Changes in Cardiac Autonomic Activity During a Passive 8 Hour Acute Exposure to 5 500 m Normobaric Hypoxia are not Related to the Development of Acute Mountain Sickness

• Published in: International journal of sports medicine 2012-03, Vol.33 (3), p.186-191
• Main Authors: Wille, M., Mairer, K., Gatterer, H., Philippe, M., Faulhaber, M., Burtscher, M.
• Format: Article
• Language: English
• Subjects: Adult; Altitude; Altitude Sickness - physiopathology; Autonomic Nervous System - physiology; Biological and medical sciences; Evaluation; Fundamental and applied biological sciences. Psychology; Heart rate; Heart Rate - physiology; Humans; Hypoxia; Hypoxia - physiopathology; Illness; Lactic acid; Lactic Acid - blood; Male; Mountains; Nervous system; Physiology & Biochemistry; Recording; Sports medicine; Stress; Time Factors; Vertebrates: body movement. Posture. Locomotion. Flight. Swimming. Physical exercise. Rest. Sports; Young Adult
• ISSN: 0172-4622; 1439-3964
• DOI: 10.1055/s-0031-1291325

Abstract Alterations in the autonomic nervous system after ascent to high altitude may be related to the development of acute mountain sickness (AMS). So far, the time course of cardiac autonomic modulation in relation to AMS development during the early hours at altitude is not well established. As AMS develops sometimes as early as 1 h and typically within 6 to 10 h at altitude, evaluating this time period provides information on cardiac autonomic responses with regard to AMS development. Prior studies exclusively investigated autonomic modulations in hypobaric hypoxia. Because barometric pressure per se might influence autonomic nervous system activity, the evaluation of cardiac autonomic alterations caused by hypoxia alone might give new insights on the role of the autonomic nervous system in AMS development. To assess the early responses of acute hypoxia on cardiac autonomic modulation and its association to the development of AMS, 48 male subjects were exposed for 8 h to acute normobaric hypoxia (F i O 2 11.0%, 5 500 m respectively). Heart rate variability (HRV) was determined by 5-min recordings of successive NN-intervals in normoxia and after 2, 4, 6 and 8 h in hypoxia. Compared with normoxia, acute exposure to hypoxia decreased total power (TP), high frequency (HF) and low frequency (LF) components as well as the standard deviation of all NN intervals (SDNN), the root mean square of differences of successive NN intervals (rMSSD) and the proportion of differences between adjacent NN intervals of more than 50 ms (pNN50). LF:HF ratio, heart rate (HR) and blood lactate (LA) were augmented, indicating an increase in cardiac sympathetic activity. No differences were found between those who developed AMS and those who did not. Our results confirm reduced HRV with a shift towards sympathetic predominance during acute exposure to hypoxia. However, changes in cardiac autonomic modulations are not related to AMS development in acute normobaric hypoxia.