A new myofilament contraction model with ATP consumption for ventricular cell model
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A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of Ca2+–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on Ca2+ activation and force (F b) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as F b activation by transient Ca2+ ([Ca2+]–F b), [Ca2+]–ATP hydrolysis relations, sarcomere length–F b, and F b recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model.
KeywordsMyofilament model Mechano-energetics Actomyosin–ATPase Crossbridge kinetics Troponin system
YM and AN designed the study and developed the mathematical model. YM analyzed the experimental simulations and drafted the manuscript. AN and AA interpreted the data, discussed the results, and revised the manuscript. All authors have approved the final version of the submitted manuscript.
Compliance with ethical standards
The authors received no external funding for this research.
Conflict of interest
The authors declare that they have no conflict of interest.
This article does not contain any studies with human participants or animals performed by any of the authors.
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