Whether prior stress increases acute stress reactivity is unresolved. The impact of life events (within the past 12 months) and social support on cardiovascular responses was investigated in 90 young male firefighters. Cardiovascular and cortisol measures were collected across baseline, arithmetic, and speech tasks; intertask recovery; and three recovery trials. Reactivity differences were not independently associated with life events. High social support was associated with greater arithmetic cardiovascular reactivity and faster recovery. Combined life events and social support grouping showed that effects of support were accentuated when event frequency was high, suggesting that life events and support interacted to sensitize future stressor responses. Support may promote the alerting response mobilization but prevent chronic allostatic load by enhancing recovery.

Acutely, cigarette smoking stimulates increases in blood pressure (BP), heart rate (HR), and cortisol, but little evidence is available concerning the impact of habitual smoking status on cardiovascular stress responsivity. This relation was assessed in 86 healthy male firefighters, age 19 to 31. comprising 52 nonsmokers and 34 smokers. Measures of BP, HR, salivary free cortisol, breathing pattern, and self-reported stress and alertness were obtained while subjects performed nonverbal mental arithmetic and a socially evaluative speech task. Systolic and diastolic BP were higher at rest in nonsmokers than smokers, and a consistent difference in stress responsivity was also found. BP, HR, and cortisol responses to mental arithmetic were significantly smaller in smokers than nonsmokers, with mean changes in BP (adjusted for body weight) averaging 19.3/11.0 mmHg and 28.5/15.4 mmHg in smokers and nonsmokers, respectively. There were no effects of smoking status on task performance or subjective stress responses and no differences between groups in family health history, health-related behaviors, o r psychological characteristics that might account for the reactivity difference. Possible explanations of the results are discussed, and methodological implications for cardiovascular stress reactivity studies are outlined.

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