5 research outputs found
Sleep disturbance at simulated altitude indicated by stratified respiratory disturbance index but not hypoxic ventilatory response
At high altitudes, the clinically defined respiratory disturbance index (RDI) and high hypoxic ventilatory response (HVR) have been associated with diminished sleep quality. Increased RDI has also been observed in some athletes sleeping at simulated moderate altitude. In this study, we investigated relationships between the HVR of 14 trained male endurance cyclists with variable RDI and sleep quality responses to simulated moderate altitude. Blood oxygen saturation (SpO(2)%), heart rate, RDI, arousal rate, awakenings, sleep efficiency, rapid eye movement ( REM) sleep, non-REM sleep stages 1, 2 and slow wave sleep as percentages of total sleep time(% TST) were measured for two nights at normoxia of 600 m and one night at a simulated altitude of 2,650 m. HVR and RDI were not significantly correlated with sleep stage, arousal rate or awakening response to nocturnal simulated altitude. SpO(2) was inversely correlated with total RDI (r=-0.69, P=0.004) at simulated altitude and with the change in arousal rate from normoxia (r=-0.65, P=0.02). REM sleep response to simulated altitude correlated with the change, relative to normoxia, in arousal (r=-0.63, P=0.04) and heart rate (r=-0.61, P=0.04). When stratified, those athletes at altitude with RDI > 20 h(-1) (n=4) and those with < 10 h(-1) (n=10) exhibited no difference in HVR but the former had larger falls in SpO(2) (P=0.05) and more arousals (P=0.03). Neither RDI ( without strati. cation) nor HVR were sufficiently sensitive to explain any deterioration in REM sleep or arousal increase. However, the stratified RDI provides a basis for determining potential sleep disturbance in athletes at simulated moderate altitude
Quantitative changes in the sleep EEG at moderate altitude (1630 m and 2590 m)
BACKGROUND: Previous studies have observed an altitude-dependent increase in central apneas and a shift towards lighter sleep at altitudes >4000 m. Whether altitude-dependent changes in the sleep EEG are also prevalent at moderate altitudes of 1600 m and 2600 m remains largely unknown. Furthermore, the relationship between sleep EEG variables and central apneas and oxygen saturation are of great interest to understand the impact of hypoxia at moderate altitude on sleep.
METHODS: Fourty-four healthy men (mean age 25.0±5.5 years) underwent polysomnographic recordings during a baseline night at 490 m and four consecutive nights at 1630 m and 2590 m (two nights each) in a randomized cross-over design.
RESULTS: Comparison of sleep EEG power density spectra of frontal (F3A2) and central (C3A2) derivations at altitudes compared to baseline revealed that slow-wave activity (SWA, 0.8-4.6 Hz) in non-REM sleep was reduced in an altitude-dependent manner (∼4% at 1630 m and 15% at 2590 m), while theta activity (4.6-8 Hz) was reduced only at the highest altitude (10% at 2590 m). In addition, spindle peak height and frequency showed a modest increase in the second night at 2590 m. SWA and theta activity were also reduced in REM sleep. Correlations between spectral power and central apnea/hypopnea index (AHI), oxygen desaturation index (ODI), and oxygen saturation revealed that distinct frequency bands were correlated with oxygen saturation (6.4-8 Hz and 13-14.4 Hz) and breathing variables (AHI, ODI; 0.8-4.6 Hz).
CONCLUSIONS: The correlation between SWA and AHI/ODI suggests that respiratory disturbances contribute to the reduction in SWA at altitude. Since SWA is a marker of sleep homeostasis, this might be indicative of an inability to efficiently dissipate sleep pressure