Objective
We investigated the moderating relationship of hostility on emotional and physiological arousal due to acute anger provocation; stress reactivity and recovery were measured.
Method
Forty-five participants completed a measure of trait hostility (CMHQ) and performed a mental arithmetic (serial 7s) task while receiving scripted comments at set intervals designed to provoke anger (harassment). The impact of trait hostility (high, medium or low) on arousal and recovery was examined.
Results
Participants low in self-reported hostility showed greater HR reactivity to the task but recovered quickly. Participants high in hostility showed noticeably slower recovery in SBP maintained after task completion.
Conclusions
The findings underscore the importance of examining both reactivity and recovery data in anger provocation research because the apparent influence of trait hostility on cardiovascular functioning would have been missed if recovery had not been systematically studied.
Research on stress and CVD has partly focused on how individual personality characteristics interact with stressors such that some people develop illness while others do not. Although many researchers have examined subjective and physiological reactivity to a variety of stressors, much less attention has been given to factors that prevent recovery. The current study examined the influence of trait hostility on cardiovascular functioning both during and after interpersonal conflict. Acute emotional stress is thought to be particularly salient for the development of stress-related disease processes (Linden et al., 1998 and Schwartz et al., 2003). The focus here was on cardiovascular stress recovery because frequent exposure to challenges that prevent quick recovery are particularly promising candidates for explaining CVD development ( Linden et al., 1997 and Schwartz et al., 2003). As such, we hoped to demonstrate the importance of examining recovery paradigms in explaining personality–pathophysiology relationships.
Hostility has been conceptualized as a personality trait composed of a combination of affect, attitudes, and general aggressiveness reflecting a propensity for anger (Cook and Medley, 1954). Trait hostility has repeatedly been shown to relate to poorer prognosis for CVD (Barefoot et al., 1989), and has also been shown to relate to elevated SBP and stress reactivity (Smith and Houston, 1987). In addition, numerous studies suggest that cardiovascular reactivity bears some relationship to CVD development. Diagnosed hypertensives show greater cardiovascular reactivity to laboratory stressors than normotensives (Fredrikson et al., 1991 and Marrero et al., 1997) and normotensive individuals with a positive family history of hypertension show greater reactivity to laboratory stressors than those without family history of hypertension (Light et al., 1999). Evidence from studies such as these has led to the conclusion that chronic cardiovascular hyperreactivity may be a marker of, or contributor to, primary hypertension ( Treiber et al., 2003 and Schwartz et al., 2003).
More recently, interest has turned towards examination of the rate of recovery following a laboratory stressor (Linden et al., 1997 and Schwartz et al., 2003). It has been theorized that negative valence emotions such as anger induce greater physiological arousal that is initially adaptive in mobilizing an organism to better deal with an acute stressor but prolonged departure from homeostasis results in exhaustion and impaired functioning. Effective coping is therefore characterized by quick recovery from arousal (McEwen, 1998). Despite these compelling reasons for studying stress recovery in relation to CVD development, relatively few studies have done so (Linden et al., 1997) and there is scant knowledge of the factors that account for slow recovery.
The present study explicitly focused on recovery to better understand personality–stress relationships. To do so, we exposed study participants to emotional stress, operationalized as verbal harassment (a situational manipulation known to elicit anger), while they performed an emotionally neutral stress task (mental arithmetic). We hypothesized that trait hostility would moderate the response to the task (i.e., highly hostile individuals would show a greater magnitude increase in HR and BP) and that high hostility would result in attenuated recovery, because one would expect more highly hostile individuals to remain angry longer. The advantage of this particular protocol was to permit detection of factors affecting reactivity but not recovery and vice versa.
