## 4 Discussion
* Difference in maximal value of VO2, heart rate, RPE, and training parameters between the NONPLAT and PLAT groups or NONEND and END ones. The occurrence of VO2 pl was not dependent on specialty and therefore on maximum VO2, given that, unsurprisingly, the END group had a higher VO2 max than the NONEND group. Thus, given that the END and NONEND athletes were equally distributed in the NONPLAT and PLAT groups, we can consider that specialty does not influence the occurrence of VO2 pl. Since this factor (specially) also has no impact on RCP, we can assume that they did not have contract a significant oxygen deficit before reaching VO2 max (with or without plateau). * The occurrence of VO2 pl  
The \"plateau phenomenon\", described by [PERSON] and [PERSON] in 1971 [68], was observed during 3 consecutive workloads. Before them, in 1955, [PERSON] and colleagues introduced a criterion for identifying a VO2 pl during exercise [69]. This threshold was set at \(\leq\)150 mL/min (or \(\leq\)2.1 mL-min-1.kg-1) based on the average increase in subjects' VO2 over incremental exercise increments. However, this method has been criticized [5,11]. Moreover, according to the positioning of eminent colleagues [4] on this issue, we did not consider the so-called \"secondary\" criteria (heart rate (HR) \(\leq\)10 beats/min or \(\leq\)5% of the maximum predicted by age (220-age), blood lactate concentration \(\geq\)8 mM, or respiratory exchange ratio (RER) \(>\)1.00, 1.10, or 1.15). Thus, when we obtain these criteria without an individual reaching a plateau, the \"VO2 peak\" referred to the highest VO2 reached during a graded exercise test, as has been done in most research on maximal exercise tests in children for whom there was some difficulty in demonstrating a VO2 pl [70]. Thus, in this study, to compare the EEG response during IET as a function of the occurrence of a VO2 pl, this was defined as less than half the expected increase. According to this definition, we observed a VO2 pl occurrence in 52.6% of our subjects, in accordance with previous studies [4,5,9,11,18,19,71,72]. * RPE response between the groups  
[PERSON]'s model emphasizes the concept of a \"critical metabolic state\" in which metabolite accumulation reaches a threshold level, triggering fatigue and necessitating a reduction in exercise intensity to avoid metabolic imbalance and potential damage to muscle tissue. In essence, [PERSON] proposed that fatigue is a protective mechanism that prevents excessive muscular strain and maintains physiological homeostasis [1,73,74]. The central governor theory challenged (or we might say, achieved) [PERSON]'s peripheral model of fatigue by emphasizing the role of the brain as a central regulator of exercise performance. The founders and protagonists of this \"central governor theory\" argue that while peripheral factors, such as muscle fatigue and metabolic stress, undoubtedly contribute to fatigue, the brain's role in pacing and regulating exercise intensity is paramount [75,76]. They suggest that the brain integrates sensory feedback from the muscles, cardiovascular system, and other physiological systems to modulate exercise effort and prevent catastrophic failure [59,71]. Here, we used perceived exertion to measure the subjective experience of intensity, stress, discomfort, and/or fatigue during physical activity. The RPE scale, first introduced in 1970 and subsequently refined by [PERSON] [77], remains the predominant tool for assessing perceived exertion in adults [78]. Some studies suggest an even stronger correlation between RPE and VO2 [79,80]. The widespread adoption of RPE to assess exercise intensity may be explained by the ability of human beings to perceive effort, which derives from continuous use of a well-developed sensory system. During exercise, individuals are aware of their overall effort and can discern the location of the effort, allowing them to gauge the intensity of the exercise and estimate their endurance at a given level [81, 82].