Altitude and Sleep Quality: Hypoxia, Periodic Breathing, and Acclimatization
Altitude above 2,500 m disrupts sleep architecture via hypoxia-driven periodic breathing (Cheyne-Stokes respiration); SWS decreases up to 40% and arousals double within the first 2 nights at 3,500 m.
| Measure | Value | Unit | Notes |
|---|---|---|---|
| Altitude threshold for sleep disruption | 2,500 | m elevation | Below this, most people sleep normally; periodic breathing onset above this altitude |
| SpO2 at 3,500 m during sleep | 85–90 | % saturation | Compared to ~97% at sea level; triggers hypoxic ventilatory response |
| SWS reduction at 3,500 m (first 2 nights) | 40 | % decrease | Reite et al.; slow-wave sleep most suppressed by altitude-related arousals |
| Prevalence of periodic breathing at 3,500–4,000 m | 25–50 | % of sleepers | Cheyne-Stokes variant; higher loop gain in hypoxic environment |
| Acetazolamide efficacy (AMS/sleep) | Significant | improvement | 250 mg twice daily reduces periodic breathing and improves SpO2 during sleep |
Altitude Hypoxia and Sleep Architecture
Above 2,500 m, reduced atmospheric oxygen pressure (PaO2) begins to destabilize the respiratory control system during sleep. The core mechanism is increased loop gain: the respiratory control system overreacts to CO2 fluctuations because the hypoxic chemoreceptor drive amplifies the feedback signal.
The consequence is periodic breathing — rhythmic alternation between hyperpnea and apnea lasting 15–40 seconds per cycle. Each apneic pause ends with arousal or lighter sleep stage, preventing deep sleep consolidation.
Cheyne-Stokes Respiration at Altitude
Cheyne-Stokes respiration (CSR) at altitude differs from its cardiac-failure variant:
| Feature | Altitude CSR | Cardiac-failure CSR |
|---|---|---|
| Cause | Hypocapnia from hypoxic hyperventilation | Pulmonary congestion + circulatory delay |
| Loop gain | High due to hypoxia | High due to long circulation time |
| SpO2 nadir | 75–85% at cycle end | Variable |
| Altitude-specific | Yes | No |
Effect on Sleep Architecture
Research from Reite et al. (1975) and subsequent polysomnographic studies document:
- SWS reduction: Up to 40% less N3 on first 2 nights at 3,500 m
- REM suppression: Altitude-naive subjects spend less time in REM on nights 1–2
- Arousal index: 2–3× higher than sea level baseline
- Sleep efficiency: Falls from ~92% to 70–80% on first nights
By night 4–7 (acclimatization), most metrics partially normalize. SWS and REM recover faster than periodic breathing frequency.
Pharmacological Interventions
Acetazolamide (Diamox): Carbonic anhydrase inhibitor. Creates metabolic acidosis, stimulating ventilation, raising baseline CO2, and stabilizing the respiratory rhythm. Standard dose 125–250 mg twice daily. Reduces AMS symptoms and measurably improves SpO2 during sleep. Most evidence-based pharmacological intervention for altitude sleep disruption.
Temazepam / Zolpidem: Blunt arousals but do not address underlying hypoxia. Used by some expeditions but carry risk of respiratory depression at extreme altitude (>5,000 m). Not recommended above 4,000 m without careful monitoring.
Practical Ascent Strategy
Evidence from Bloch et al. (2010) and wilderness medicine guidelines:
- Limit sleeping altitude gains to 300–500 m/day above 3,000 m
- Rest day every 3rd day (“climb high, sleep low”)
- Avoid alcohol and sedatives first 2 nights at new altitude
- Consider prophylactic acetazolamide for rapid ascents (e.g., Kilimanjaro, Aconcagua)
Related Pages
Sources
- Khoo MC et al. — Factors inducing periodic breathing in humans: a general model. J Appl Physiol (1982)
- Reite M et al. — Sleep at high altitude: disturbed nocturnal ventilation and sleep at high altitude. Arch Intern Med (1975)
- Bloch KE et al. — Effect of ascent protocol on acute mountain sickness and sleep quality at high altitude. J Appl Physiol (2010)
- Burgess KR & Ainslie PN — Central sleep apnea at high altitude. Adv Exp Med Biol (2016)
Frequently Asked Questions
Why does altitude disrupt sleep so severely?
Altitude reduces atmospheric oxygen partial pressure (PaO2). The hypoxic ventilatory response drives hyperventilation, which lowers CO2 (hypocapnia). Since CO2 is the primary driver of the respiratory rhythm, lowered CO2 causes breathing to pause (apnea). When apnea triggers CO2 to rise again, breathing resumes — producing the characteristic crescendo-decrescendo pattern of Cheyne-Stokes respiration. Each cycle (15–30 s) causes partial arousal, fragmenting sleep. The brain's chemoreceptor loop gain is higher in hypoxia, making this instability worse.
Does acclimatization improve sleep quality at altitude?
Yes, significantly. By night 4–7 at a given altitude, most people show substantial improvement: fewer arousals, less periodic breathing, improved SpO2, and partial recovery of SWS. Acclimatization involves erythropoietin-driven increase in red cell mass, rightward shift of the oxygen-hemoglobin dissociation curve, and blunting of the chemoreceptor hypersensitivity. Gradual ascent (gain no more than 300–500 m of sleeping altitude per day above 3,000 m) prevents the worst disruption.