Abstract

Introduction Constant suppliance of oxygen plays one of the crucial roles in normal brain functioning. Examining brain at high altitude can provide us useful information about how brain functions are impacted by high altitude hypoxia. Recent studies have shown that high altitude can lead to (i) structural changes in the brain, (ii) functional changes in the brain, and (iii) changes in cognitive functioning. However, how these brain changes are moderated by oxygen saturation (SaO2) and physical fitness (PF) of high altitude climbers still remains an ongoing debate, while (iv) correlation between SaO2 and high altitude sickness has already been found. The aim of our study was to assess to which extent can SaO2 and PF predict brain changes at high altitude. Methods Ten healthy, non-professional climbers from Muztagh Ata (7546 m) expedition were included in our study. Participants’ brain activity was measured by 36-channel EEG while they were performing checkerboard (visual evoked potentials - VEP) and oddball task (event related potentials - P300) before and during the expedition. Afterwards, EEG signals were averaged and event-related potentials were calculated. SaO2 was measured in normobaric hypoxia before the expedition and in hypobaric hypoxia during the expedition at the altitude of 4400 m (Base Camp). Climbers also performed in an incremental multi-stage ergometer test until exhaustion at sea level. VO2max and other parameters of aerobic function were observed. Results Multiple linear regression method was used to calculate the predictive power of SaO2 and PF in changes of brain activity. In first model latency and amplitude of visual evoked potentials measured at high altitude were included as dependent variable while SaO2 and PF were included as predictors. While SaO2 and PF showed no predictive power in variability of VEP latency [ F (2, 5) = 0.62, p = 0.855, R 2 = 0.061], we found significant regression equation when VEP amplitude was included as dependent variable [ F (2, 5) = 8.236, p = 0.026, R 2 = 0.767]. Additional analysis showed that only SaO2 was significant predictor of VEP amplitude ( t = 4.027, p = 0,010). In second model latency and amplitude of P300 were included as dependent variables and SaO2 and PF as predictors. In this case, neither P300 latency [ F (2, 5) = 1.035, p = 0.421, R 2 = 0.293] nor P300 amplitude [ F (2, 5) = 0.788, p = 0,504, R 2 = 0.240] were predicted by SaO2 and PF. Conclusions The aim of our study was to observe if brain changes at high altitude can be predicted by some physiological factors. We found that physical fitness didn’t play any role in brain activity changes. On the other hand climbers who acclimatised faster to high altitude, which is reflected in greater SaO2 changes, showed less decrease in VEP amplitude than climbers with slower acclimatisation process. We believe that our results might represent first step in detecting subjects who are more vulnerable to detrimental brain and cognitive changes at high altitude. Acknowledgment We hereby thank the administrative and technical staff of Brain Products GmbH which gave us access to their EEG equipment (BrainAmp 32 channel EEG amplifier, ActiCap active electrode system and the MOVE wireless add-on) to perform these measurements. This study would not have been possible without the versatility and ease of EEG recording that this equipment offered. References Stivalet P, Leifflen D, Poquin D, Savourey G, Launay J. in Barraud, P. A. Positive expiratory pressure as a method for preventing the impairment of attentional processes by hypoxia. Ergonomics 2000; 43 :474–85. Thakur L, Singh SB, Anand JP, Panjwani U. in Banerjee, P. K. Effect of hypobaric hypoxia on visual evoked potential at high altitude. Journal of environmental Biology 2005; 26 (3):593–6. Virues-Ortega J, Buela-Casal G, Garrido E. in Alcazar B. Neurobehavioural functioning associated with high-altitude exposure. Neuropsychology Review 2004; 14 (4):197–224. Burtscher M, Flatz M, Faulhaber, M. Prediction of susceptibility to acute mountain sickness by SaO2 values during short-term exposure to hypoxia. High Alt Med Biol 2004; 5 (3):335–40.

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