The right ventricle (RV) is often overlooked in the evaluation of cardiac performance and treatment of left ventricular (LV) heart diseases. However, recent evidence suggests the RV may play an important role in maintaining systemic cardiac function and delivering stroke volume (SV). We used exercise cardiac magnetic resonance and biomechanical modeling to investigate the role of the RV in LV stroke volume regulation. We studied SV augmentation during exercise by pharmacologically inducing negative chronotropy (sHRi) in healthy volunteers and investigating training-induced SV augmentation in endurance athletes. SV augmentation during exercise after sHRi is achieved differently in the two ventricles. In the RV, the larger SV is driven by increasing contraction down to lower end-systolic volume (ESV; p<.001). In the LV, SV augmentation is achieved through an increase in end-diastolic volume (EDV; p<.001), avoiding contraction to a lower ESV. The same mechanism is underlies the enhanced SV response observed in athletes. Changes in atrial area during SV augmentation suggest that the improved LV EDV response is sustained by the larger RV contractions. Using our biomechanical model, we explain this behavior and show that the RV systolic function driven regulation of LV SV optimizes the energetic cost of LV contraction, and leads to minimization of the total costs of biventricular contraction. In conclusion, this work provides mechanistic understanding of the pivotal role of the RV in optimizing LV SV during exercise. It demonstrates why optimizing RV function needs to become a key part of therapeutic strategies in patients and training for athletes.

中文翻译：

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心脏的协同作用：RV 收缩功能在运动期间优化 LV 性能方面起着关键作用。

在评估心脏功能和治疗左心室 (LV) 心脏病时，右心室 (RV) 经常被忽视。然而，最近的证据表明 RV 可能在维持全身心脏功能和提供每搏输出量 (SV) 方面发挥重要作用。我们使用运动心脏磁共振和生物力学模型来研究 RV 在 LV 每搏输出量调节中的作用。我们通过药理学诱导健康志愿者的负变时性 (sHRi) 和调查耐力运动员训练引起的 SV 增加来研究运动期间的 SV 增加。sHRi 后运动期间的 SV 增强在两个心室中实现不同。在 RV 中，较大的 SV 是由收缩增加到较低的收缩末期容积驱动的（ESV；p<.001）。在LV里，通过增加舒张末期容积（EDV；p<.001）来增加 SV，避免收缩至较低的 ESV。同样的机制是在运动员中观察到的增强的 SV 反应的基础。SV 增加期间心房面积的变化表明，改善的 LV EDV 反应是由较大的 RV 收缩维持的。使用我们的生物力学模型，我们解释了这种行为，并表明 RV 收缩功能驱动的 LV SV 调节优化了 LV 收缩的能量成本，并使双心室收缩的总成本最小化。总之，这项工作提供了对 RV 在运动期间优化 LV SV 的关键作用的机械理解。它说明了为什么优化 RV 功能需要成为患者治疗策略和运动员训练的关键部分。