ArticleJournal of muscle research and cell motility1997
Models of calcium activation account for differences between skeletal and cardiac force redevelopment kinetics.
Article in Journal of muscle research and cell motility, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
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- Eliminating the First Inactive State and Stabilizing the Active State of the Cardiac Regulatory System Alters Behavior in Solution and in Ordered Systems.Biochemistry · 2020Article
- Familial Dilated Cardiomyopathy Associated With a Novel Combination of Compound HeterozygousFrontiers in physiology · 2019Article
- Structural and functional impact of troponin C-mediated CaJournal of molecular and cellular cardiology · 2018Article
- Effects of cross-bridge compliance on the force-velocity relationship and muscle power output.PloS one · 2017Article
- Slowed Dynamics of Thin Filament Regulatory Units Reduces CaCellular and molecular bioengineering · 2013Article
- The force-frequency relationship: insights from mathematical modeling.Advances in physiology education · 2013Review
- Tropomyosin flexural rigidity and single ca(2+) regulatory unit dynamics: implications for cooperative regulation of cardiac muscle contraction and cardiomyocyte hypertrophy.Frontiers in physiology · 2012Article
- Approximate model of cooperative activation and crossbridge cycling in cardiac muscle using ordinary differential equations.Biophysical journal · 2008Article
- Thin filament Ca2+ binding properties and regulatory unit interactions alter kinetics of tension development and relaxation in rabbit skeletal muscle.The Journal of physiology · 2008Article
- Sarcomere lattice geometry influences cooperative myosin binding in muscle.PLoS computational biology · 2007Article
- Thin-filament regulation of force redevelopment kinetics in rabbit skeletal muscle fibres.The Journal of physiology · 2007Article
- Sarcomeric determinants of striated muscle relaxation kinetics.Pflugers Archiv : European journal of physiology · 2005Review
- Cardiac length dependence of force and force redevelopment kinetics with altered cross-bridge cycling.Biophysical journal · 2004Article
- Cross-bridge versus thin filament contributions to the level and rate of force development in cardiac muscle.Biophysical journal · 2004Article
- Activation kinetics of skinned cardiac muscle by laser photolysis of nitrophenyl-EGTA.Biophysical journal · 2004Article
- Cooperative mechanisms in the activation dependence of the rate of force development in rabbit skinned skeletal muscle fibers.The Journal of general physiology · 2001Article
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3 authors at 2 institutions in 1 country.
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Abstract
To explain observed differences in the activation dependence of force redevelopment kinetics between cardiac and skeletal muscle, two numerical models of contractile regulation by Ca2+ were investigated. Ca2+ binding and force production were each modelled as two-state processes with forward and reverse rate constants taken from the literature. The first model incorporates four possible thin-filament states. In the second model Ca2+ is assumed not to dissociate from a thin-filament unit in the force-generating state, resulting in three states. The four-state model can account for the activation dependence of the rate constant of tension redevelopment (ktr) seen in skeletal muscle, without requiring that Ca2+ directly modulates the kinetics of any step in the cross-bridge cycle. Using identical kinetic parameters, the three-state model shows no activation dependence of ktr, consistent with our results in cardiac muscle. Following a step increase in [Ca2+], the rate of rise in tension (as described by the rate constant kCa) varies with the final [Ca2+] for both models, consistent with experimental results from skeletal and cardiac muscle. These numerical models demonstrate that experimental measurements thought to reveal changes in kinetic parameters may simply reflect coupling between the two kinetic processes of Ca2+ binding and force generation. Furthermore, the models present possible differences in the Ca2+ activation scheme between cardiac and skeletal muscle which can account for the contrasting activation dependencies of force redevelopment kinetics.
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