Differential negative effects of acute exhaustive swim exercise on the right ventricle is associated with disproportionate hemodynamic loading

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.