## 4 Discussion  
### Autonomic Mechanisms of Emotional Pain  
This study aims to clarify the relationship between subjective (psychological) and objective (physiological) indicators of emotional pain by examining psychophysiological responses to anger-induced pain across varying levels of perceived pain intensity. Our findings reveal significant increases in RMSSD, pNN50, HFNu, SCL, and SCR, which were associated with emotional pain, and significant decreases in LF/HF, RR, BVP, and PTT (Table 4). These results align with our previous research that examined social pain induced by a social loss stimulus and revealed a similar pattern of physiological changes in SCL, SCR, RR, BVP, and PTT in response to the stimulus [31].  
RR is one of the most commonly used respiratory indices, in addition to respiratory period, respiratory depth, tidal volume, duty cycle, and respiratory variability [32]. Negative affect can induce shallower and faster breathing, potentially lowering blood carbon dioxide levels [33]. Decreases in RR have also been linked to anxious personality traits, particularly under mental stress or a physical load [34; 35]. BVP reflects the volume of blood flowing through peripheral vessels such as those in the fingers and can also indicate vascular or blood pressure changes resulting from vasoconstriction or vasodilation [36]. Reduced BVP suggests peripheral vasoconstriction in the fingers, and this is often associated with arousal triggered by emotional pain [37]. PTT represents the duration from the ECG R-peak to the arrival of the pulse wave at the fingertip [38] and is influenced by cardiac contractility and mean arterial pressure. The significant decrease in PTT observed during pain stimulation aligns with the findings of our previous social pain study [31], indicating blood pressure elevation under stress. Increased SC activity signifies sympathetic nervous system (SNS) activation. SC reflects a psychogalvanic reflex wherein SNS excitation of eccrine sweat glands in the palms and soles occurs in response to stress or fear [39]. When sympathetic activity intensifies, more sweat is secreted at the skin surface, leading to elevated EDA. Increases in SCL and SCR indicate sweat secretion attributable to SNS activation, suggesting a physiological response to emotional distress or social rejection.  
Elevated HFnu, RMSSD, and pNN50 and lower LF/HF ratios during emotional pain indicate increased parasympathetic nervous system (PNS) activity. In this study, the LF/HF ratio, which reflects the balance between sympathetic and parasympathetic activation, decreased, suggesting a relative reduction in sympathetic influence and a shift towards parasympathetic dominance, as evidenced by the increase in other parasympathetic metrics. HRV indices represent the autonomic regulation of the HR and can serve as objective indicators of emotional states [40]. RMSSD reflects short-term fluctuations driven predominantly by a vagal (parasympathetic) tone [41], correlates with HF power [36], and reflects self-regulatory capacity. Similarly, pNN50 is primarily governed by parasympathetic influence. Hence, the increased parasympathetic activity during emotional pain suggests that emotional engagement or recovery processes may be more pronounced than sympathetic arousal. Our findings suggest that emotional pain does not merely represent a simple stress response; rather, it entails a complex emotional state that prompts the coactivation of the PNS and SNS under heightened emotional arousal.