Key result
New ventricular myofilament contraction model accounts for ~60% of total cellular ATP consumption.
A new computational model of cardiac muscle contraction successfully incorporates biochemical and biophysical characteristics and estimates that contraction accounts for ~60% of total ATP usage in a ventricular cell.
Supports detailed modeling of myofilament energetics; leaves open in vivo confirmation and therapeutic implications.
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.
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Muangkram et al. (2017) studied Cardiac muscle contraction. New myofilament contraction model was evaluated on ATP consumption. A new myofilament contraction model incorporated into a ventricular cell model accounted for approximately 60% of the total ATP usage in the cell model.
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