Effect of rapid ascent to high altitude on autonomic cardiovascular modulation

Effect of acute hypobaric hypoxia on autonomic nervous activities remains unclear. We evaluated the effect of rapid ascent to high altitude on autonomic cardiovascular modulation and compared the differences between the subjects with and without acute mountain sickness (AMS).

Twenty-seven unacclimatized healthy subjects were included for this study. The sleep and study altitude (3180 m) was reached by car from low level (555 m) within 3 hours. The stationary spectral heart rate variability was measured 3 days before ascent (T0), 2 nights at high altitude (T1 and T2), and 2 days after descent (T3). AMS occurrence was evaluated by the Lake Louise score system.

At high altitude, RR intervals (RRI), standard deviation of RRI (SDRR), total power (TP), low-frequency power (LF), high-frequency power (HF), and normalized HF decreased significantly but normalized LF and LF/HF ratio increased significantly in subjects irrespective of AMS. AMS developed in 13 of 27 (48.1%) subjects. Compared with the data at T1, SDRR, TP, LF, and HF increased at T2 in AMS group but decreased in non-AMS group, and the differences in these variables (data at T2 minus data at T1) between the 2 groups showed statistical significance.

After rapid ascent to high altitude, autonomic nervous activities were suppressed and sympathetic activity was relatively predominant. At high altitude, the discordant changes in SDRR, TP, LF, and HF may reflect varying capacity of acute hypobaric hypoxic adaptation between the subjects with and without AMS.