Right ventricular performance during acute hypoxic exercise.
Lindsay M Forbes, Todd M Bull, Tim Lahm, Tyler Sisson, Katie O'Gean, Justin S Lawley, Kendall Hunter, Benjamin D Levine, Andrew Lovering, Robert C Roach, Andrew W Subudhi, William K Cornwell
Author Information
Lindsay M Forbes: Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado, Aurora, CO, USA.
Todd M Bull: Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado, Aurora, CO, USA.
Tim Lahm: Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado, Aurora, CO, USA.
Tyler Sisson: Clinical Translational Research Center, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Katie O'Gean: Clinical Translational Research Center, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Justin S Lawley: Department of Sport Science, University of Innsbruck, Innsbruck, Austria. ORCID
Kendall Hunter: Department of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Benjamin D Levine: Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, TX, USA. ORCID
Andrew Lovering: Department of Physiology, University of Oregon, Eugene, OR, USA. ORCID
Robert C Roach: Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado, Aurora, CO, USA.
Andrew W Subudhi: Department of Physiology, University of Colorado, Colorado Springs, CO, USA.
William K Cornwell: Clinical Translational Research Center, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Acute hypoxia increases pulmonary arterial (PA) pressures, though its effect on right ventricular (RV) function is controversial. The objective of this study was to characterize exertional RV performance during acute hypoxia. Ten healthy participants (34 ± 10 years, 7 males) completed three visits: visits 1 and 2 included non-invasive normoxic (fraction of inspired oxygen ( ) = 0.21) and isobaric hypoxic ( = 0.12) cardiopulmonary exercise testing (CPET) to determine normoxic/hypoxic maximal oxygen uptake ( ). Visit 3 involved invasive haemodynamic assessments where participants were randomized 1:1 to either Swan-Ganz or conductance catheterization to quantify RV performance via pressure-volume analysis. Arterial oxygen saturation was determined by blood gas analysis from radial arterial catheterization. During visit 3, participants completed invasive submaximal CPET testing at 50% normoxic and again at 50% hypoxic ( = 0.12). Median (interquartile range) values for non-invasive values during normoxic and hypoxic testing were 2.98 (2.43, 3.66) l/min and 1.84 (1.62, 2.25) l/min, respectively (P < 0.0001). Mean PA pressure increased significantly when transitioning from rest to submaximal exercise during normoxic and hypoxic conditions (P = 0.0014). Metrics of RV contractility including preload recruitable stroke work, dP/dt, and end-systolic pressure increased significantly during the transition from rest to exercise under normoxic and hypoxic conditions. Ventricular-arterial coupling was maintained during normoxic exercise at 50% . During submaximal exercise at 50% of hypoxic , ventricular-arterial coupling declined but remained within normal limits. In conclusion, resting and exertional RV functions are preserved in response to acute exposure to hypoxia at an = 0.12 and the associated increase in PA pressures. KEY POINTS: The healthy right ventricle augments contractility, lusitropy and energetics during periods of increased metabolic demand (e.g. exercise) in acute hypoxic conditions. During submaximal exercise, ventricular-arterial coupling decreases but remains within normal limits, ensuring that cardiac output and systemic perfusion are maintained. These data describe right ventricular physiological responses during submaximal exercise under conditions of acute hypoxia, such as occurs during exposure to high altitude and/or acute hypoxic respiratory failure.
