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SLAPNEA

Maladaptive consequences of nocturnal periodic breathing at high altitude

Humans sleeping at high altitude (HA) commonly experience periodic breathing (PB), characterized by apneas alternating with periods of hyperventilation. PB is a consequence of the increased pulmonary ventilation at HA, which reduces arterial CO2 tension (PaCO2) towards the apneic threshold. During sleep, a small further PaCO2 reduction triggers an apnea, followed by an exaggerated hyperventilation that reverts PaCO2 below the apneic threshold and initiates the next apnea.
We aim to investigate whether PB contributes to maladaptive responses to HA that are currently incompletely understood, namely activation of the sympathetic nervous system, acute mountain sickness, and deterioration of sleep quality.

Project duration: August 2020 - December 2022
Project status:
Funding:
Public institutions (Other projects /Project)
Institutes: Institute of Mountain Emergency Medicine, terraXcube

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Credit: Eurac Research | Annelie Bortolotti

Scientific Publications

Journal article2025

Sympathetic transduction to blood pressure following a three-day sojourn in hypobaric hypoxia: influence of nocturnal periodic breathing

Fisher F, Roche J, Duffy A, Ibrahim A, Turner R, Vinetti G, Cesari M, Furian M,

Rachel Turner, Giovanni Vinetti, Hannes Gatterer, Christoph Siebenmann

The vascular responsiveness to sympathetic nerve activity (i.e., sympathetic transduction) is preserved with acute hypoxia but diminishes with acclimation to chronic hypoxia. However, it is unclear whether such reductions in sympathetic transduction are already present after three days, which would be a typical time for recreational mountaineers to be at high altitude. Furthermore, the mechanisms for the reduced sympathetic transduction with chronic hypoxia are unclear but could relate to the nocturnal periodic breathing (nPB) that characterizes sleep in hypoxia since, at sea level, sleep-disordered breathing is also associated with blunted sympathetic transduction. Using a randomized, placebo-controlled, cross-over protocol, we thus explored whether nPB diminishes sympathetic transduction during a three-day sojourn in hypoxia. In twelve young, healthy males, muscle sympathetic nerve activity (MSNA; microneurography) and beat-to-beat blood pressure (finger photoplethysmography) were measured first in normoxia, and then at the end of two three-day sojourns in hypobaric hypoxia (equivalent to 4,000m altitude), where nPB was either allowed to occur (PB+) or prevented by increased inspiratory carbon dioxide (PB-). Sympathetic transduction was quantified using burst-triggered signal-averaging, where the mean arterial pressure (MAP) response to a MSNA burst was tracked over 15 cardiac cycles. At the end of the nPB+ and nPB- sojourns, MSNA burst frequency was increased by 118±103% and 107±101%, respectively, with no difference between sojourns (p≥0.80). The transient increase in MAP following a sympathetic burst was not different between measurement time points (peak +2.8±2.2, +2.8±2.0 and +3.3±2.3 mmHg, for normoxia, nPB+ and nPB-, respectively; p=0.208). Conversely, the transient decrease in MAP following cardiac cycles without a sympathetic burst tended to be similarly increased at the end of nPB+ and nPB- sojourns compared to normoxia (nadir -1.3±0.6, -2.0±0.9 and -2.3±1.6 mmHg, for normoxia, nPB+ and nPB- respectively; p=0.051). In summary, three days exposure to hypobaric hypoxia did not diminish the pressor response following a spontaneous MSNA burst, regardless of the severity of nPB. The larger drop in MAP following cardiac cycles without a sympathetic burst, however, suggests that hypoxia increases the importance of the sympathetic vasoconstrictor support of beat-to-beat MAP.

DOI

DOI: 10.1152/physiol.2025.40.S1.0665

Journal article2024

Effects of periodic breathing on sleep at high altitude: a randomized, placebo-controlled, crossover study using inspiratory CO2

Ibrahim A, Stefani A, Cesari M, Roche J, Gatterer H, Holzknecht E, Turner R, Vinetti G,

Rachel Turner, Giovanni Vinetti, Hannes Gatterer, Christoph Siebenmann

Hypoxia at high altitude facilitates changes in ventilatory control that can lead to nocturnal periodic breathing (nPB). Here, we introduce a placebo-controlled approach to prevent nPB by increasing inspiratory CO2 and used it to assess whether nPB contributes to the adverse effects of hypoxia on sleep architecture. In a randomized, single-blinded, crossover design, 12 men underwent two sojourns (three days/nights each, separated by 4 weeks) in hypobaric hypoxia corresponding to 4000 m altitude, with polysomnography during the first and third night of each sojourn. During all nights, subjects' heads were encompassed by a canopy retaining exhaled CO2 , and CO2 concentration in the canopy (i.e. inspiratory CO2 concentration) was controlled by adjustment of fresh air inflow. Throughout the placebo sojourn inspiratory CO2 was ≤0.2%, whereas throughout the other sojourn it was increased to 1.76% (IQR, 1.07%-2.44%). During the placebo sojourn, total sleep time (TST) with nPB was 54.3% (37.4%-80.8%) and 45.0% (24.5%-56.5%) during the first and the third night, respectively (P = 0.042). Increased inspiratory CO2 reduced TST with nPB by an absolute 38.1% (28.1%-48.1%), the apnoea-hypopnoea index by 58.1/h (40.1-76.1/h), and oxygen desaturation index ≥3% by 56.0/h (38.9.1-73.2/h) (all P < 0.001), whereas it increased the mean arterial oxygen saturation in TST by 2.0% (0.4%-3.5%, P = 0.035). Increased inspiratory CO2 slightly increased the percentage of N3 sleep during the third night (P = 0.045), without other effects on sleep architecture. Increasing inspiratory CO2 effectively prevented hypoxia-induced nPB without affecting sleep macro-architecture, indicating that nPB does not explain the sleep deterioration commonly observed at high altitudes. KEY POINTS: Periodic breathing is common during sleep at high altitude, and it is unclear how this affects sleep architecture. We developed a placebo-controlled approach to prevent nocturnal periodic breathing (nPB) with inspiratory CO2 administration and used it to assess the effects of nPB on sleep in hypobaric hypoxia. Nocturnal periodic breathing was effectively mitigated by an increased inspiratory CO2 fraction in a blinded manner. Prevention of nPB did not lead to relevant changes in sleep architecture in hypobaric hypoxia. We conclude that nPB does not explain the deterioration in sleep architecture commonly observed at high altitude.

DOI

DOI: 10.1113/JP285397

All Publications

Effects of nocturnal periodic breathing on sympathetic nerve activity and ventilatory control at high altitude: a randomised, crossover study
Roche J, Fisher JP, Rasmussen P, Ibrahim A, Ainslie PN, Turner R, Vinetti G, Cesari M, Furian M, Stefani A, Netzer N, Gatterer H, Högl B, Siebenmann C (2025)
Journal article
The Journal of Physiology

https://doi.org/10.1113/JP288700

Sympathetic transduction to blood pressure following a three-day sojourn in hypobaric hypoxia: influence of nocturnal periodic breathing
Fisher F, Roche J, Duffy A, Ibrahim A, Turner R, Vinetti G, Cesari M, Furian M, Stefani A, Gatterer H, Högl B, Siebenmann C (2025)
Journal article
Physiology

https://doi.org/10.1152/physiol.2025.40.S1.0665

Effects of periodic breathing on sleep at high altitude: a randomized, placebo-controlled, crossover study using inspiratory CO2
Ibrahim A, Stefani A, Cesari M, Roche J, Gatterer H, Holzknecht E, Turner R, Vinetti G, Furian M, Heidbreder A, Högl B, Siebenmann C (2024)
Journal article
The Journal of Physiology

https://doi.org/10.1113/JP285397

Our partners

Medical University Innsbruck, Universitätsklinik für Neurologie

Project Team

Christoph Siebenmann

Rachel Turner

Diane Martinelli

Giovanni Vinetti

Miriam Gottardi

Hannes Gatterer

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Journal article2025

Sympathetic transduction to blood pressure following a three-day sojourn in hypobaric hypoxia: influence of nocturnal periodic breathing

Fisher F, Roche J, Duffy A, Ibrahim A, Turner R, Vinetti G, Cesari M, Furian M,

Rachel Turner, Giovanni Vinetti, Hannes Gatterer, Christoph Siebenmann

DOI

DOI: 10.1152/physiol.2025.40.S1.0665

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