Daily chronic intermittend hypobaric hypoxia does not induce chronic increase in pulmonary arterial pressure

Background: Acute exposure to high-altitude increases pulmonary arterial pressure by hypoxic pulmonary vasoconstriction. Chronic hypoxia causes pulmonary vascular remodeling resulting in persistently increased pulmonary arterial pressures even after return to normoxia. Recently, interest in chronic intermittent hypobaric hypoxia (CIHH) was raised because it occurs in subjects working at high-altitude but living in lowland. However, effects of daily CIHH on pulmonary arterial pressure at rest and exercise are unknown. Methods: We studied 8 (4 men and 4 women) healthy subjects working at 2600 m each workday for 8 – 9h while living and sleeping at lowland and 8 matched control subjects living and working at lowland. Baseline measurements including pulmonary function tests, echocardiography, blood gas analysis and blood laboratory workup were performed at lowland Munich (530 m asl). Further, subjects underwent echocardiography and blood gas analysis at rest and during exercise at high-altitude (Umweltforschungsstation Schneefernerhaus, Zugspitze, 2600 m asl). Results: Baseline characteristics including age, sex, BMI, physical activity and pre-existing medical conditions were similar in both groups. Baseline PFTs were normal in all subjects. Hemoglobin was significantly higher in CIHH compared to controls. Echography at lowland showed normal right and left cardiac dimensions and function and absence of cardiac disease in all subjects. Right heart function as measured by TAPSE was similar in both groups. Resting BGA at lowland as well as at high-altitude revealed significantly decreased pCO2 in CIHH compared to controls. sPAP at rest did not significantly differ, however it was not measurable in some subjects due to lack of TI. During exercise sPAP was significantly lower in CIHH subjects compared to controls while SpO2 was significantly higher. Endothelin-1 levels were increased at high-altitude compared to lowland, however there were no significant differences between the groups. Conclusions: In subjects exposed to CIHH there were no signs of pulmonary vascular remodeling. Interestingly, sPAP at altitude under exertion was significantly lower in CIHH subjects than in controls. This might be explained by increased hyperventilation as mechanism of adaptation to CIHH.