Impact of modulating pulmonary artery pressure on resting right ventricular function in endurance-trained and untrained individuals

Abstract

Prolonged endurance training is associated with critical adaptations to right ventricular (RV) structure and function that facilitate the achievement of higher exercise capacity, peak cardiac output, and RV stroke volume in the face of large increases in pulmonary artery pressures (afterload) and RV wall stress. Compared to the left ventricle, the RV is more sensitive to increases in afterload during exercise. However, the independent effect of increased afterload on RV function in endurance trained (Trained) vs untrained individuals remain unknown. Trained were considered those with a maximal oxygen consumption ( V̇O2max) >60ml/kg/min (male) or >55ml/kg/min (female) while untrained were defined as V̇O2max <45ml/kg/min. Using echocardiography, this retrospective study sought to evaluate RV systolic function (RV global longitudinal strain [GLS]) and ventriculo-arterial coupling (ratio of RV GLS to pulmonary artery systolic pressure [PASP]) in Trained and untrained individuals while manipulating PASP. Ten participants (5 Trained and 5 Untrained) underwent resting echocardiography while breathing moderate (pressure of inspired oxygen; PiO2=89 mmHg) and severe hypoxia (PiO2=79 mmHg; order randomized) to increase PASP. Separately, eight participants (4 Trained and 4 untrained) inhaled nitric oxide (iNO; 40ppm) during echocardiography to lower PASP. Moderate and severe hypoxia increased PASP by 2.3 ± 1.3mmHg and 3.5 ± 1.8mmHg, respectively, while iNO decreased PASP by 2.6 ± 2.4mmHg, with no between group differences observed. Cardiac output was not different between any condition. A fitness-by-hypoxia interaction was observed in RV GLS in moderate hypoxia suggesting Trained had lower RV function during moderate hypoxia as compared to untrained (Untrained: -23.1 ± 4.4% vs. Trained: -20.2 ± 2.7%; p<0.01). No differences in RV GLS were observed with iNO (p=0.98). The ratio of RV GLS to PASP was significantly different between groups at moderate hypoxia (Untrained: -1.06 ± 0.09%/mmHg vs. Trained: -0.85 ± 0.12%/mmHg; p=0.04) but not severe hypoxia (p=0.78). These findings suggest reducing PASP did not alter RV function or ventriculo-arterial coupling, however, Trained individuals experienced differential RV function responses when PASP is experimentally increased with hypoxia. Natural Sciences and Engineering Research Council of Canada. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.