Fear-induced bradycardia is a physiological response to fear, characterized by a temporary decrease in heart rate. It has been studied extensively in both animals and humans, with recent research focusing on its role in fear conditioning experiments. Fear conditioning involves pairing a neutral stimulus (CS+) with an unpleasant stimulus (US) to elicit a conditioned response (CR). This process is crucial for predicting aversive events and ensuring survival. In humans, fear conditioning is often assessed using psychophysiological measures such as electrodermal activity (SCR), fear-potentiated startle (FPS), and pupillary responses. Heart rate (HR) is also used, though its application in fear conditioning is still in its early stages. Recent studies have shown that fear-induced bradycardia can be influenced by various factors, including the type of conditioning paradigm, the timing of the unconditioned stimulus (US), and the participant's reactivity to aversive stimuli. For example, participants classified as 'accelerators' show increased heart rate in response to threatening stimuli, while 'decelerators' show decreased heart rate. These differences are linked to the reactivity of the aversive motivational system, which is crucial for preparing the organism to avoid threats. The use of heart period (HP) as a more precise measure of cardiac rhythm has gained attention, as it provides a more accurate reflection of autonomic activity compared to beats per minute (BPM). Studies have shown that HP can detect specific components of the cardiac response, such as early deceleration (D1), acceleration (A1), and late deceleration (D2), which are associated with fear conditioning. Additionally, spectral analysis of HRV has revealed that parasympathetic activity, particularly high-frequency (HF) components, is linked to fear-induced bradycardia. Research has also highlighted the importance of HRV in safety learning and fear extinction. Lower HRV is associated with impaired safety learning and difficulty in inhibiting fear responses. The neurovisceral integration model suggests that HRV reflects the functionality of a system that integrates physiological, affective, and cognitive processes for appropriate responses to the environment. Therefore, lower HRV may indicate a reduced ability to integrate cognitive information with physiological processes. In conclusion, fear-induced bradycardia is a valuable psychophysiological measure in fear conditioning research, providing insights into the mechanisms underlying fear learning and extinction. Recent studies have emphasized the importance of using precise measures such as HP and HRV to better understand the role of the autonomic nervous system in fear responses. These findings underscore the need for standardized methodologies and further research to fully elucidate the complexities of fear-induced bradycardia.Fear-induced bradycardia is a physiological response to fear, characterized by a temporary decrease in heart rate. It has been studied extensively in both animals and humans, with recent research focusing on its role in fear conditioning experiments. Fear conditioning involves pairing a neutral stimulus (CS+) with an unpleasant stimulus (US) to elicit a conditioned response (CR). This process is crucial for predicting aversive events and ensuring survival. In humans, fear conditioning is often assessed using psychophysiological measures such as electrodermal activity (SCR), fear-potentiated startle (FPS), and pupillary responses. Heart rate (HR) is also used, though its application in fear conditioning is still in its early stages. Recent studies have shown that fear-induced bradycardia can be influenced by various factors, including the type of conditioning paradigm, the timing of the unconditioned stimulus (US), and the participant's reactivity to aversive stimuli. For example, participants classified as 'accelerators' show increased heart rate in response to threatening stimuli, while 'decelerators' show decreased heart rate. These differences are linked to the reactivity of the aversive motivational system, which is crucial for preparing the organism to avoid threats. The use of heart period (HP) as a more precise measure of cardiac rhythm has gained attention, as it provides a more accurate reflection of autonomic activity compared to beats per minute (BPM). Studies have shown that HP can detect specific components of the cardiac response, such as early deceleration (D1), acceleration (A1), and late deceleration (D2), which are associated with fear conditioning. Additionally, spectral analysis of HRV has revealed that parasympathetic activity, particularly high-frequency (HF) components, is linked to fear-induced bradycardia. Research has also highlighted the importance of HRV in safety learning and fear extinction. Lower HRV is associated with impaired safety learning and difficulty in inhibiting fear responses. The neurovisceral integration model suggests that HRV reflects the functionality of a system that integrates physiological, affective, and cognitive processes for appropriate responses to the environment. Therefore, lower HRV may indicate a reduced ability to integrate cognitive information with physiological processes. In conclusion, fear-induced bradycardia is a valuable psychophysiological measure in fear conditioning research, providing insights into the mechanisms underlying fear learning and extinction. Recent studies have emphasized the importance of using precise measures such as HP and HRV to better understand the role of the autonomic nervous system in fear responses. These findings underscore the need for standardized methodologies and further research to fully elucidate the complexities of fear-induced bradycardia.