Acute exhaustive endurance exercise can differentially impact the right ventricle (RV) versus the left (LV). However, the hemodynamic basis for these differences and its impact on post-exercise recovery remains unclear. Therefore, we assessed cardiac structure and function along with hemodynamic properties of mice subjected to single bouts (216±8min) of exhaustive swimming (ES). One-hour after ES, LVs displayed mild diastolic impairment compared to sedentary (SED) mice. Following dobutamine administration to assess functional reserve, diastolic and systolic function were slightly impaired. Twenty-four hours after ES, LV function was largely indistinguishable from SED. By contrast, one-hour post-swim, RVs showed pronounced impairment of diastolic and systolic function with and without dobutamine, which persisted twenty-four hours later. The degree of RV impairment correlated with time-to-exhaustion. To identify hemodynamic factors mediating chamber-specific responses to ES, LV pressure was recorded during swimming. Swimming initiated immediate increases in heart rates (HRs), systolic pressure, dP/dt_max and -dP/dt_min, which remained stable for ~45min. LV end-diastolic pressures (LVEDP) increased to ≥45mmHg during the first 10min and subsequently declined. After 45 mins, HR and -dP/dt_min declined, which correlated with gradual elevations in LVEDP (to ~45mmHg) as mice approached exhaustion. All parameters rapidly normalized post-exercise. Consistent with human studies, our findings demonstrate a disproportionate negative impact of acute exhaustive exercise on RVs that persisted for at least 24-hours. We speculate that the differential effects of exhaustive exercise on the ventricles arise from a ~2-fold greater hemodynamic load in the RV versus LV originating from profound elevations in LVEDPs as mice approach exhaustion.

中文翻译：

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急性力竭游泳运动对右心室的不同负面影响与不均衡的血流动力学负荷相关

急性力竭运动可以对右心室（RV）和左心室（LV）产生不同的影响。但是，这些差异的血液动力学基础及其对运动后恢复的影响仍不清楚。因此，我们评估了一次力竭游泳（ES）的单次发作（216±8min）小鼠的心脏结构和功能以及血液动力学特性。ES后一小时，与久坐（SED）小鼠相比，LVs表现出轻度舒张功能障碍。多巴酚丁胺给药后评估功能储备，舒张和收缩功能略有受损。ES后二十四小时，LV功能与SED在很大程度上没有区别。相比之下，游泳后一小时，RV在有和没有多巴酚丁胺的情况下表现出明显的舒张和收缩功能受损，这种现象在二十四小时后持续存在。RV损害的程度与疲劳时间相关。为了确定介导腔室对ES的特异性反应的血液动力学因素，在游泳过程中记录了LV压力。游泳导致心率（HRs），收缩压，dP / dt立即升高_max和-dP / dt _min，它们在〜45min内保持稳定。在最初的10分钟内，LV舒张末期压力（LVEDP）升高至≥45mmHg，随后下降。45分钟后，HR和-dP / dt _min下降，这与小鼠接近精疲力竭时LVEDP逐渐升高（至〜45mmHg）有关。所有参数在运动后迅速标准化。与人体研究一致，我们的研究结果表明，急性力竭运动对至少持续24小时的RV产生不成比例的负面影响。我们推测，力竭运动对心室的差异作用是由于LV相对于LV的血流动力学负荷增加了约2倍，这是由于小鼠接近力竭时LVEDPs明显升高所致。