N C Netzer1,2,3, K P Strohl3, J Högel4, H Gatterer5, R Schilz3. 1. Department of Sport Science, Hermann Buhl Institute for Hypoxia and Sleep Medicine Research, University Innsbruck, Bad Aibling, Germany. 2. Division of Sports- and Rehabilitative Medicine, Department of Medicine, University Hospitals Ulm, Ulm, Germany. 3. Pulmonary and Critical Care Division, Department of Medicine, University Hospitals, Case Western Reserve University, Cleveland, OH, USA. 4. Department of Human Genetics, University Hospitals Ulm, Ulm, Germany. 5. Department of Sport Science, University Innsbruck, Innsbruck, Austria.
Abstract
AIM: Acute hypoxia produces acute vasoconstriction in the pulmonary circulation with consequences on right ventricular (RV) structure and function. Previous investigations in healthy humans have been restricted to measurements after altitude acclimatization or were interrupted by normoxia. We hypothesized that immediate changes in RV dimensions in healthy subjects in response to normobaric hypoxia differ without the aforementioned constraints. METHODS: Transthoracic echocardiography was performed in 35 young, healthy subjects exposed to 11% oxygen, as well as six controls under sham hypoxia (20.6% oxygen, single blind) first at normoxia and after 30, 60, 100, 150 min of hypoxia or normoxia respectively. A subgroup of 15 subjects continued with 3-min cycling exercise in hypoxia with subsequent evaluation followed by an assessment 1 min at rest while breathing 4 L min-1 oxygen. RESULTS: During hypoxia, there was a significant linear increase of all RV dimensions (RVD1 + 29 mm, RVD2 + 42 mm, RVD3 + 41 mm, RVOT + 13 mm, RVEDA + 18 mm, P < 0.01) in the exposure group vs. the control group. In response to hypoxia, right ventricular systolic pressure (RVSP) showed a modest increase in hypoxia at rest (+7.3 mmHg, P < 0.01) and increased further with physical effort (+11.8 mmHg, P < 0.01). After 1 min of oxygen at rest, it fell by 50% of the maximum increase. CONCLUSION: Acute changes in RV morphology occur quickly after exposure to normobaric hypoxia. The changes were out of proportion to a relatively low-estimated increase in pulmonary pressure, indicating direct effects on RV structure. The results in healthy subjects are basis for future clinically oriented interventional studies in normobaric hypoxia.
AIM: Acute hypoxia produces acute vasoconstriction in the pulmonary circulation with consequences on right ventricular (RV) structure and function. Previous investigations in healthy humans have been restricted to measurements after altitude acclimatization or were interrupted by normoxia. We hypothesized that immediate changes in RV dimensions in healthy subjects in response to normobaric hypoxia differ without the aforementioned constraints. METHODS: Transthoracic echocardiography was performed in 35 young, healthy subjects exposed to 11% oxygen, as well as six controls under sham hypoxia (20.6% oxygen, single blind) first at normoxia and after 30, 60, 100, 150 min of hypoxia or normoxia respectively. A subgroup of 15 subjects continued with 3-min cycling exercise in hypoxia with subsequent evaluation followed by an assessment 1 min at rest while breathing 4 L min-1oxygen. RESULTS: During hypoxia, there was a significant linear increase of all RV dimensions (RVD1 + 29 mm, RVD2 + 42 mm, RVD3 + 41 mm, RVOT + 13 mm, RVEDA + 18 mm, P < 0.01) in the exposure group vs. the control group. In response to hypoxia, right ventricular systolic pressure (RVSP) showed a modest increase in hypoxia at rest (+7.3 mmHg, P < 0.01) and increased further with physical effort (+11.8 mmHg, P < 0.01). After 1 min of oxygen at rest, it fell by 50% of the maximum increase. CONCLUSION: Acute changes in RV morphology occur quickly after exposure to normobaric hypoxia. The changes were out of proportion to a relatively low-estimated increase in pulmonary pressure, indicating direct effects on RV structure. The results in healthy subjects are basis for future clinically oriented interventional studies in normobaric hypoxia.
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