## 4 Discussion
Despite years of research, the characteristics of the optimal hypoxia 'dose' (magnitude, duration, frequency) are not clear [28]. This dose may be highly individual [28]. Undoubtedly, the results of previous studies may be influenced by the selection of participants to take part in the study because this type of study typically involves well-trained athletes in whom there may already be limited possibilities for improving VO2 max due to already high physical performance. Also, the variety of hypoxic and training protocols used or genetic factors [19] may have a significant impact on the effectiveness of IHT. Although the hypoxia applied in our study was found to be ineffective in improving VO2 max, our results indicate that IHT affected other aspects affecting endurance performance, which is consistent with what has been previously reported [31]. The IHT used was effective in improving maximal power output, power output and absolute VO2 at VT2. These results confirm other previously published data, where improvement in maximal power output was observed in a graded test, while reporting an unclear effect of IHT on the anaerobic threshold and VO2 max [32]. In another similar study, [PERSON] et al. [33] reported no beneficial effect of IHT on Pmax and VO2 max. Improvements in maximal and/or threshold power output can be attributed to non-hematological effects of IHT, while beneficial changes in skeletal muscle--e.g., mitochondrial density, capillary-to-fiber ratio and fiber cross-sectional area [14,34]--have been reported in untrained participants after hypoxia training. Improved non-hematological factors may also be the cause of improved anaerobic power, which has also been reported after IHT [35]. Improved anaerobic metabolism and sprint performance after IHT may possibly be through enhanced glycolysis [36]. Enhanced glycolysis after IHT may also affect the anaerobic threshold (second ventilatory threshold), as observed in this study. To maximize the effects of applied training, we used interval training in this study in which loads were determined based on metabolic (ventilation) thresholds, and further strengthened by normobaric hypoxia stimulation. The interval loads used in this study allowed us to control the exercise metabolism of this training, and exercise bout was performed with power output at VT2, i.e., the highest intensity at which there is still a balance between lactate production and lactate removal [25]. In contrast, active recovery was performed with power output at VT1, i.e., the intensity corresponding to the highest intensity of aerobic metabolism [25]. By applying the workloads in this way, it was possible to adapt to high concentrations of lactate, and at the same time perform effective recovery based on aerobic metabolism. In this study, interval training was relatively short (4 weeks)--shorter than the usual 6-12 weeks used to improve VO2 max [20]--and proved to be an effective training method. Our training (both in normoxia and normobaric hypoxia) proved to be effective in improving VO2 max, which is an important practical application of the results of our study, especially in sports where the pre-season is short and coaches have little time for effective physical conditioning in athletes