Effects of acute hypoxia on heart rate variability, sample entropy and cardiorespiratory phase synchronization

Abstract

Background: Investigating the responses of autonomic nervous system (ANS) in hypoxia may provide some knowledge about the mechanism of neural control and rhythmic adjustment. The integrated cardiac and respiratory system display complicated dynamics that are affected by intrinsic feedback mechanisms controlling their interaction. To probe how the cardiac and respiratory system adjust their rhythms in different simulated altitudes, we studied heart rate variability (HRV) in frequency domain, the complexity of heartbeat series and cardiorespiratory phase synchronization (CRPS) between heartbeat intervals and respiratory cycles.

Methods: In this study, twelve male subjects were exposed to simulated altitude of sea level, 3000 m and 4000 m in a hypobaric chamber. HRV was assessed by power spectral analysis. The complexity of heartbeat series was quantified by sample entropy (SampEn). CRPS was determined by cardiorespiratory synchrogram.

Results: The power spectral HRV indices at all frequency bands depressed according to the increase of altitude. The SampEn of heartbeat series increased significantly with the altitude (P < 0.01). The duration of CRPS epochs at 3000 m was not significantly different from that at sea level. However, it was significantly longer at 4000 m (P < 0.01).

Conclusions: Our results suggest the phenomenon of CRPS exists in normal subjects when they expose to acute hypoxia. Further, the autonomic regulation has a significantly stronger influence on CRPS in acute hypoxia. The changes of CRPS and HRV parameters revealed the different regulatory mechanisms of the cardiac and respiratory system at high altitude.

Figure 1

Experimental protocol described with a diagram showing altitude vs. time. Each subject stayed at each simulated altitude for 15 minutes. The physiological data of the last 10 minutes was considered as steady state and adopted for analysis. The simulated altitude ascended from sea level (SL) to 3000 m and 3000 m to 4000 m at the rate of 3 m/s.

Figure 2

ECG (a), respiratory signal (b) and the instantaneous phase of the respiratory signal (c) for subject 5 at sea level.

Figure 3

The cardiorespiratory synchrogram for subject 5 at sea level was plotted at the top. The solid dots located at 48 s to 88 s and 230 s to 251 s respectively composed 7 parallel lines in synchrogram and demonstrated CRPS with the ratio of 7:2 (n = 7 heartbeats within m = 2 consecutive respiratory cycles) during the 300 s periods. f_HR/f_RespR which was the instantaneous ratio of heart rate (f_HR) to respiratory rate (f_RespR) was plotted at the bottom.

Figure 4

Synchronization time T (s) changed with the simulated altitude. The value was 60 ± 26 s, 80 ± 41 s and 113 ± 48 s at sea level (SL), 3000 m and 4000 m, respectively. The T at 4000 m was significantly longer than the value at SL (asterisk indicates P = 0.003) and 3000 m (plus indicates P = 0.040), but there was non-significantly change between at 3000 m and at SL (P = 0.214). The error bars indicated the standard deviation.