Effects of exercise and hypoxia on heart rate variability and acute mountain sickness.

Acute mountain sickness (AMS) is a common condition among non-acclimatized individuals ascending to high altitude. Exercise, a characteristic feature of hiking and mountaineering, has been suggested to exacerbate AMS prevalence and to cause modifications of the autonomic nervous system. A reduction of the heart rate variability (HRV) is a common finding during acute hypoxia, however characteristics of HRV during exercise in subjects suffering from AMS are unknown. Therefore, the aim of the present study was to investigate the effects of acute normobaric hypoxia (FiO2=11.0% ≙ 5 500 m) at rest (PHE) and during exercise (AHE) on the cardiac autonomic function and the development of AMS in 20 healthy, male individuals. HRV recordings were performed during normoxia and after 2, 4, 6 and 8 h in hypoxia during PHE and AHE, respectively. AMS was assessed using the Lake Louise Score. During PHE 50% of participants developed AMS and 70% during AHE (p=0.22). The analysis of HRV data showed a significant reduction of total power (TP), high frequency (HF) and low frequency (LF) components and an increase of the LF:HF ratio during PHE, however without further modification during AHE. Exercise did not increase AMS prevalence or severity, but increased "non-gastrointestinal" symptoms including headache, fatigue and dizziness. HRV indices were not related to the overall incidence of AMS or the development of "non-gastrointestinal" symptoms but we detected significant correlations between gastrointestinal complaints and HRV components. Thus, we suggest that the cardiac autonomic modulation during acute normobaric hypoxia does not play an important role in the development of AMS, but seems to be related to gastrointestinal complaints at high altitude. However, the influence of moderate exercise on HRV and AMS is minor, only "non-GI" symptoms seem to be exacerbated when exercise is applied.

Short-term intermittent hypoxia reduces the severity of acute mountain sickness.

Intermittent hypoxia (IH) is a promising approach to induce acclimatization and hence lower the risk of developing acute mountain sickness (AMS). We hypothesized that a short-term IH protocol in normobaric hypoxia (7 × 1 h to 4500 m) effectively increases the hypoxic ventilatory response (HVR) and reduces the incidence and severity of AMS. Therefore, 26 men (25.5 ± 4.4 years), assigned in a double-blinded fashion to the hypoxia group (HG) or placebo group (PG), spent 8 h at 5300 m before (PRE) and 2 days after cessation of the IH protocol (POST). Measurements included the evaluation of the Lake Louise Score (LLS) and the HVR. The severity of AMS decreased from PRE to POST in the HG (from 6.0 ± 2.7 at PRE to 4.1 ± 2.1 at POST), whereas the LLS in the PG stayed high (from 5.7 ± 2.9 to 5.5 ± 2.8, respectively). The HVR in the HG increased from 0.73 ± 0.4 L/min/% at PRE to 1.10 ± 0.5 L/min/% at POST and did not increase in the PG. The reduction of the LLS was inversely related to the changes in the HVR (r = -0.434), but the AMS incidence was not different between the HG and the PG at POST. In conclusion, short-term IH reduced the severity of AMS development during a subsequent 8-h exposure to normobaric hypoxia.

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.

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 (FiO2 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.