The Neurovisceral Integration Model and the Vagal Tank Theory propose that cardiac vagal activity (CVA) changes dynamically in response to self-regulatory demands, yet empirical support remains limited. In Study 1, state anxiety was induced using the Velten mood induction procedure, followed by a 2-min emotional incubation period. CVA—indexed by vagally mediated heart rate variability (vmHRV), specifically high-frequency (HF) component and root mean square of successive differences (RMSSD)—was quantified from electrocardiogram (ECG) recordings during resting, anxiety induction, and recovery phases. Based on findings from Study 1, Study 2 implemented a 10-day HRV biofeedback intervention in healthy college students to evaluate its effects on tonic and phasic CVA. The protocol involves slow-paced breathing (SPB) to enhance cardiorespiratory coupling and modulate vmHRV, with real-time feedback generated from respiratory sinus arrhythmia (RSA)-related heart rate fluctuations. Results showed that CVA during anxiety was significantly higher than during both resting and recovery phases. Additionally, resting CVA was positively correlated with phasic CVA, including both reactivity and recovery. Following biofeedback training, phasic CVA—comprising reactivity and recovery—significantly increased. These findings indicate that CVA increases during emotional regulation, and higher resting CVA facilitates more adaptive vagal responses. Moreover, short-term biofeedback training appears to enhance regulatory capacity under conditions of state anxiety by modulating CVA. Together, this study offers empirical support for both the Neurovisceral Integration Model and the Vagal Tank Theory.
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