International Journal of Psychophysiology 92 (2014) 79–84

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International Journal of Psychophysiology journal homepage: www.elsevier.com/locate/ijpsycho

Trait dominance is associated with vascular cardiovascular responses, and attenuated habituation, to social stress Eimear M. Lee a,⁎, Brian M. Hughes b a b

Anglia Ruskin University, Cambridge, UK National University of Ireland, Galway, Galway, Ireland

a r t i c l e

i n f o

Article history: Received 9 August 2013 Received in revised form 28 February 2014 Accepted 5 March 2014 Available online 13 March 2014 Keywords: Cardiovascular reactivity Individual differences Stress

a b s t r a c t Both exaggerated and diminished levels of cardiovascular reactivity have been associated with cardiovascular ill health. Dysregulation of hemodynamic mechanisms which control cardiovascular functioning may account for some individual differences in health outcomes. Trait dominance has also been associated with poor cardiovascular health in studies of humans and animals. The current study investigated the relationship between trait dominance and cardiovascular habituation to repeated social stress in humans. Forty-seven undergraduate women completed two consecutive speech tasks, preceded by a baseline period, and separated by an inter-task resting phase. Continuous cardiovascular functioning was monitored using the Finometer device. The trait dominance subscale of the Jackson Personality Research Form was completed. Mixed ANCOVA with trait dominance revealed a significant 3 (dominance) × 4 (phase) interaction for total peripheral resistance (TPR), such that TPR varied across experimental phases and was associated with trait dominance, F(1, 43) = 12.88, p = .001, partial η2 = .23. Further mixed ANCOVA for TPR reactivity to Exposures 1 and 2 revealed a significant 3 × 2 interaction with trait dominance, F(2, 40) = 7.77, p = .001, partial η2 = .28, such that higher dominance was associated with attenuated TPR habituation to Exposure 2. Trait dominance was significantly associated with vascular-oriented cardiovascular functioning, and with attenuated habituation to social stress. Vascular-dominated stress responses have in some instances been associated with ill-health, suggesting that a failure to habituate to stress, and a vascular response style could reflect potential mechanisms through which dominance is associated with poor future cardiovascular health. © 2014 Elsevier B.V. All rights reserved.

1. Introduction It is increasingly acknowledged that both smaller and larger physiological stress responses may be associated with poorer long-term cardiovascular health (Carroll et al., 2009). Extending the wide research on the harmful effects of exaggerated cardiovascular functioning stemming from the cardiovascular reactivity (CVR) hypothesis (Obrist, 1976), a range of other physiological stress response profiles have since been implicated in the aetiology of cardiovascular disease (CVD), including delayed recovery following stress (Schuler and O'Brien, 1997; Stewart et al., 2006), disrupted habituation to stress (Hughes et al., 2011), and blunted reactivity to stress (Phillips et al., 2013). While there is robust evidence that CVR to stress can predict future negative health outcomes, many of the moderating and mediating mechanisms are not yet fully understood (Treiber et al., 2003). For cardiovascular stress responses, determining whether reactivity is exaggerated or blunted is complicated by the way blood pressure is derived from a dynamic and compensatory interaction between cardiac ⁎ Corresponding author at: Department of Psychology, Anglia Ruskin University, Cambridge, UK. E-mail address: [email protected] (E.M. Lee).

http://dx.doi.org/10.1016/j.ijpsycho.2014.03.001 0167-8760/© 2014 Elsevier B.V. All rights reserved.

output (CO) and total peripheral resistance (TPR). The operation of this reciprocal relationship can be conceptualised as a process of flow and resistance (Levick, 2010). Increased CO results in greater ejection of blood from the ventricles of the heart to surrounding arteries, reflecting a physiological preparedness of the body to execute an action. In contrast, increased TPR reflects increased vascular constriction, causing an opposition or resistance in the blood vessels that serves to regulate blood flow (Levick, 2010). The term hemodynamic profile has been advocated by as a means of describing this specific compensatory relationship (James et al., 2012). This complexity of the cardiovascular system is such that it is possible for two different people to have the same mean level of blood pressure, despite their individual blood pressure having different hemodynamic determinants (as long noted by Brod et al., 1959). Individual variations in the magnitude, pattern, and duration of stress-induced hemodynamic responses could have implications for the nature and extent of pathophysiological changes leading to CVD (James et al., 2012). In terms of the hemodynamics underlying blood pressure changes, individuals may be referred to as either vascular (TPR-dominated) or cardiac (CO-dominated) reactors, categories which have been shown to have some temporal stability (Sherwood et al., 1990). Additionally, it should be considered whether the classification of hemodynamic patterns (and cardiovascular functioning more

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broadly), stems from higher general levels of cardiovascular activity, or whether such classifications are derived from large changes in cardiovascular functioning over time, such as in response to a stressor, and are thus indicative of reactivity. Active stress tasks (like public speaking or mental arithmetic) have been shown to be associated with increased myocardial reactivity, which may be adaptive initially, demonstrating an increased active physiological response to something that is stressful. Subsequent exposures to the same stressor have shown reduced myocardial stress responses in several studies (al'Absi et al., 1997; Frankish and Linden, 1991; Kelsey et al., 1999). In contrast, vascular profiles of stress responding are typically evoked by tasks requiring passive coping, such as the cold pressor task. Prolonged vascular responses to stress have been associated with negative cardiovascular health outcomes, including increased vascular resistance and excessive vascular reactivity (Palatini and Julius, 2009). Stronger dispositions towards some trait dimensions of personality, such as neuroticism, anger and hostility, and a desire for social dominance have been shown to be associated with future cardiovascular ill-health, such as increased incidence of coronary heart disease (CHD) and atherosclerosis (see Booth-Kewley and Friedman, 1987; Everson-Rose and Lewis, 2005; Suls and Bunde, 2005). Trait (or social) dominance is an individual difference variable encapsulating social competitiveness and the degree to which persons innately desire to exert a dominant position within their social group (Pratto et al., 1994). While dominance may have conferred evolutionary advantages, higher levels of dominance in modern society may have health consequences. Trait dominance has been linked to CVD consequences, including increased odds of both fatal and non-fatal cardiovascular events (Siegman et al., 2000). In contrast, greater submissiveness has been found in some instances to be protective against ill-health (Siegman et al., 2000; Whiteman et al., 2000). Socially-salient stressors have been shown to elicit considerable and reliable cardiovascular stress responses (e.g., al'Absi et al., 1997; Gramer, 2003), and such forms of stress may be especially pertinent for individuals with strongest interpersonal trait influences such as trait dominance. Research has supported a positive association between trait dominance and CVR to socially-relevant forms of stress, but not asocial stress (Gramer and Berner, 2005; Hughes and Callinan, 2007; Newton, 2009). A recent review (Newton, 2009) concluded that in the main, studies involving socially relevant stressors show significant positive associations between trait dominance and acute cardiovascular responses. Investigation of individual differences in personality, coupled with a consideration of the diversity of hemodynamic responding to repeated stress could elucidate variations in CVR more clearly. Thus, the present study sought to assess whether individual differences in trait dominance influenced the extent to which healthy adults adapted to stress across time, as represented by hemodynamic responses observed during repeated exposures to a stress-inducing social stress task.

2. Materials and methods 2.1. Participants Participants were 54 undergraduate women. For the purposes of this study, only women under the age of 35 years (ages ranged from 17 to 34; M = 20.98, SD = 3.42), without a personal history of hypertension, with baseline blood pressure within normal ranges (blood pressure b 140/90 mm Hg), and with a BMI of less than 30 (M = 22.92, SD = 2.98) were included in the final sample (n = 46). Nine smokers were included for reasons of power as it was determined that the inclusion of smokers did not alter the trend of the results. No restrictions were placed on participants prior to participation in the study with regard to smoking, exercise, or caffeine intake. All procedures and

materials were approved by an institutional ethics review panel prior to commencement of the research. 2.2. Measures 2.2.1. Cardiovascular responses Cardiovascular functioning was assessed using a Finometer hemodynamic cardiovascular monitor (Finapres Medical Systems BV, BT Arnhem, The Netherlands). The Finometer measures beat-to-beat cardiovascular functioning non-invasively and is the successor of previous cardiovascular monitoring devices, the TNO Finapres-model-5 and the Ohmeda Finapres 2300e, which have been used in the previous research (e.g., Beckham et al., 2002; Gregg et al., 2002; Philippsen et al., 2007; Van Rooyen et al., 2004). The Finometer has been shown to provide accurate blood pressure measurement in young populations (Schutte et al., 2003). Determination of cardiovascular functioning using the Finometer is premised on the volume-clamp method, first developed by Peňaz (1973), while individualised determination of the volume at which the artery should be clamped is automatically calculated using the Physiocal algorithm (see Wesseling et al., 1995). Continuous measures of arterial CO, and TPR are estimated from arterial blood pressure waveforms using the validated Modelflow modelling method (Wesseling et al., 1995; Wesseling et al., 1993). Some of the precise operating procedures of the Finometer have been detailed elsewhere (see Hughes et al., 2011). 2.2.2. Psychometric measurement Trait dominance was measured using the Jackson Personality Research Form (JPRF) social dominance subscale (Jackson, 1999). Sixteen items assessed trait dominance (M = 5.24, SD = 4.10; possible scores ranged 0–16). Sample items include I feel confident when directing the activities of others, and I would make a poor military leader (reversescored). High scorers on the trait dominance subscale of the JPRF attempt to control their environments and influence or direct other people; they are forceful, decisive, authoritative, and domineering (Pratto et al., 1994). Reliability in the current study for trait dominance was good (α = .88). 2.2.3. Subjective task ratings Participants provided subjective ratings for three separate items measuring task engagement; perceived stress, interest, and difficulty. Participants were asked how stressful/interesting/difficult did you find the task following their completion of the stress tasks. Answers were obtained using a five-point Likert response scale, with possible scores ranging from 0 (not at all; stressful, interesting or difficult) to 4 (extremely; stressful, interesting or difficult). 2.2.4. Speech task Participants were asked to perform two of three possible speech task scenarios. Assignment to the speech tasks was randomised by the experimenter, and participants each performed two different speech tasks during the course of the experiment. The speech tasks chosen were similar in format and content to procedures previously employed in published research (e.g., Bostock et al., 2011; Hamer et al., 2006, 2007). The scenario was described, participants were given 2 min to prepare their defensive speech, and following this they were asked to deliver their speech to a video camera for 2 min, and they were aware that their performance was being video recorded. The scenarios involved false accusations of shoplifting, cheating on an exam, or an accusation of occupational disinterest. Participants were told that their speeches would be recorded, and that the tape would later be evaluated by the researcher for overall content, clarity and delivery. The experimenter remained in the room throughout the duration of the experiment, but remained behind an opaque screen, except when delivering instructions to the participant.

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2.3. Procedure Participants were seated on a comfortable chair in a small psychophysiological laboratory and familiarised with the Finometer apparatus. It was attached to their non-dominant hand, adjusted for participant comfort, but remained switched off. For 10 min, participants were asked to relax while completing some psychometric questionnaires. After 10 min, participants were asked to put aside the questionnaires and to relax for a further 10 min. A magazine was provided to assist with this relaxation (Jennings et al., 1992). Continuous blood pressure monitoring began at this time. After a further 10-minute baseline period spent relaxing and reading the magazine, participants were given instructions for the first stress task and asked to spend 2 min preparing for this task. The two-minute speech task was followed by a threeminute resting period, and the second speech stressor instructions, preparation, and task time. Each speech exposure period was defined as precisely the time period during which each participant was delivering their speech, and did not include the instruction or preparation phases. 2.4. Overview of analyses For the purposes of analyses, social dominance was reduced to a three group variable indicative of low (M = 1.13, SD = 0.81, n = 16), medium (M = 5.00, SD = 1.46, n = 17), and high (M = 10.62, SD = 2.33, n = 13) levels of dominance. Beat-to-beat cardiovascular data for systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), CO, and TPR were reduced to 30 second intervals, and mean values were then computed for each experimental phase, namely baseline, Exposure 1, resting post-Exposure 1, and Exposure 2 phases. Throughout, violations of estimates of Sphericity were corrected using Greenhouse–Geisser epsilon corrections as appropriate. To examine initially if the stressor was successful in eliciting CVR, a repeated measures ANOVA, with post hoc comparisons of means, was conducted for each cardiovascular parameter, with experimental phase entered as the within subjects factor. Polynomial functions were considered, and significant main effects were taken to indicate a change in cardiovascular functioning over the phases of the experiment. Post hoc paired samples t-tests assessed whether each cardiovascular parameter had returned to baseline levels during the inter-stressor resting period. Cardiovascular functioning during the resting phase that was equivalent to or lower than baseline levels was taken to be indicative of adaptation, and thus was calculated as the arithmetic difference between stressor exposure and the immediately preceding baseline (or resting) period. For cardiovascular parameters that failed to return to baseline levels during the resting phase, adaptation was computed as the arithmetic difference between stressor and baseline levels of that parameter. For parameters that did not achieve adaptation, 3 × 2 mixed ANCOVAs were conducted, with levels of trait dominance and reactivity to Exposures 1 and 2 included as factors. Baseline levels of each cardiovascular parameter were entered as a covariate to control for initial values (Benjamin, 1967). For each parameter that reached adaptation, a 3 × 4 mixed ANOVA was conducted, with dominance and experimental phase entered as the factors. Patterns of cardiovascular functioning were assessed using polynomial functions. 3. Results 3.1. Subjective task ratings Several 3 × 2 mixed ANOVAs revealed no significant differences between women categorised as having low, medium, or high levels of trait dominance for subjective ratings of Exposures 1 or 2 as stressful, interesting, or difficult (all ps N .46). Significant main effects for Exposure

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were found for ratings of stressfulness, F(1, 43) = 11.84, p = .001, partial η2 = .22, and difficulty, F(1, 43) = 9.30, p = .004, partial η2 = .18. Although it was found that Exposure 1 was rated as more stressful and more difficult generally by participants, these ratings did not significantly interact with trait dominance, suggesting that irrespective of dispositional dominance, similar levels of stress, difficulty, and interest were experienced by all participants. 3.2. Confirmation of reactivity Separate 4 × 1 repeated measures ANOVAs conducted using mean values of the cardiovascular parameters revealed significant linear and polynomial effects (significant at the cubic level) for all parameters (all ps b .001), except TPR (p = .89). In the case of TPR, trends were found to be significant at the level of both the linear and quadratic function (p = .001). The polynomial effects were supportive of the premise that there was a significant change in cardiovascular parameters over successive phases of the experiment for all parameters, except for TPR (see Table 1 for descriptive and reliability statistics of cardiovascular parameters). Post hoc paired samples t tests investigated differences between baseline and resting periods. The results showed that only HR and TPR were found to return to baseline levels during the post-Exposure 1 resting period, such that non-significant differences between baseline and resting cardiovascular functioning were observed (all ps N .09). For SBP, DBP, MAP, and CO, mean cardiovascular functioning during the resting period was found to be significantly higher than at baseline (all ps b .001). Thus, during calculations of CVR to tasks, the reference point of baseline values of cardiovascular parameters was chosen for SBP, DBP, MAP, and CO, rather than the immediately preceding resting period (which was chosen for HR and TPR). 3.3. Cardiovascular reactivity 3.3.1. Blood pressure (SBP, DBP, MAP and HR) Several 3 × 4 mixed ANOVAs were conducted to examine the effects of low, medium, and high levels of trait dominance on cardiovascular functioning over the four experimental phases. No statistically significant interaction effects between blood pressure (SBP, DBP, MAP, or HR) and trait dominance, or main effects for dominance were found (all ps N .05), suggesting that these parameters of cardiovascular functioning remained at similar levels for those higher and lower in trait dominance across successive stressor exposures. Significant main effects for phase were observed for SBP, F(1.84, 79.14) = 118.13, p b .001, partial η2 = .73; DBP, F(1.77, 75.99) = 214.00, p b .001, partial η2 = .83; MAP, F(1.71, 73.71) = 195.86, p b .001, partial η2 = .82; and HR, F(1.71, 73.71) = 195.86, p b .001, partial η2 = .82, such that blood pressure was higher during Exposure 2 than Exposure 1. Separate 3 × 2 mixed ANCOVAs were conducted to analyse potential differences between low, medium, and high dominant participants in relation to SBP, DBP, MAP, and HR reactivity to stress across the two stress-task exposures, with baseline values entered as a covariate. No significant interaction effects between blood pressure and trait dominance were found for SBP, DBP, MAP, or HR, suggesting that these parameters remained at similar levels for those with varying levels of trait dominance across successive stressor exposures. 3.3.2. Cardiac output A 3 × 4 ANOVA for CO revealed a significant main effect for phase, F(1.63, 69.92) = 37.25, p b .001, partial η2 = .46; a significant main effect for dominance, F(2, 43) = 4.70, p = .01, partial η2 = .18; and a significant phase × dominance interaction at the level of the cubic function, F(2, 43) = 5.27, p = .01, partial η2 = .20. Post hoc Tukey tests clarified the phase × dominance interaction and revealed that participants with lower dominance had significantly higher CO than those higher in dominance during Exposure 1 (p = .01), post task

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Table 1 Descriptives of cardiovascular parameters by phase for women (n = 46) with reliability statistics. Variable

Baseline α

a

SBP DBPa HRb MAPa COc TPRd

.98 .99 .99 .99 .99 .99

Exposure 1 Mean 117.21 72.32 78.60 90.62 5.18 1.17

SD 9.98 7.76 11.37 8.62 1.18 0.50

α .96 .96 .97 .96 .98 .97

Mean 137.84 86.65 92.46 108.81 6.31 1.15

Resting SD 14.66 10.41 14.17 12.09 1.65 0.44

Exposure 2

Cubic trend

α

Mean

SD

α

Mean

SD

p

η2

.96 .97 .98 .96 .98 .99

129.71⁎⁎⁎ 79.25⁎⁎⁎

11.18 8.21 11.84 9.02 1.33 0.47

.97 .97 .98 .97 .99 .98

139.48 88.92 89.70 110.72 5.90 1.27

15.35 9.94 14.11 11.54 1.62 0.05

b.001 b.001 b.001 b.001 b.001 .89

.72 .81 .72 .80 .50 .24

79.52 100.43⁎⁎⁎ 5.73⁎⁎⁎ 1.16

Note. Asterisks refer to significance values of post hoc paired samples t tests conducted to compare baseline and post task resting values for cardiovascular parameters. a mm Hg. b bpm. c lpm. d pru. ⁎⁎⁎ p b .001.

resting (p = .03), and Exposure 2 (p = .01). No other comparisons of CO between participants with lower and medium, and medium and higher levels of dominance were statistically significant. Examination of a 3 × 2 ANCOVA for the analysis of CO reactivity to Exposures 1 and 2, with baseline CO entered as a covariate, revealed no significant main effects for Exposure, trait dominance, or baseline CO. Additionally, no significant dominance × exposure, exposure × baseline, baseline × dominance, or dominance × exposure × baseline interactions were found. 3.3.3. Total peripheral resistance The results of 3 × 4 ANOVA for the analysis of TPR showed a significant main effect for phase, F(1.61, 69.02) = 7.05, p = .003, partial η2 = .14, which was also significant at the level of a quadratic function, F(1, 43) = 12.88, p = .001, partial η 2 = .23; and a borderline significant main effect for dominance, F(2, 43) = 3.13, p = .05, partial η2 = .13. Post hoc Tukey tests revealed that significant differences in TPR lay only between those lowest and highest in trait dominance (p = .04), whereby TPR was greatest for those with the highest levels of trait dominance (see Fig. 1). A cubic level dominance × phase interaction was not statistically significant, falling just outside the conventional cut offs allowed, p = .08. The cubic nature of the trait dominance × phase interaction observed for TPR suggested that further examination of the effects of trait dominance on TPR reactivity stressor exposures was warranted. A 3 × 2 repeated measures ANCOVA was conducted with three levels of trait dominance as the between subjects factor, and TPR reactivity to Exposure 1 and Exposure 2 entered as the within-subject factors (see Fig. 2). Continuous baseline TPR was entered as a covariate. The results of this 3 × 2 ANCOVA revealed significant main effects for exposure, F(1, 40) = 11.04, p = .002, partial η2 = .23, and for baseline TPR,

F(1, 40) = 8.05, p = .01, partial η2 = .17. For TPR, significant interactions were observed for exposure × baseline, F(1, 40) = 24.59, p b .001, partial η 2 = .38; and trait dominance × exposure × baseline, F(2, 40) = 14.87, p b .001, partial η2 = .43. No significant main effect for dominance was revealed. However, a significant trait dominance × exposure interaction was observed, F(2, 40) = 7.77, p = .001, partial η2 = .28, suggesting that, independent of the effect of baseline TPR, trait dominance was associated with TPR reactivity to Exposures 1 and 2. Post hoc paired samples t-tests showed that there was greater TPR reactivity to Exposure 2 than Exposure 1 for those categorised with low (p = .02) or medium (p = .03) levels of trait dominance. No significant difference in TPR reactivity between Exposures 1 or 2 was observed for participants categorised as high in trait dominance (p =.14). While during Exposure 1, only those lowest and highest in dominance had TPR reactivity significantly different from each other (p =.05), at Exposure 2 it was found that TPR reactivity for those with medium levels of dominance was significantly higher than for participants rated as lower in dominance (p = .02). While the differences between low and high dominance were marginally not statistically significant (p = .06), it was also found that there was no statistically significant difference between TPR reactivity during Exposure 2 for participants with high and medium levels of trait dominance (p = .81), suggesting parity between high and medium dominant participants. 4. Discussion Trait dominance was found to be associated with greater vascular patterns of CVR, lower myocardial functioning, and with attenuated habituation to repeated social stress.

Fig. 1. Patterns of CO (a) and TPR (b) across successive stressor exposures with lower (n = 16), medium (n = 17), and higher (n = 13) trait dominance. p values represent significance of the changes from each experimental change to the next. Error bars denote standard error of the mean.

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Fig. 2. Reactivity of CO (a) and TPR (b) to Exposures 1 and 2 for participants with lower (n = 16), medium (n = 17), and higher (n = 13) trait dominance. Error bars denote standard error of the mean.

Higher trait dominant participants were characterised by higher levels of sustained vascular stress activity during Exposures 1 and 2, compared to participants with lower and medium trait dominance, who exhibited significant higher levels of TPR activity during Exposure 2. Patterns of myocardial functioning over the experimental phases were similar for those with lower, medium, and higher levels of dominance, such that CO during Exposure 2 was lower than that observed during Exposure 1. During repeated stressor exposures, cardiovascular parameters characterised as myocardial factors (e.g., CO) typically attenuate over subsequent stressor presentations, while other, vascular, factors (e.g., TPR) may not decrease or may in fact increase (Kelsey et al., 1999). As mentioned previously, optimal regulation of the hemodynamic profile is characterised by simultaneous increases in either CO or TPR, with parallel decreases in the other parameter. While patterns of cardiovascular functioning were similar to this optimal profile for participants with medium and lower levels of dominance, for those higher in dominance, sustained higher levels of vascular stress activity (i.e., TPR) for both stressor exposures could be indicative of maladaptive stress responding. Cardiovascular profiles characterised by an initial myocardial response to stress, followed by a habituation of that response on subsequent exposures to similar stress are healthful. In contrast, sustained vascular profiles of cardiovascular responding are associated with CVD risk (Julius et al., 1986; Palatini and Julius, 2009). The results are consistent with evidence that points to an association between maladaptive patterns of CVR and trait dominance. It should also be noted that in this study, participants scoring lower in dominance had higher changes in CO during Exposures 1 and 2, and concurrently had consistently lower TPR. Such a hemodynamic pattern is consistent with a fight or flight response, or an appropriate response to a new (stressful) event. It may be that this group of low dominant individuals characteristically respond to stressor events in this manner. As levels of TPR were found to increase over time for participants with lower and medium levels of dominance, such changes could also reflect an increasing sense of ease with the stress tasks. In tandem, CO activity reduced for these participants too. In contrast, the higher dominant group evidenced lower cardiovascular activity changes, with higher levels of TPR across all experimental phases, and a corresponding lower profile of CO activity, relative to participants with lower and medium levels of dominance. Such differences in the ways in which individuals higher and lower in trait dominance respond to the same set of socially-oriented stressors could potentially reflect characteristic ways of experiencing and reacting to stress, which may have longterm implications for health, should these patterns be sustained over a long period of time. As participants higher in dominance had a pattern of cardiovascular functioning that was relatively stable, this could in another way point to the detrimental effects of sustained patterns of

vascular forms of cardiovascular activity, with impaired ability to physiologically distinguish between stress and non-stress times. Although the exact mechanisms involved in the negative health outcomes associated with failed or delayed adaptation to stress remain unclear, some potential explanations for increases in vascular factors (and thus failure to adapt to stress over time) have been posited, most recently by Hughes et al. (2011). The authors suggest that increased vascular resistance during stress could reflect a process of auto-regulation, whereby increases in vascular factors could be prompted by the hemodynamic factors that underlie increases in myocardial factors. Alternatively, increases in parameters such as TPR which are indicative of systemic vascular restriction could be a consequence of increased vasoconstriction, or some combination of myocardial driven vasodilatation, and vascular vasoconstriction (Carroll et al., 1990; Kelsey et al., 1999). Whatever the mechanism for lack of physiological attenuation to stress, it seems that vascular responses during repeated stressor exposures are implicated in ways that are harmful to cardiovascular health. The findings support the evidence that dominance is associated with maladaptive patterns of cardiovascular responding (e.g., Newton, 2009), and shed further light on some of the physiological processes that may underlie increased cardiovascular risk associated with trait dominance. The study shows that repeated social stress exposures can prompt potentially maladaptive cardiovascular responses in women with a greater dominant disposition. The results support the findings of previous studies that employed repeated stressor exposure protocols to other active stressors (e.g., mental arithmetic; Kelsey et al., 1999, 2004), which reported general attenuations in myocardial, but not levels of vascular activity with repeated stress exposures. The innate desire of people higher in trait dominance to exert a controlling influence to the attainment of social hierarchy may be a feature of the increased vascular profile of responding. Higher trait dominant individuals persist in the exhibition of underlying vascular hemodynamic responses to stress, even when it appears that blood pressure is stable. Interestingly, only those lower in social dominance reported Exposure 2 as significantly less stressful and less difficult, compared to Exposure 1. Some small declines in subjective appraisals of stress and difficulty between the two stressors for those higher in dominance were not statistically significant. Despite no observed between-subject effects for trait dominance relating to subjective task appraisals, the fact that lower trait dominant participants found Exposure 2 to be less stressful and less difficult reflects their attenuated physiological functioning during Exposure 2. In contrast, even the task appraisals of those higher in dominance did not demonstrate habituation of perceived stressfulness or difficulty of the tasks, mirroring their physiological responding. The results of the current study add to the debate surrounding blunting of cardiovascular functioning. As argued by James et al.

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(2012), examination of hemodynamic processes can reveal added value to the interpretation of findings that may at first appear to reflect blunted physiological function. James et al. (2012) suggested that blunted blood pressure responses could be the result of a particular personality's tendency towards a characteristic vascular or myocardial response pattern (i.e., high-dominant individuals may trend towards more vascular-oriented cardiovascular response patterns). Therefore, as suggested by James et al. (2012), an alternative explanation to cardiovascular blunting, less pronounced blood pressure could be an indication of augmented vascular tendencies. The current findings indicate the potential for an association between trait dominance and patterns of hemodynamic function to affect lifetime health trajectories, should such hemodynamic patterns be sustained over the course of a lifetime. Hemodynamic profiles of stress responding have previously been shown to have good temporal stability (Sherwood et al., 1990). Limitations of the study could be addressed by including an extended protocol with further stressor exposures to demonstrate whether the current trends could be replicated. Variations of the speech task could be interesting to examine, such as conditions where an independent observer is present during the task, rating participant's speech rather than using a video camera. The findings extend previous research with repeated mental arithmetic tasks (Howard et al., 2011; Hughes et al., 2011), and suggest that individual differences in dominance may moderate profiles of hemodynamic responses. The observed sustained vascular-oriented pattern of cardiovascular activity to repeated social stress for those higher in dominance could point to a potential mechanism though which trait dominance and patterns of hemodynamic responses could be linked to poorer cardiovascular health outcomes, which warrants closer future investigation. Acknowledgment This work was supported by funding from the Higher Education Authority of Ireland, Programme for Research in Third Level Institutions, Cycle 4 (Irish Social Sciences Platform). References al'Absi, M., Bongard, S., Buchanan, T., Pincomb, G.A., Licinio, J., Lovallo, W.R., 1997. Cardiovascular and neuroendocrine adjustment to public speaking and mental arithmetic stressors. Psychophysiology 34, 266–275. Beckham, J.C., Vrana, S.R., Barefoot, J.C., Feldman, M.E., Fairbank, J., Moore, S.D., 2002. Magnitude and duration of cardiovascular response to anger in Vietnam veterans with and without posttraumatic stress disorder. J. Consult. Clin. Psychol. 70, 228. Benjamin, L.S., 1967. Facts and artifacts in using analysis of covariance to “undo” the law of initial values. Psychophysiology 4, 187–206. Booth-Kewley, S., Friedman, H.S., 1987. Psychological predictors of heart disease: a quantitative review. Psychol. Bull. 101, 343–362. Bostock, S., Hamer, M., Wawrzyniak, A.J., Mitchell, E.S., Steptoe, A., 2011. Positive emotional style and subjective, cardiovascular and cortisol responses to acute laboratory stress. Psychoneuroendocrinology 36, 1175–1183. Brod, J., Fencl, V., Hejl, Z., Jirka, J., 1959. Circulatory changes underlying blood pressure elevation during acute emotional stress (mental arithmetic) in normotensive and hypertensive subjects. Clin. Sci. 18, 269–279. Carroll, D., Cross, G., Harris, M.G., 1990. Physiological activity during a prolonged mental stress task: evidence for a shift in the control of pressor reactions. J. Psychophysiol. 4, 261–269. Carroll, D., Lovallo, W.R., Phillips, A.C., 2009. Are large physiological reactions to acute psychological stress always bad for health? Soc. Personal. Psychol. Compass 3, 725–743. Everson-Rose, S.A., Lewis, T.T., 2005. Psychosocial factors and cardiovascular diseases. Annu. Rev. Public Health 26, 469–500. Frankish, J., Linden, W., 1991. Is response adaptation a threat to the high-low reactor distinction among female college students? Health Psychol. 10, 224–227. Gramer, M., 2003. Cognitive appraisal, emotional and cardiovascular responses of high and low dominant subjects in active performance situations. Pers. Individ. Differ. 34, 1303–1318. Gramer, M., Berner, M., 2005. Effects of trait dominance on psychological and cardiovascular responses to social influence attempts: the role of gender and partner dominance. Int. J. Psychophysiol. 55, 279–289.

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Trait dominance is associated with vascular cardiovascular responses, and attenuated habituation, to social stress.

Both exaggerated and diminished levels of cardiovascular reactivity have been associated with cardiovascular ill health. Dysregulation of hemodynamic ...
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