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

Abstract

Acute exhaustive endurance exercise can differentially impact the right ventricle (RV) versus the left ventricle (LV). However, the hemodynamic basis for these differences and its impact on postexercise recovery remain unclear. Therefore, we assessed cardiac structure and function along with hemodynamic properties of mice subjected to single bouts (216 ± 8 min) of exhaustive swimming (ES). One-hour after ES, LVs displayed mild diastolic impairment compared with that in 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 that in SED. By contrast, 1-h post swim, RVs showed pronounced impairment of diastolic and systolic function with and without dobutamine, which persisted 24 h later. The degree of RV impairment correlated with the 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/dtmax and -dP/dtmin, which remained stable for ∼45 min. LV end-diastolic pressures (LVEDP) increased to ≥45 mmHg during the first 10 min and subsequently declined. After 45 min, HR and -dP/dtmin declined, which correlated with gradual elevations in LVEDP (to ∼45 mmHg) as mice approached exhaustion. All parameters rapidly normalized postexercise. Consistent with human studies, our findings demonstrate a disproportionate negative impact of acute exhaustive exercise on RVs that persisted for at least 24 h. We speculate that the differential effects of exhaustive exercise on the ventricles arise from a ∼2-fold greater hemodynamic load in the RV than in LV originating from profound elevations in LVEDPs as mice approach exhaustion.NEW & NOTEWORTHY Acute exhaustive exercise differentially impacts the right ventricle (RV) versus left ventricle (LV), yet the underlying hemodynamic basis remains unclear. Using pressure-volume analyses and pressure-telemetry implantation in mice, we confirmed a marked disproportionate and persistent negative impact of exhaustive exercise on the RV. These differences in responses of the ventricles to exhaustive exercise are of clinical relevance, reflecting ∼2-fold greater hemodynamic RV loads versus LVs arising from massive (∼45 mmHg) increases in LV end-diastolic pressures at exhaustion.