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Updated: Nov 25, 2025

Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
Published on: March 15, 2019
Exercise-Induced Cardiac Fatigue after a 45-Minute Bout of High-Intensity Running Exercise Is Not Altered under
Geert Kleinnibbelink1, Arie P J van Dijk2, Alessandro Fornasiero3
1Department of Physiology, Research Institute for Health Sciences, Radboud University Medical Center, Nijmegen, the Netherlands; Department of Cardiology, Research Institute for Health Sciences, Radboud University Medical Center, Nijmegen, the Netherlands; Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.
Background:
Acute exercise promotes transient exercise-induced cardiac fatigue, which affects the right ventricle and to a lesser extent the left ventricle. Hypoxic exposure induces an additional increase in right ventricular (RV) afterload. Therefore, exercise in hypoxia may differently affect both ventricles. The aim of this study was to investigate the acute effects of a bout of high-intensity exercise under hypoxia versus normoxia in healthy individuals on right- and left-sided cardiac function and mechanics.
Methods:
Twenty-one healthy individuals (mean age, 22.2 ± 0.6 years; 14 men) performed 45-min high-intensity running exercise under hypoxia (fraction of inspired oxygen 14.5%) and normoxia (fraction of inspired oxygen 20.9%) in a randomized order. Pre- and post-exercise echocardiography, at rest and during low-to-moderate intensity recumbent exercise ("stress"), was performed to assess RV and left ventricular (LV) cardiac function and mechanics. RV structure, function, and mechanics were assessed using conventional two-dimensional, Doppler, tissue Doppler, speckle-tracking echocardiographic, and novel strain-area loops.
Results:
Indices of RV systolic function (RV fractional area change, Tricuspid annular plane systolic excursion, RV s', and RV free wall strain) and LV function (LV ejection fraction and LV global longitudinal strain) were significantly reduced after high-intensity running exercise (P < .01). These exercise-induced changes were more pronounced when echocardiography was examined during stress compared with baseline. These responses in RV and LV indices were not altered under hypoxia (P > .05).
Conclusions:
There was no impact of hypoxia on the magnitude of exercise-induced cardiac fatigue in the right and left ventricles after a 45-min bout of high-intensity exercise. This finding suggests that any potential increase in loading conditions does not automatically exacerbate exercise-induced cardiac fatigue in this setting.
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