## 4 Discussion  
The main finding is that acute fatigue increases resting muscle oxygen consumption and is associated with increased sympathetic nervous system (SNS) activity. Therefore, previous exercise can affect resting muscle oxygenation data measured by VOT-NIRS. Resting muscle oxygen consumption increased under acute fatigue conditions, showing greater desaturation (\(-20.5\%\)) and resaturation (\(+19.5\%\)). This aligns with [PERSON] et al. (2020), who found that acute fatigue increased SmO\({}_{2}\) slopes following an official soccer match and persisted for 24 h, correlating with elevated lactate dehydrogenase (LDH) levels. This increase is primarily due to Excess Post-Exercise Oxygen Consumption (EPOC) [41]. The rapid phase of EPOC occurs immediately post-exercise and can last up to 3 h [42]. A SmO\({}_{2}\) increase and an accelerated slope pattern (tau, MRT, desaturation, and resaturation) at rest are necessary to restore muscle homeostasis. This process aids in eliminating accumulated CO\({}_{2}\), rapidly redistributing blood flow to the vastus lateralis muscles post-exercise, and increasing thermogenesis to restore ATP and phosphocreatine levels. Furthermore, increased eccentric work from jumps raises the total energy cost covered by oxidative and glycolytic pathways in the muscle post-exercise [43]. Also, in conditions of muscle damage, the physiological mechanisms explaining the interaction between HRV and SmO\({}_{2}\) at rest have been studied [13; 44; 45]. The reduction in HRV is associated at the cellular level with increased levels of Creatine Phosphokinase (CPK) and reactive oxygen species (ROS) as byproducts of mitochondrial metabolism [46; 47]. Additionally, there is an increase in peripheral vasodilation resulting from the activation of H1 and H2 histamine receptors. When muscle oxygen consumption increases at rest due to greater metabolic demand or fatigue, as measured by NIRS, vasodilatory substances such as prostaglandandins, adenosine, and nitric oxide are present in ischemic tissue and are modulated by sympathetic vascular tone controlled by the autonomic nervous system (ANS) [48]. The post-exercise increase in SmO\({}_{2}\) depends on the training status, which is related to endothelial capacity, likely attributed to the release of endothelial-derived factors such as nitric oxide (NO), which possesses antiproliferative, anti-inflammatory, and antithrombotic properties and promotes vasodilation [49]. This interaction between the increase in HRV and oxygen consumption reflects a complex adaptive response in which the muscle seeks to enhance its ability to manage metabolic and oxidative stress while optimizing recovery after exercise. Although these mechanisms have not been exhaustively studied, they are related to increased SmO\({}_{2}\) at rest and mitochondrial capacity. The hyperemic response showed a reduction under fatigue conditions (\(-2.8\%\)), but this was not significant. This response indicates greater endothelial capacity, which was not evident in our study. Hyperemia responds immediately to exercise and returns to baseline within minutes; its stabilization speed depends on muscle oxygen consumption and the vasodilatory response [50]. Acute fatigue showed lower values 30 min post-exercise, with hyperemic response stabilizing faster due to increased oxygen transport speed [51]. These results align with the finding that reoxygenation kinetics were affected by acute fatigue, resulting in faster tau constant values [16]. Reoxygenation kinetics indirectly indicate mitochondrial function, which can significantly improve oxygen utilization and mitochondrial respiration, facilitating muscle homeostasis recovery [52]. Conversely, slower mitochondrial respiration is associated with poorer fitness [53]. Rapid reoxygenation may also aid in converting lactate to pyruvate, enhancing muscle recovery [54].