## 4 Discussion
### Mechanism Exploration of tPCS Intervention on HRV and HbO\({}_{2}\)  
In this study, fNIRS and HRV were used to monitor the effect of tPCS intervention on the elimination of different degrees of exercise-induced physical fatigue. It was found that the changes in the HRV and the concentration of HbO\({}_{2}\) were similar in subjects with moderate and severe physical fatigue, which indicates that there may be some relationship between the change in the HRV and the change in the HbO\({}_{2}\). [PERSON] et al. found that the frontal lobe is located in the central area of the \"fatigue network\" [62]. When fatigue occurs, the neural connections between different brain regions decrease, especially between the frontal lobe and other brain regions, and the frontal lobe plays an important role in the regulation of physical fatigue [63]. Some scholars have found that the stimulation of tPCS in the frontal lobe can cause the change in the concentration of HbO\({}_{2}\) in the frontal lobe [64]. It has also been proved that the frontal lobe is part of the sympathetic and parasympathetic pathway [65], which means that the stimulation of tPCS in the frontal lobe can affect the HRV and concentration of HbO\({}_{2}\) at the same time, which makes it possible to explore the mechanism of tPCS intervention on the HRV and the concentration of HbO\({}_{2}\). There have been studies on the combination of fNIRS and HRV as a means of fatigue monitoring, but few studies have combined them to analyze the mechanism. When individuals experience physical fatigue, the concentration of HbO\({}_{2}\) in the brain decreases, and the concentration of HbO\({}_{2}\) in the brain is negatively correlated with the degree of physical fatigue [66]. Compared with the normal state, tired individuals find it more difficult to maintain their original exercise level, which would force the brain area to be in a state of high activation, so more blood oxygen supply is needed to combat fatigue. [PERSON] proved this in experiments and further considered that the demand for oxygenated hemoglobin is positively related to the difficulty of the task. When the task is more difficult, the demand for oxygenated hemoglobin is higher, and when the task is simpler, the demand for oxygenated hemoglobin is lower [67, 68]. [PERSON] et al. found that the stimulation of tPCS in the frontal lobe can improve the excitability of the cerebral cortex, strengthen the connection between brain regions, and improve the blood oxygen transport capacity of the stimulated region [69, 70]. Therefore, we speculate that this may be one of the reasons why tPCS can increase the concentration of HbO\({}_{2}\) in the frontal lobe. At the same time, the stimulation of tPCS in the frontal lobe increased the overall level of HRV, which was consistent with the increase in the HbO\({}_{2}\) concentration in the prefrontal lobe after stimulation. [PERSON] et al. pointed out that the pathways involved in sympathetic and parasympathetic nerves include the frontal lobe, anterior cingulate gyrus, insular, hypothalamus, and brainstem [71]. The mediator of the cortical-subcortical pathway of the frontal parasympathetic nerves and sympathetic nervous system can effectively regulate HRV [72]. The prefrontal cortex, including the orbital prefrontal cortex and medial prefrontal cortex, inhibits the amygdala by connecting \(\gamma\)-aminobutyric acid (gamma-aminobutyric acid, GABA) neurons in the amygdala. The overactivation of the prefrontal cortex inhibits the sympathetic excitation circuit of the amygdala, and the amygdala nuclear energy regulates the output of autonomic nervous regulation through the hypothalamus-brain stem pathway, thus leading to changes in the HRV [73, 74, 75]. Applying tDCS stimulation above the prefrontal cortex increases parasympathetic activity and decreases sympathetic activity, and when parasympathetic activity increases, it affects HRV, especially RMSSD and HF indicators [76].