One night at 1,900 m prompts ventilatory acclimatization without altering cardiac autonomic regulation at 3,000 m in males with coronary artery disease

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 1,900 m (intervention) or in control conditions (250 m, placebo) before being decompressed to 3,000 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 before the overnight stay (at 250 m) and after the simulated ascent to 3,000 m. The intervention night was associated with a greater number of apneas/hypopneas (33 [9, 51] h-1) than placebo (6 [3, 13] h-1, P = 0.02). At 3,000 m, SpO2 was higher after intervention (88 ± 2%) than placebo (87 ± 2%, P = 0.03), PETCO2 was lower after intervention (34 ± 3 mmHg) than placebo (36 ± 3 mmHg, P = 0.002), cTSI decrease was smaller after intervention (-3.6 ± 2.2%) than placebo (-6.5 ± 3.1%, P = 0.02), and PASP was higher after intervention (30 ± 8 mmHg) than after placebo (28 ± 7 mmHg, P = 0.04), whereas BRS and HRV indices showed no differences. We conclude that a single night at 1,900 m is sufficient to trigger measurable ventilatory acclimatization in persons with CAD without altering BRS and HRV at 3,000 m, but likely enhancing pulmonary hypoxic vasoconstriction.