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 ([Formula: see text]), end-tidal partial pressure of CO<sub>2</sub> ([Formula: see text]), 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<sup>-1</sup>) than placebo (6 [3, 13] h<sup>-1</sup>, <i>P</i> = 0.02). At 3,000 m, [Formula: see text] was higher after intervention (88 ± 2%) than placebo (87 ± 2%, <i>P</i> = 0.03), [Formula: see text] was lower after intervention (34 ± 3 mmHg) than placebo (36 ± 3 mmHg, <i>P</i> = 0.002), cTSI decrease was smaller after intervention (-3.6 ± 2.2%) than placebo (-6.5 ± 3.1%, <i>P</i> = 0.02), and PASP was higher after intervention (30 ± 8 mmHg) than after placebo (28 ± 7 mmHg, <i>P</i> = 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.<b>NEW & NOTEWORTHY</b> We found that a single night spent at simulated moderate altitude (1,900 m) prompts measurable ventilatory acclimatization when ascending to simulated high altitude (3,000 m) in males with coronary artery disease. We also found that, although sleeping at 1,900 m increases the occurrence of apneas and/or hypopneas, this did not modify heart rate variability and baroreflex sensitivity responses at 3,000 m.

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Journal
Journal of Applied Physiology
Published
2025-12-27
DOI
https://doi.org/10.1152/japplphysiol.00416.2025
Primary Topic
High Altitude and Hypoxia
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article
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article

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

Michela Masè, Giacomo Strapazzon, G Parati, Grzegorz Bilo et al.
Journal of Applied Physiology
High Altitude and Hypoxia
article

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

Michela Masè, Giacomo Strapazzon, G Parati, Grzegorz Bilo, Giovanni Vinetti, Anna Taboni, Johanna Roche, Hannes Gatterer, Rachel Turner, Carolina Lombardi
article en

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 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 ([Formula: see text]), end-tidal partial pressure of CO<sub>2</sub> ([Formula: see text]), 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<sup>-1</sup>) than placebo (6 [3, 13] h<sup>-1</sup>, <i>P</i> = 0.02). At 3,000 m, [Formula: see text] was higher after intervention (88 ± 2%) than placebo (87 ± 2%, <i>P</i> = 0.03), [Formula: see text] was lower after intervention (34 ± 3 mmHg) than placebo (36 ± 3 mmHg, <i>P</i> = 0.002), cTSI decrease was smaller after intervention (-3.6 ± 2.2%) than placebo (-6.5 ± 3.1%, <i>P</i> = 0.02), and PASP was higher after intervention (30 ± 8 mmHg) than after placebo (28 ± 7 mmHg, <i>P</i> = 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.<b>NEW & NOTEWORTHY</b> We found that a single night spent at simulated moderate altitude (1,900 m) prompts measurable ventilatory acclimatization when ascending to simulated high altitude (3,000 m) in males with coronary artery disease. We also found that, although sleeping at 1,900 m increases the occurrence of apneas and/or hypopneas, this did not modify heart rate variability and baroreflex sensitivity responses at 3,000 m.

Journal of Applied PhysiologyVol. 140(2)
Eurac Research (IT), University of Padua (IT), University of Trento (IT), Brescia University (US), Institute of Mountain Emergency Medicine (IT), University Hospital of Zurich (CH), IRCCS Istituto Auxologico Italiano (IT), Istituti di Ricovero e Cura a Carattere Scientifico (IT), University of Milano-Bicocca (IT), University of Brescia (IT)
Openalex Percentile: Top 25%
High Altitude and Hypoxia
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