Abstract
Spending a single night at moderate altitude before ascending to high altitude may enhance ventilatory acclimatization but also exacerbate sympathetic activation, a response that should be carefully pondered in persons with coronary artery disease (CAD). Ten males with CAD participated in this randomized placebo-controlled crossover trial in a hypobaric chamber where they slept either at simulated 1900 m (intervention) or in control conditions (250 m, placebo) before being decompressed to 3000 m the following morning. Respiratory polygraphy was performed each night. Peripheral oxygen saturation (SpO2), end-tidal partial pressure of CO2 (PetCO2), cerebral tissue oxygen saturation index (cTSI), baroreflex sensitivity (BRS), heart rate variability (HRV), and pulmonary artery systolic pressure (PASP) were recorded during wakeful rest each morning, both prior to the overnight stay (at 250 m) and after the simulated ascent to 3000 m. The intervention night was associated with a greater number of apneas/hypopneas (32.6 [8.8, 51.4] h-1) than placebo (5.8 [2.7, 13.4] h-1, p=0.0216). At 3000 m, SpO2 was higher after intervention (88±2%) than placebo (87±2%, p=0.0279), PetCO2 was lower after intervention (34±3 mmHg) than placebo (36±3 mmHg, p=0.0022), cTSI decrease was smaller after intervention (-3.6±2.2%) than placebo (-6.5±3.1%, p=0.0192), PASP was higher after intervention (30±8 mmHg) than after placebo (28±7 mmHg, p=0.0413), whereas BRS and HRV indices showed no differences. We conclude that a single night at 1900 m is sufficient to trigger measurable ventilatory acclimatization in persons with CAD without altering BRS and HRV at 3000 m, but likely enhancing pulmonary hypoxic vasoconstriction.