Contraction of the heart is driven by cyclical interactions between myosin and actin filaments powered by ATP hydrolysis. The modular structure of heart muscle and the organ-level synchrony of the heartbeat ensure tight reciprocal coupling between this myosin ATPase cycle and the macroscopic cardiac cycle. The myosin motors respond to the cyclical activation of the actin and myosin filaments to drive the pressure changes that control the inflow and outflow valves of the heart chambers. Opening and closing of the valves in turn switches the myosin motors between roughly isometric and roughly isotonic contraction modes. Peak filament stress in the heart is much smaller than in fully activated skeletal muscle, although the myosin filaments in the two muscle types have the same number of myosin motors. Calculations indicate that only ~5% of the myosin motors in the heart are needed to generate peak systolic pressure, although many more motors are needed to drive ejection. Tight regulation of the number of active motors is essential for the efficient functioning of the healthy heart — this control is commonly disrupted by gene variants associated with inherited heart disease, and its restoration might be a useful end point in the development of novel therapies.

心脏的收缩是由 ATP 水解驱动的肌球蛋白和肌动蛋白丝之间的周期性相互作用驱动的。心肌的模块化结构和心跳的器官水平同步确保了该肌球蛋白 ATP 酶循环和宏观心动周期之间的紧密往复耦合。肌球蛋白马达响应肌动蛋白和肌球蛋白丝的周期性激活，以驱动控制心腔流入和流出阀的压力变化。依次打开和关闭阀门，在大致等长和大致等张收缩模式之间切换肌球蛋白马达。心脏中的峰值细丝应力比完全激活的骨骼肌小得多，尽管两种肌肉类型的肌球蛋白丝具有相同数量的肌球蛋白马达。计算表明，心脏中只需要 ~5% 的肌球蛋白马达即可产生峰值收缩压，尽管需要更多的马达来驱动射血。严格调节主动马达的数量对于健康心脏的有效运作至关重要——这种控制通常被与遗传性心脏病相关的基因变异所破坏，其恢复可能是开发新疗法的有用终点。