ArticleBiophysical journal2002
Relaxation kinetics following sudden Ca(2+) reduction in single myofibrils from skeletal muscle.
Article in Biophysical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 139 citations in OpenAlex.
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- Molecular mechanisms of altered contraction with the β-myosin R403Q mutation in porcine ventricular muscle and a human stem cell-derived cardiomyocyte model.Journal of molecular and cellular cardiology · 2025Article
- The G256E HCM mutation prolongs cardiac muscle relaxation via altered nucleotide handling.Research square · 2025Article
- Myosin-binding protein C slows cardiac myofibril relaxation kinetics.The Journal of physiology · 2025Article
- The elementary step that generates force and sinusoidal analysis in striated muscle fibers.Journal of muscle research and cell motility · 2025Review
- Myosin Isoform-Dependent Effect of Omecamtiv Mecarbil on the Regulation of Force Generation in Human Cardiac Muscle.International journal of molecular sciences · 2024Article
- A novel kinetic model to demonstrate the independent effects of ATP and ADP/Pi concentrations on sarcomere function.PLoS computational biology · 2024Article
- Oscillatory work and the step that generates force in single myofibrils from rabbit psoas.Pflugers Archiv : European journal of physiology · 2024Article
- A Laing distal myopathy-associated proline substitution in the β-myosin rod perturbs myosin cross-bridging activity.The Journal of clinical investigation · 2024Article
- Strain rate of stretch affects crossbridge detachment during relaxation of intact cardiac trabeculae.PloS one · 2024Article
- Influence of age on force and re-lengthening dynamics after tetanic stimulation withdrawal in the tibialis anterior muscle.European journal of applied physiology · 2023Article
- Multiscale characterization of left ventricle active behavior in the mouse.Acta biomaterialia · 2023Article
- Gaining new understanding of sarcomere length non-uniformities in skeletal muscles.Frontiers in physiology · 2023Article
- Pressing physiology to move our understanding of cytosolic calcium dynamics.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Alpha and beta myosin isoforms and human atrial and ventricular contraction.Cellular and molecular life sciences : CMLS · 2021Review
- Single-molecule imaging reveals the concerted release of myosin from regulated thin filaments.eLife · 2021Article
- Mavacamten has a differential impact on force generation in myofibrils from rabbit psoas and human cardiac muscle.The Journal of general physiology · 2021Article
- Changes in electromyographic activity, mechanical power, and relaxation rates following inspiratory ribcage muscle fatigue.Scientific reports · 2021Observational
- The relation between sarcomere energetics and the rate of isometric tension relaxation in healthy and diseased cardiac muscle.Journal of muscle research and cell motility · 2021Article
32 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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