degrees C. However, at 10 degrees C, the scup could swim to only 54 cm s-1 before recruiting their white muscle whereas, at 20 degrees C, they could swim to 80 cm s-1. The difference in speed of initial white muscle recruitment, as well as information on muscle mechanics, suggests that the scup compress their recruitment order into a narrow speed range at low temperatures, thereby recruiting more muscle fibres. Quantitative analysis of red muscle electromyograms in this paper supports this hypothesis.

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44

Givli, Sefi, and Kaushik Bhattacharya. "A coarse-grained model of the myofibril: Overall dynamics and the evolution of sarcomere non-uniformities." Journal of the Mechanics and Physics of Solids 57, no. 2 (February 2009): 221–43. http://dx.doi.org/10.1016/j.jmps.2008.10.013.

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45

Toepfer, Christopher N., Markus B. Sikkel, Valentina Caorsi, Anupama Vydyanath, Iratxe Torre, O'Neal Copeland, Alexander R. Lyon, et al. "A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation." American Journal of Physiology-Heart and Circulatory Physiology 311, no. 2 (August 1, 2016): H465—H475. http://dx.doi.org/10.1152/ajpheart.00899.2015.

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Myocardial remodeling in response to chronic myocardial infarction (CMI) progresses through two phases, hypertrophic “compensation” and congestive “decompensation.” Nothing is known about the ability of uninfarcted myocardium to produce force, velocity, and power during these clinical phases, even though adaptation in these regions likely drives progression of compensation. We hypothesized that enhanced cross-bridge-level contractility underlies mechanical compensation and is controlled in part by changes in the phosphorylation states of myosin regulatory proteins. We induced CMI in rats by left anterior descending coronary artery ligation. We then measured mechanical performance in permeabilized ventricular trabecula taken distant from the infarct zone and assayed myosin regulatory protein phosphorylation in each individual trabecula. During full activation, the compensated myocardium produced twice as much power and 31% greater isometric force compared with noninfarcted controls. Isometric force during submaximal activations was raised >2.4-fold, while power was 2-fold greater. Electron and confocal microscopy demonstrated that these mechanical changes were not a result of increased density of contractile protein and therefore not an effect of tissue hypertrophy. Hence, sarcomere-level contractile adaptations are key determinants of enhanced trabecular mechanics and of the overall cardiac compensatory response. Phosphorylation of myosin regulatory light chain (RLC) increased and remained elevated post-MI, while phosphorylation of myosin binding protein-C (MyBP-C) was initially depressed but then increased as the hearts became decompensated. These sensitivities to CMI are in accordance with phosphorylation-dependent regulatory roles for RLC and MyBP-C in crossbridge function and with compensatory adaptation in force and power that we observed in post-CMI trabeculae.

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46

Caramani, Marco, Luca Melli, Mario Dolfi, Vincenzo Lombardi, and Marco Linari. "Half-Sarcomere Mechanics and Energetics Indicate that Myosin Motors Slip Between Two Consecutive Actin Monomers during their Working Stroke." Biophysical Journal 102, no. 3 (January 2012): 17a. http://dx.doi.org/10.1016/j.bpj.2011.11.118.

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47

Hanft, Laurin M., and Kerry S. McDonald. "Sarcomere length dependence of power output is increased after PKA treatment in rat cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 5 (May 2009): H1524—H1531. http://dx.doi.org/10.1152/ajpheart.00864.2008.

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The Frank-Starling relationship of the heart yields increased stroke volume with greater end-diastolic volume, and this relationship is steeper after β-adrenergic stimulation. The underlying basis for the Frank-Starling mechanism involves length-dependent changes in both Ca2+ sensitivity of myofibrillar force and power output. In this study, we tested the hypothesis that PKA-induced phosphorylation of myofibrillar proteins would increase the length dependence of myofibrillar power output, which would provide a myofibrillar basis to, in part, explain the steeper Frank-Starling relations after β-adrenergic stimulation. For these experiments, adult rat left ventricles were mechanically disrupted, permeabilized cardiac myocyte preparations were attached between a force transducer and position motor, and the length dependence of loaded shortening and power output were measured before and after treatment with PKA. PKA increased the phosphorylation of myosin binding protein C and cardiac troponin I, as assessed by autoradiography. In terms of myocyte mechanics, PKA decreased the Ca2+ sensitivity of force and increased loaded shortening and power output at all relative loads when the myocyte preparations were at long sarcomere length (∼2.30 μm). PKA had less of an effect on loaded shortening and power output at short sarcomere length (∼2.0 μm). These changes resulted in a greater length dependence of myocyte power output after PKA treatment; peak normalized power output increased ∼20% with length before PKA and ∼40% after PKA. These results suggest that PKA-induced phosphorylation of myofibrillar proteins explains, in part, the steeper ventricular function curves (i.e., Frank-Starling relationship) after β-adrenergic stimulation of the left ventricle.

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48

Garcia-Webb, M. G., A. J. Taberner, N. C. Hogan, and I. W. Hunter. "A modular instrument for exploring the mechanics of cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (July 2007): H866—H874. http://dx.doi.org/10.1152/ajpheart.01055.2006.

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The cardiac ventricular myocyte is a key experimental system for exploring the mechanical properties of the diseased and healthy heart. Millions of primary myocytes, which remain viable for 4–6 h, can be readily isolated from animal models. However, currently available instrumentation allows the mechanical properties of only a few physically loaded myocytes to be explored within 4–6 h. Here we describe a modular and inexpensive prototype instrument that could form the basis of an array of devices for probing the mechanical properties of single mammalian myocytes in parallel. This device would greatly increase the throughput of scientific experimentation and could be applied as a high-content screening instrument in the pharmaceutical industry. The instrument module consists of two independently controlled Lorentz force actuators-force transducers in the form of 0.025 × 1 × 5 mm stainless steel cantilevers with 0.5 m/N compliance and 360-Hz resonant frequency. Optical position sensors focused on each cantilever provide position and force resolution of <1 nm/√Hz and <2 nN/√Hz, respectively. The motor structure can produce peak displacements and forces of ±200 μm and ±400 μN, respectively. Custom Visual Basic.Net software provides data acquisition, signal processing, and digital control of cantilever position. The functionality of the instrument was demonstrated by implementation of novel methodologies for loading and attaching healthy mammalian ventricular myocytes to the force sensor and actuator and use of stochastic system identification techniques to measure their passive dynamic stiffness at various sarcomere lengths.

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49

Weinert, Stefanie, Nora Bergmann, Xiuju Luo, Bettina Erdmann, and Michael Gotthardt. "M line–deficient titin causes cardiac lethality through impaired maturation of the sarcomere." Journal of Cell Biology 173, no. 4 (May 15, 2006): 559–70. http://dx.doi.org/10.1083/jcb.200601014.

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Titin, the largest protein known to date, has been linked to sarcomere assembly and function through its elastic adaptor and signaling domains. Titin's M-line region contains a unique kinase domain that has been proposed to regulate sarcomere assembly via its substrate titin cap (T-cap). In this study, we use a titin M line–deficient mouse to show that the initial assembly of the sarcomere does not depend on titin's M-line region or the phosphorylation of T-cap by the titin kinase. Rather, titin's M-line region is required to form a continuous titin filament and to provide mechanical stability of the embryonic sarcomere. Even without titin integrating into the M band, sarcomeres show proper spacing and alignment of Z discs and M bands but fail to grow laterally and ultimately disassemble. The comparison of disassembly in the developing and mature knockout sarcomere suggests diverse functions for titin's M line in embryonic development and the adult heart that not only involve the differential expression of titin isoforms but also of titin-binding proteins.

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50

Coirault, Catherine, Denis Chemla, Jean-Claude Pourny, Francine Lambert, and Yves Lecarpentier. "Instantaneous force-velocity-length relationship in diaphragmatic sarcomere." Journal of Applied Physiology 82, no. 2 (February 1, 1997): 404–12. http://dx.doi.org/10.1152/jappl.1997.82.2.404.

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Coirault, Catherine, Denis Chemla, Jean-Claude Pourny, Francine Lambert, and Yves Lecarpentier. Instantaneous force-velocity-length relationship in diaphragmatic sarcomere. J. Appl. Physiol. 82(2): 404–412, 1997.—The simultaneous analysis of muscle force, length, velocity, and time has been shown to precisely characterize the mechanical performance of isolated striated muscle. We tested the hypothesis that the three-dimensional force-velocity-length relationship reflects mechanical properties of sarcomeres. In hamster diaphragm strips, instantaneous sarcomere length (S L) and muscle length were simultaneously measured during afterloaded twitches. S L was measured by means of laser diffraction. We also studied the influence of initial S L, abrupt changes in total load, and 2 × 10−7 M dantrolene. Baseline resting S L at the apex of the length-active tension curve was 2.2 ± 0.1 μm, whereas S L at peak shortening was 1.6 ± 0.1 μm in the preloaded twitch and 2.1 ± 0.1 μm in the “isometric” twitch. Over the whole load continuum and at any given level of isotonic load, there was a unique relationship between instantaneous sarcomere velocity and instantaneous S L. Part of this relationship was time independent and initial S L independent and was markedly downshifted after dantrolene. When five different muscle regions were considered, there were no significant variations of S L and sarcomere kinetics along the muscle. These results indicate that the time- and initial length-independent part of the instantaneous force-velocity-length relationship previously described in muscle strips reflects intrinsic sarcomere mechanical properties.

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