RATIONALE: Long-term smoking can lead to changes in autonomic function, including decreased vagal tone and altered stress responses. One index of the inability to adapt to stress may be blunted vagal reactivity. Stress is a primary mechanism involved in relapse to smoking, but mechanisms leading to stress-precipitated relapse are not well understood. OBJECTIVES: Using an experimental paradigm of stress-precipitated smoking behavior, we examined whether autonomic reactivity mediates the relationship between stress and smoking. High-frequency heart rate variability (HF-HRV), a putative measure of vagal tone, and the ratio of low-to-high frequency HRV (LF/HF), a measure of sympathovagal balance, were assessed. METHODS: Using a within-subjects design, 32 nicotine-dependent, 15-h abstinent smokers (a subgroup from McKee et al. (J Psychopharmacol 25(4):490-502, 2011)) were exposed to individualized script-driven imagery of stressful and relaxing scenarios and assessed on the ability to resist smoking and subsequent ad-lib smoking. HRV was monitored throughout each laboratory session (maximum 60 min following imagery). RESULTS: As expected, stress and ad-lib smoking additively decreased HF-HRV and increased LF/HF. Blunted stress-induced HF-HRV responses reflecting decreased vagal reactivity were associated with less time to initiate smoking and increased craving relief and reinforcement from smoking. These relationships were specific to HF-HRV following stress as neither baseline HF-HRV, HF-HRV following relaxing imagery, or LF/HF predicted smoking behavior. CONCLUSIONS: The current findings are the first to experimentally demonstrate that stress-precipitated decreased vagal reactivity predicts the ability to resist smoking. Findings suggest that strategies that normalize vagal reactivity in early abstinent smokers may lead to improved smoking cessation outcomes.
RATIONALE: Long-term smoking can lead to changes in autonomic function, including decreased vagal tone and altered stress responses. One index of the inability to adapt to stress may be blunted vagal reactivity. Stress is a primary mechanism involved in relapse to smoking, but mechanisms leading to stress-precipitated relapse are not well understood. OBJECTIVES: Using an experimental paradigm of stress-precipitated smoking behavior, we examined whether autonomic reactivity mediates the relationship between stress and smoking. High-frequency heart rate variability (HF-HRV), a putative measure of vagal tone, and the ratio of low-to-high frequency HRV (LF/HF), a measure of sympathovagal balance, were assessed. METHODS: Using a within-subjects design, 32 nicotine-dependent, 15-h abstinent smokers (a subgroup from McKee et al. (J Psychopharmacol 25(4):490-502, 2011)) were exposed to individualized script-driven imagery of stressful and relaxing scenarios and assessed on the ability to resist smoking and subsequent ad-lib smoking. HRV was monitored throughout each laboratory session (maximum 60 min following imagery). RESULTS: As expected, stress and ad-lib smoking additively decreased HF-HRV and increased LF/HF. Blunted stress-induced HF-HRV responses reflecting decreased vagal reactivity were associated with less time to initiate smoking and increased craving relief and reinforcement from smoking. These relationships were specific to HF-HRV following stress as neither baseline HF-HRV, HF-HRV following relaxing imagery, or LF/HF predicted smoking behavior. CONCLUSIONS: The current findings are the first to experimentally demonstrate that stress-precipitated decreased vagal reactivity predicts the ability to resist smoking. Findings suggest that strategies that normalize vagal reactivity in early abstinent smokers may lead to improved smoking cessation outcomes.
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