# Acute Effects of Combined Hypoxia and Fatigue on Balance in Young Men
## 1 Introduction  
The ability to maintain a vertical posture is the basis of typical human motor activity. The mechanisms of postural stability are affected in a variety of ways at any point in our lives, originating from both internal and external factors. Motor activity is accompanied by fatigue of varying intensity, affecting the effectiveness of postural stability mechanisms [(1; 2; 3)]. These influences are multiplied when motor activity is undertaken in adverse external environmental conditions, such as high altitude [(4; 5; 6; 7)]. The balance control mechanisms may respond differently to changes in each of these factors. It is therefore important to determine their influence on the organization of the balance-maintenance process. This is particularly important for a wide variety of sports activities (skiing, snow-boarding, skitouring), with competitions in most of these disciplines taking place at altitudes approaching 2000 m and not infrequently above 2500 m. In these high-altitude sports/physical activities, excellent coordination and balance are usually required. This provokes questions about the extent to which fatigue, influenced by the additional factor of hypoxia, has a negative effect on athletes' performance. This problem will increasingly affect recreational activities as well. As a result of climate change, the practice of these activities (in the case of winter sports) will require increased adaptation to higher altitudes above sea level. The main factor that reduces performance is fatigue, which, depending on the type of exertion and intensity, can affect balance in different ways. The effectiveness of the postural system depends on the integration of information between receptors, effectors and the central nervous system. If any of these links is impaired, a limitation in the effectiveness of the balance mechanisms is possible. Fatigue (increase in lactate levels) and consequent hyperventilation are determined by the type of exercise, intensity and duration [8], having a detrimental effect on postural stability. Prolonged exercise, through metabolic (e.g., interleukin-6 production), structural (e.g., cell membrane aging), functional and behavioral modifications, leads to central and peripheral fatigue [9]. These changes vary according to the intensity of exercise, the type of contraction or the muscle group working [10]. Running has been shown to disrupt balance parameters more than walking and cycling [11; 12]. Short-duration, rapidly initiated maximal exercises disturb balance more than long-term exercises with less anaerobic glycolysis [13; 14]. They lead to a transient change in global postural control [15] or are only limited to certain muscle groups [16]. The extent to which muscle fatigue can affect postural control is not entirely clear and may have both a metabolic and a neurosensory basis. Fatigue is a complex phenomenon. There are several mechanisms associated with fatigue at different levels of the nervous system that may affect the regulation of forces necessary for balance. At the peripheral level, these are likely to be pre- and postsynaptic mechanisms, including lack of nerve signal transmission or lack of muscle response to nerve excitation [17]. At the central level, fatigue may be induced by a lack of excitation of motor neurons, which is caused by changes in the nervous system [18; 19]. Changes in motor neuron excitation are attributed to intrinsic motor neuron properties, inhibition or impaired reflexes [20]. The effects of normobaric and hypobaric hypoxia on postural balance have been reported for both long exposure (24 h) [21] and short exposure (less than 60 min) [22]. Balance impairment can lead to falls and stumbles, and these issues have been observed at both high (1500-3500 m) and very high altitudes (above 3500 m) [5; 6; 7]. High altitude negatively affects postural stability and balance due to acute hypoxia [23; 24; 25; 26]. The most commonly analyzed inducer of static imbalance is hyperventilation, which is a compensatory response to oxygen deficit [26].