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.

心脏收缩是由肌球蛋白和肌动蛋白丝之间的周期性相互作用驱动的，而肌球蛋白和肌动蛋白丝由 ATP 水解提供动力。心肌的模块化结构和心跳的器官级同步确保了肌球蛋白 ATP 酶循环与宏观心动周期之间的紧密相互耦合。肌球蛋白马达响应肌动蛋白和肌球蛋白丝的周期性激活，驱动压力变化，从而控制心室的流入和流出瓣膜。阀门的打开和关闭依次将肌球蛋白马达在大致等长收缩模式和大致等张收缩模式之间切换。尽管两种肌肉类型中的肌球蛋白丝具有相同数量的肌球蛋白马达，但心脏中的峰值肌丝应力比完全激活的骨骼肌中的峰值肌丝应力小得多。计算表明，尽管需要更多的电机来驱动射血，但仅需要约 5％ 的心脏中的肌球蛋白电机即可产生峰值收缩压。严格调节活跃马达的数量对于健康心脏的有效运作至关重要——这种控制通常会被与遗传性心脏病相关的基因变异所破坏，而其恢复可能是开发新疗法的一个有用的终点。