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Aims: Data on sleep at altitude are scant due to the limited availability of polysomnography. Therefore, we investigated whether actigraphy might serve as a simple tool for monitoring sleep during altitude field studies., Methods: Fourteen mountaineers participating in studies on dexamethasone prophylaxis of high altitude pulmonary edema were monitored by actigraphy and polysomnography during 1 night at Zurich (490 m) and 4 nights at the Regina Margherita hut (4559 m). Total sleep time (TST) estimated by actigraphy was compared to polysomnography and subjective sleep quality., Results: In 64 comparisons, mean differences±2SD (bias±limits of agreement) between actigraphy and polysomnography were 5±35 min for TST and 1±7% for sleep efficiency. Correlations between subjective and polysomnographic estimates of sleep efficiency and sleep latency were nonsignificant. Medians of nocturnal oxygen saturation were 96% at 490 m and 74%-81% during nights 1 to 4 at 4459 m (p<0.05 vs. 490 m). Medians of polysomnographic TST were similar at 490 m (451 min) and 4559 m (377-456 min during nights 1 to 4, p=NS) but the proportions of slow wave and REM sleep were reduced and arousals were more common (p<0.05 all instances)., Conclusion: Actigraphy accurately estimates sleep efficiency and duration. Due to its portability and simple use and the potential application over several weeks, it is a convenient tool for investigating altitude effects on sleep during field studies.

Background: Obstructive sleep apnoea (OSA) is highly prevalent and associated with cardiovascular and metabolic changes. OSA is usually diagnosed by polysomnography which is time-consuming and provides little information on the patient's phenotype thus limiting a personalised treatment approach. Exhaled breath contains information on metabolism which can be analysed by mass spectrometry within minutes. The objective of this study was to identify a breath profile in OSA recurrence by use of secondary-electrospray-ionization-mass spectrometry (SESI-MS).Methods: Patients with OSA effectively treated with CPAP were randomised to either withdraw treatment (subtherapeutic CPAP) or continue therapeutic CPAP for 2 weeks. Exhaled breath analysis by untargeted SESI-MS was performed at baseline and 2 weeks after randomisation. The primary outcome was the change in exhaled molecular breath pattern.Results: 30 patients with OSA were randomised and 26 completed the trial according to the protocol. CPAP withdrawal led to a recurrence of OSA (mean difference in change of oxygen desaturation index between groups +30.3/h; 95% CI 19.8/h,40.7/h, p<0.001) which was accompanied by a significant change in 62 exhaled features (16 metabolites identified). The panel of discriminating mass-spectral features allowed differentiation between treated and untreated OSA with a sensitivity of 92.9% and a specificity of 84.6%.Conclusion: Exhaled breath analysis by SESI-MS allows rapid and accurate detection of OSA recurrence. The technique has the potential to characterise an individual's metabolic response to OSA and thus makes a comprehensible phenotyping of OSA possible.Trial Registration Number: NCT02050425 (registered at ClinicalTrials.gov). [ABSTRACT FROM AUTHOR]

Study Objectives: 1) To investigate the impact of acetazolamide, a drug commonly prescribed for altitude sickness, on cortical oscillations in patients with obstructive sleep apnea syndrome (OSAS). 2) To examine alterations in the sleep EEG after short-term discontinuation of continuous positive airway pressure (CPAP) therapy. Design: Data from two double-blind, placebo-controlled randomized cross-over design studies were analyzed. Setting: Polysomnographic recordings in sleep laboratory at 490 m and at moderate altitudes in the Swiss Alps: 1630 or 1860 m and 2590 m. Patients: Study 1: 39 OSAS patients. Study 2: 41 OSAS patients. Interventions: Study 1: OSAS patients withdrawn from treatment with CPAP. Study 2: OSAS patients treated with autoCPAP. Treatment with acetazolamide (500–750 mg) or placebo at moderate altitudes. Measurements and Results: An evening dose of 500 mg acetazolamide reduced slow-wave activity (SWA; approximately 10%) and increased spindle activity (approximately 10%) during non-REM sleep. In addition, alpha activity during wake after lights out was increased. An evening dose of 250 mg did not affect these cortical oscillations. Discontinuation of CPAP therapy revealed a reduction in SWA (5–10%) and increase in beta activity (approximately 25%). Conclusions: The higher evening dose of 500 mg acetazolamide showed the “spectral fingerprint” of Benzodiazepines, while 250 mg acetazolamide had no impact on cortical oscillations. However, both doses had beneficial effects on oxygen saturation and sleep quality. [ABSTRACT FROM AUTHOR]

Background Many patients with the obstructive sleep apnoea syndrome (OSA) travel to the mountains for recreational and professional activities while temporarily discontinuing continuous positive airway pressure (CPAP) treatment. A study was undertaken to evaluate the hypothesis that altitude would aggravate their hypoxaemia, sleep-related breathing disturbances and impair daytime performance. Methods Thirty-four patients with OSA of median age 62 years (IQR 57e65), median apnoea/hypopnoea index (AHI) 47.5 events/h (IQR 32.4e72.8), residing at<600 m were enrolled. A crossover trial randomised for the sequence of altitude exposure was carried out: patients spent 1 day in Zurich (490 m) and 4 days in the Swiss Alps at 1860 m and 2590 m (2 days each) during which continuous positive airway pressure was discontinued. Daily evaluations included polysomnography, symptom questionnaires, physical examination and driving simulator tests. Results Polysomnography revealed median oxygen saturations at 490 m and in the first and second nights at 1860 and 2590 m, respectively, of 94%, 90%, 90%, 86% and 87% (p<0.01 between altitudes). Corresponding median AHI were 47.5, 85.1, 74.6, 90.0 and 90.9 events/h (p<0.01 between altitudes) with ratios of central to obstructive events of 0.1, 0.8, 1.0, 1.9 and 1.9 (p<0.01 between altitudes). Tracking performance during simulated driving was significantly impaired at 2590 m compared with 490 m. Systolic blood pressure and cardiac arrhythmias were increased at altitude. Conclusions Altitude exposure in untreated patients with OSA aggravates hypoxaemia, increases sleeprelated breathing disturbances due to frequent central apnoeas/hypopnoeas, impairs driving simulator performance and induces cardiovascular stress. These findings have implications for counselling and treating patients with OSA planning to travel to high altitude. [ABSTRACT FROM AUTHOR]