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Clinical Trial
. 2007 Sep;30(9):1195-203.
doi: 10.1093/sleep/30.9.1195.

Nocturnal hypoxia exposure with simulated altitude for 14 days does not significantly alter working memory or vigilance in humans

Affiliations
Clinical Trial

Nocturnal hypoxia exposure with simulated altitude for 14 days does not significantly alter working memory or vigilance in humans

Robert Joseph Thomas et al. Sleep. 2007 Sep.

Abstract

Study objectives: To assess the effect of 2 weeks of nocturnal hypoxia exposure using simulated altitude on attention and working memory in healthy adult humans.

Design: Prospective experimental physiological assessment.

Setting: General Clinical Research Center.

Participants: Eleven healthy, nonsmoking, subjects (7 men, 4 women). The subjects had a mean age of 27 +/- 1.5 years and body mass index of 23 +/- 0.9 kg/m2.

Interventions: Subjects were exposed to 9 hours of continuous hypoxia from 2200 to 0700 hours in an altitude tent. Acclimatization was accomplished by graded increases in "altitude" over 3 nights (7700, 10,000 and 13,000 feet), followed by 13,000 feet for 13 consecutive days (FIO2 0.13).

Measurements and results: Polysomnography that included airflow measurements with a nasal cannula were done at baseline and during 3 time points across the protocol (nights 3, 7, and 14). Attention (10-minute Psychomotor Vigilance Task) and working memory (10-minute verbal 2-back) were assessed at baseline and on day 4, 8, 9, and 15. Nocturnal hypoxia was documented using endpoints of minimum oxygen saturation, oxygen desaturation index, and percentage of total sleep time under 90% and 80%. Total sleep time was reduced, stage 1 sleep was increased, and both obstructive and nonobstructive respiratory events were induced by altitude exposure. There was no difference in subjective mood, attention, or working memory.

Conclusions: Two weeks of nocturnal continuous hypoxia in an altitude tent did not induce subjective sleepiness or impair objective vigilance and working memory. Caution is recommended in the extrapolation to humans the effects of hypoxia in animal models.

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Figures

Figure 1
Figure 1
Hypoxia with periodic breathing, unstable non-rapid eye movement (NREM) sleep. A 25-year old woman after 2 weeks of exposure to 13,000 feet altitude for 2 weeks shows short cycle periodic breathing (20–25 seconds) in this 120-second snapshot from Stage 2 sleep. Saturations fluctuate between 89% and 81%. Small cardiogenic oscillations can be seen on the flow and effort traces, suggesting that the airway was open during the apnea. The traces from the top of the figure are electroencephalogram (EEG) channels C4-A1, C3-A2, O2-A1, O1-A2 (50 μV between lighter horizontal lines), right and left electrooculogram (EOG), mentalis electromyogram (EMG), nasal pressure (Pres), computed flow from the pressure signal (Flow), thoracic (Thor) and abdominal (Abd) effort with piezo-bands, electrocardiogram (ECG), joined (right and left) tibialis anterior electromyogram (Tib), and finger pulse oximetry (Ox).
Figure 2
Figure 2
Hypoxia without periodic breathing, stable non-rapid eye movement (NREM) sleep. The same subject, traces, and screen compression as in Figure 1 during stable stage 2 NREM sleep, showing an absence of respiratory events. There is minimal flow limitation and no arousals; oxygen saturation is 84%-83%. The traces from the top of the figure are electroencephalogram (EEG) channels C4-A1, C3-A2, O2-A1, O1-A2 (50 μV between lighter horizontal lines), right and left electrooculogram (EOG), mentalis electromyogram (EMG), nasal pressure (Pres), computed flow from the pressure signal (Flow), thoracic (Thor) and abdominal (Abd) effort with piezo-bands, electrocardiogram (ECG), joined (right and left) tibialis anterior electromyogram (Tib), and finger pulse oximetry (Ox).
Figure 3
Figure 3
Hypoxia without periodic breathing, rapid eye movement (REM) sleep. The same subject, traces, and screen compression as in Figure 1 during REM sleep, showing an absence of respiratory events. Altitude-induced periodic breathing is minimal or mildest during REM sleep. There is minimal flow limitation, especially during phasic REM sleep and no arousals; oxygen saturation fluctuates from 87% to 83%, probably secondary to tidal volume changes typical of REM sleep. The traces from the top of the figure are electroencephalogram (EEG) channels C4-A1, C3-A2, O2-A1, O1-A2 (50 μV between lighter horizontal lines), right and left electrooculogram (EOG), mentalis electromyogram (EMG), nasal pressure (Pres), computed flow from the pressure signal (Flow), thoracic (Thor) and abdominal (Abd) effort with piezo-bands, electrocardiogram (ECG), joined (right and left) tibialis anterior electromyogram (Tib), and finger pulse oximetry (Ox).

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