Stress-induced Cardiovascular Reactivity Research Articles

Can Acute Exercise Lower Cardiovascular Stress Reactivity? Findings from a Scoping Review.

Exaggerated cardiovascular reactivity to and delayed recovery from stress increase the risk of cardiovascular diseases in the future. While exercise training has been shown to attenuate stress-induced cardiovascular reactivity and enhance recovery from stress, the effects with acute exercise are less characterized. The aim of this scoping review was to explore the range and characteristics of published evidence regarding acute exercise on cardiovascular reactivity and stress recovery. The secondary objective was to highlight research gaps and implications for future research. A total of 36 articles met the review inclusion/exclusion criteria, involving 1200 participants from various age groups, fitness and health status. Blood pressure (BP) reactivity was the most measured outcome, followed by heart rate (HR) reactivity, and to some extent, heart rate variability. Overall, acute exercise particularly of the moderate-intensity aerobic type effectively reduced stress-induced BP reactivity in the general population. The effects on HR reactivity and cardiovascular recovery were inconclusive. Further research would be recommended to establish if other forms of exercise intensity or type are equally beneficial to lower exaggerated cardiovascular responses to stress. Despite methodological differences and limitations, the available evidence supports the therapeutic potential of acute exercise in addressing the ill effects of stress on cardiovascular health.

Attenuation of stress-induced cardiovascular reactivity following high-intensity interval exercise in untrained males

ABSTRACT Exaggerated cardiovascular (CV) reactivity to stress is associated with negative cardiovascular outcomes. This study aimed to investigate the effects of acute high-intensity interval exercise (HIIE) and moderate-intensity exercise (MIE) on CV reactivity in response to a stress challenge in untrained males. Thirteen, normotensive males (age: 22.8 ± 2 years, BMI: 21.9 ± 3.6 kg/m2) underwent three conditions in counterbalanced order: HIIE (bodyweight exercises; 80–90% HRR), MIE (treadmill-jog; 55–60% HRR) and seated rest (CON) separated by 7–10 days. Thirty minutes after performing HIIE, MIE or CON, subjects underwent a 2-min cold pressor task (CPT). Blood pressure (BP) and heart rate (HR) were measured before, during, and after CPT. CV reactivity, i.e., the change in BP and HR responses were compared across conditions. Systolic BP reactivity were attenuated following HIIE (−60%, p = 0.015) and MIE (−42%, p = 0.033) compared to CON, but no differences were observed between HIIE and MIE. HR reactivity was not different across all conditions. We conclude that performing HIIE or MIE 30 minutes prior to acute stress exposure lowers BP reactivity compared to rest in untrained males. These findings highlight the potential benefits of HIIE in lowering stress-induced elevations in blood pressure

Attenuated cardiovascular reactivity is related to higher anxiety and fatigue symptoms in truck drivers.

Depression and anxiety have been linked with reduced stress-induced cardiovascular reactivity (CVR), which could be indicative of autonomic dysregulation. Less is known about the association between work-related fatigue and CVR. Truck drivers experience high levels of depression, anxiety, and fatigue, with repeated psychophysiological stressors on the road, yet little is known about the effects of these conditions on their CVR. Three hundred eighty six truck drivers completed the Hospital Anxiety and Depression Scale (HADS) and the Occupational Fatigue Exhaustion/Recovery Scale (OFER-15). Systolic (SBP) and diastolic (DBP) blood pressure and heart rate (HR) were measured at rest and during a stressor protocol to measure CVR. Multivariate regression analyses were used to determine relationships between variables and adjusted for nine key covariates. Higher symptoms of persistent fatigue were related to a reduced SBP reactivity (β=-.236, p=.009) and reduced DBP reactivity (β=-.257, p=.005), whereas there was a positive trend between acute fatigue and DBP reactivity (β=.169, p=.052). Higher symptoms of anxiety were related to a reduced SBP reactivity (β=-.164, p=.016). This study demonstrated in a population of truck drivers that both anxiety and persistent fatigue were related to an attenuated SBP reactivity in a combined model, whereas there was a positive trend between acute fatigue solely and DBP reactivity. These novel findings may have serious implications for cardiovascular disease risk in truck drivers, and future research should attempt to establish the causal effect of these associations and the underlying physiological mechanisms.

325 Stress-Induced Physiological Profiles Among Different Phenotype Insomniacs

Abstract Introduction Stress reactivity and autonomic nervous system (ANS) dysregulation have been suggested to be the pathophysiology of insomnia. Based on the finding PSG-measured short sleep duration was associated with higher morbidity of metabolic and cardiovascular disease. Vgontzas and Fernandez-Mandoza (2013) proposed that objective sleep duration is a biomarker for insomnia phenotypes. The phenotype with short objective sleep duration is associated with increased stress-related physiological hyperarousal. The present study aims to test this hypothesis by comparing the stress-induced cardiovascular reactivity between insomnia patients with short and long objective sleep durations. Methods 27 insomnia patients (age mean 34.48 ±12.87, Male: Female= 6:21) without comorbidity of psychiatric, medical or sleep disorders participated in this study. They went through one night of 8-hour PSG recording and were divided into two groups by their total sleep time with a cutoff of 6 hours. Nine participants were in short sleep duration group and 18 in longer sleep duration group. Psychophysiological reactivity profile, as recorded with EKG, skin conductance (SC), body temperature (BT), blood volume pulse (BVP), respiration rate (RR), was measured under three conditions: baseline resting state, arithmetic word problems solving, and recovery resting state. Results Both groups showed similar stress physiological response with increased heart rate (HR) and SC, nearly equivalent BT and BVP, and decreased RR when solving arithmetic problems, and opposite reaction during recovery resting state. Mann-Whitney U test comparing the changes from baseline resting state on all the psychophysiological measures between two phenotypes of insomnia showed no significant differences: stress-induced heart-rate (U=106, p=.119.) recovery heart-rate (U=44, p=.095), stress-induced skin conductance (U=104.5, p=.132),recovery skin conductance (U=51.5, p=.198), stress-induced body temperature (U=79, p=.897),recovery body temperature (U=60.5, p=.418), stress-induced blood volume pulse amplitude (U=77, p=1.0), and recovery blood volume pulse amplitude (U=69, p=.735), stress-induced respiration rate (U=76, p =.696), and recovery respiration rate (U=85, p=.658). Conclusion Our results indicate that the insomnia phenotypes with short and long objective sleep duration are not different in their stress-induced physiological responses. Future studies are needed to confirm these results and to explore other mechanisms for the increased metabolic and cardiovascular disease risk in insomnia patients with short objective sleep duration. Support (if any):

The Effects of Nicotine and Nicotine Abstinence on Stress-Induced Cardiovascular Reactivity

Abstract. The effects of 12 hr nicotine administration and abstinence on stress-induced cardiovascular reactivity were assessed within Light/Intermittent cigarette smokers and Habitual cigarette smokers. One hundred thirty-two male smokers (66 Habitual, 66 Light/Intermittent) were assigned to a Nicotine (21 mg) or Placebo patch condition. Cardiovascular reactivity was assessed during Baseline, a 6-min mental arithmetic task (Paced Auditory Serial Arithmetic Task) and a 5-min mirror-tracing task (Star Mirror Tracing Task). Within the Nicotine condition, Light/Intermittent smokers showed greater cardiac output (CO) increases, smaller stroke volume decreases, and smaller total peripheral resistance (TPR) increases than Light/Intermittent smokers in the Placebo condition. No condition differences in cardiovascular reactivity were demonstrated for Habitual smokers. Light/Intermittent smokers also showed greater CO increases than Habitual smokers during the mirror-tracing task but during the Nicotine condition only. During mental arithmetic, Light/Intermittent smokers had greater CO increases and smaller TPR increases than Habitual smokers across nicotine conditions. Habitual smokers responded to stress with increases in peripheral responses whereas Light/Intermittent smokers responded myocardially. Light/Intermittent smokers may have increased density of β-adrenergic receptors whereas Habitual smokers may have decreased density due to chronic smoking.

The Stress-Induced Cardiovascular Reactivity in the Fasting and Fed States of Healthy Young Indian Males

Low blood glucose levels have been associated with a hostile behaviour. The individuals who show aggressiveness and hostility are more likely to develop hypertension and cardiac diseases. The future hypertension has been linked with a high cardiovascular reactivity to stress. We have investigated the association of the blood glucose levels with the Cardio Vascular Reactivity (CVR) to stress. Fourty six volunteers were subjected to stress (which was induced by the cold pressor task) in the fasting state and again, half an hour after the ingestion of 75 grams of glucose. The CVR in both conditions was compared in terms of an increase in the heart rate and the blood pressure. The resting pulse was lower and the blood pressure was higher in the fasting condition, as compared to the values which were obtained in the ½ hour post-prandial condition. The CVR to stress was significantly higher in the fasting condition. The increased resting heart rate and the decreased resting blood pressure in the ½ hourPost-Prandial (PP) condition was due to the higher levels of histamine in the post-prandial state. Low blood glucose levels are associated with a higher CVR to stress. This suggests that the persons are prone to develop future hypertension, those with frank hypertension, and the chronic pain sufferers should avoid prolonged fasts, in order to lower their CVR to the stress stimuli which are encountered in the daily life.

Cardiovascular reactivity, stress, and physical activity

Psychological stress has been proposed as a major contributor to the progression of cardiovascular disease (CVD). Acute mental stress can activate the sympathetic-adrenal-medullary (SAM) axis, eliciting the release of catecholamines (NE and EPI) resulting in the elevation of heart rate (HR) and blood pressure (BP). Combined stress (psychological and physical) can exacerbate these cardiovascular responses, which may partially contribute to the elevated risk of CVD and increased proportionate mortality risks experienced by some occupations (e.g., firefighting and law enforcement). Studies have supported the benefits of physical activity on physiological and psychological health, including the cardiovascular response to acute stress. Aerobically trained individuals exhibit lower sympathetic nervous system (e.g., HR) reactivity and enhanced cardiovascular efficiency (e.g., lower vascular reactivity and decreased recovery time) in response to physical and/or psychological stress. In addition, resistance training has been demonstrated to attenuate cardiovascular responses and improve mental health. This review will examine stress-induced cardiovascular reactivity and plausible explanations for how exercise training and physical fitness (aerobic and resistance exercise) can attenuate cardiovascular responses to stress. This enhanced functionality may facilitate a reduction in the incidence of stroke and myocardial infarction. Finally, this review will also address the interaction of obesity and physical activity on cardiovascular reactivity and CVD.

Stress-induced cardiovascular reactivity and atherogenesis in adolescents

ObjectiveTo examine the association between cardiovascular reactivity to a set of psychological stressors and carotid artery intima-media thickness, a marker of subclinical cardiovascular disease in healthy adolescents. MethodsParticipants were 25 boys and 23 girls age 14.2±0.9 years who were measured for heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressure reactivity to mirror-tracing, reaction time, speech preparation and ad lib speech tasks and for common carotid artery intima-media thickness. Sequential regression analyses were used to establish the incremental increase in R2(Rinc2) for the prediction of intima-media thickness due to cardiovascular reactivity independent of age, BMI percentile, sex, socioeconomic status, and resting HR or BP. ResultsSBP reactivity while preparing (β=0.0019, Rinc2=0.09) and giving the speech (β=0.0014, Rinc2=0.10) and an aggregate reactivity score based on all 4 tasks (β=0.0026, Rinc2=0.11) independently predicted (p≤0.05) mean carotid artery intima-media thickness. Neither DBP reactivity nor HR reactivity during any task were independent predictors of intima-media thickness. ConclusionStress-induced cardiovascular reactivity, and especially SBP reactivity, is associated with carotid intima-media thickness and the early pathogenesis of cardiovascular disease. The use of an aggregate stress reactivity index provides a more reliable reflection of trait SBP reactivity to psychological stress and increases the confidence that youth with greater cardiovascular stress reactivity may indeed have greater progression of subclinical cardiovascular disease.

Stress-Induced Cardiovascular Reactivity Among African American Smokers

To test for differences in stress-induced cardiovascular functioning among hypertensive and normotensive African American (AA) smokers. Participants (n = 35) were exposed to both stress and neutral mood inductions. Repeated measures analyses of covariance produced a significant group x mood condition interaction for systolic blood pressure (P = .048), but not for diastolic blood pressure (P > .05). The most notable finding was that AA hypertensive smokers showed selectively greater elevations in their systolic responses compared with normotensive controls following the laboratory-induced stressor. Implications to an elevated risk of future cardiovascular disease among AA hypertensive smokers are discussed.

Emotion suppression affects cardiovascular responses to initial and subsequent laboratory stressors

The study of anger suppression and risk for cardiovascular disease has relied predominately on inspection of correlations between trait anger-in and cardiovascular risk factors and disease. This approach tells us little about whether inhibitory processes have anything to do with outcomes, and cannot speak to whether suppression of anger per se affects cardiovascular parameters. Drawing on the broader emotion regulation literature, we examined the effects of experimentally induced anger and general negative emotion in the context of expressive and experiential suppression on cardiovascular responses to initial and subsequent laboratory stressors. Of all participants, 201 healthy participants were randomly assigned to one of six conditions formed by crossing emotion (anxiety, anger) and suppression (experiential, expressive, control) conditions. Participants completed a mental arithmetic task with anxiety or anger induction under their respective suppression manipulation instructions, and subsequently were exposed to a cold pressor task. Systolic blood pressure (SBP), diastolic blood pressure, and heart rate values were obtained for each experimental epoch. More robust SBP responses to the initial stressor were evidenced for those in the expressive versus the control condition. In response to the subsequent stressor, those in the experiential suppression condition showed the most pronounced SBP responses, suggesting pronounced delayed effects of this type of suppression. Effects of suppression on SBP reactivity were indistinguishable across anxiety and anger conditions. Effortful suppression of negative emotion has immediate and delayed consequences for stress-induced cardiovascular reactivity. Theoretical and clinical significance of these findings are discussed.

Effect of a Simulated Active Commute to School on Cardiovascular Stress Reactivity

Stress-induced cardiovascular reactivity is associated with the pathogenesis of cardiovascular disease. This study tested whether a simulated active commute to school dampened cardiovascular reactivity to a cognitive stressor typical to what children might experience during school. Forty children (20 girls and 20 boys) aged 10-14 yr were randomly assigned to simulated sedentary drive-to-school or active-commute (walking) groups. The walking group completed a self-paced 1.6-km walk on a treadmill while images from a real 1.6-km walk through a pleasant neighborhood that finished at a school were projected in front of them. The drive-to-school group sat in a chair and watched the same slideshow of images of the neighborhood environment. Standardized residualized gain scores of cardiovascular reactivity during a cognitive stressor, the Stroop task, were calculated and used as dependent variables. Children in the walking group self-selected a walking intensity of 60.6% +/- 1.6% HRmax and covered the 1.6-km distance in 21.5 +/- 0.5 min. Children in the walking group had lower HR (2 +/- 1 vs 11 +/- 1 bpm, P < 0.001), systolic blood pressure (4 +/- 1 vs 12 +/- 1 mm Hg, P < 0.001), pulse pressure (-4 +/- 1 vs 6 +/- 1 mm Hg, P < 0.001), and perceived stress (1.4 +/- 0.1 vs 3.0 +/- 0.1 cm, P < 0.001) reactivities to cognitive stress than the control group. Active commuting to school may dampen cardiovascular reactivity and perceived stress when confronted with stressful cognitive challenges during the school day. This may help reduce the risk for cardiovascular disease later in life.

A Protective Effect of Exercise Against Interpersonal Stress-Induced Cardiovascular Reactivity in Youth

Empirical evidence suggests an association between blood pressure reactivity to psychological stress in childhood and hypertension in adulthood. Acute aerobic exercise dampens blood pressure reactivity to subsequent stress in adults. PURPOSE: To determine if a single bout of interval exercise reduces cardiovascular reactivity to an interpersonal stressor in children. METHODS: Twenty-two children (n = 11 boys, n = 11 girls), ages 8-12 completed a control television-speech protocol and an experimental interval exercise-speech protocol. The order of test days was counterbalanced across children. Heart rate, blood pressure and perceived stress measures were collected at baseline, after watching television or exercising for 25 minutes (post-television or post-exercise), after reading for 20 minutes (post-read), and then after preparing (post-speech preparation) and giving a speech (post-speech). Salivary α-amylase concentrations were measured at baseline, post-speech preparation and post-speech as a marker of sympathetic tone. Children wore an accelerometer for 7 days to assess usual physical activity. RESULTS: Diastolic (DBP) and mean arterial pressures (MAP) increased (p < 0.001) when giving a speech on both the television and exercise days; however, the slope of the increase was greater (p < 0.006) when children watched television than when they exercised. Salivary α-amylase concentrations were lower (p < 0.05) when giving a speech after exercising than when giving a speech after watching television. The changes in DBP (ρ = 0.51, p < 0.02) and MAP (ρ = 0.44, p < 0.05) were correlated with the change in α-amylase from baseline to post-speech on the exercise day. CONCLUSIONS: An acute bout of interval exercise can attenuate stress-induced blood pressure responses and dampened sympathetic output may be one mechanism whereby exercise attenuates stress-induced cardiovascular reactivity. Frequent exercise may help to reduce the risk of hypertension and cardiovascular disease in adulthood by reducing stress-induced cardiovascular reactivity.

Psychological and physical stress-induced cardiovascular reactivity and diurnal blood pressure variation in women with different work shifts.

There is increasing evidence that diurnal blood pressure (BP) variation, in addition to high BP per se, is related to target organ damage and the incidence of cardiovascular events. However, the determinants of diurnal BP variation are not adequately understood. This paper tests the hypothesis that cardiovascular reactivity to acute stress and/or delayed recovery predicts greater diurnal BP variation (i.e., a lower sleep/awake BP ratio). We studied the relationship of diurnal BP variation (assessed by ambulatory BP monitoring) to mental stress (mental arithmetic and anger recall tasks) and physical stress (treadmill)-induced cardiovascular reactivity and recovery in 87 female nurses who worked different shifts. The sleep/awake systolic BP (SBP) ratio was negatively correlated with relative SBP reactivity (maximum SBP increase/baseline SBP: r = -0.21, p = 0.06) and relative stress response (average of SBP during stress/baseline SBP:r = -0.23, p = 0.04) induced by anger recall, while the correlations of the sleep/awake SBP ratio with other parameters of reactivity or recovery in the anger recall or mental arithmetic task were not significant. When subjects were divided into day-shift workers (n=54) and night-shift workers (n = 33), the sleep/awake SBP ratio was negatively correlated with relative SBP reactivity (r = -0.41, p = 0.02) and relative stress response of SBP (r = -0.48, p = 0.006) induced by anger recall, and positively correlated with recovery rate (r = 0.34, p = 0.06) in the latter group, while these correlations were not significant in the former group. The sleep/awake SBP ratio was inversely correlated with the exercise-induced SBP increase in the day-shift workers (r = -0.30, p = 0.03), while this association was not found in the night-shift workers. In conclusion, cardiovascular reactivity triggered by psychological and physical stress in the laboratory may be a weak, but significant, determinant of diurnal BP variation; in addition, work shift (day or night) appears to moderate the relationship between these two pressor mechanisms.

Acute hemoconcentration during psychological stress: Assessment of hemorheologic factors

In this study, we examined the effects of acute psychological stress on hemorheology and hemoconcentration in humans and the associations between stress-induced cardiovascular reactivity and hemorheological changes. Stress-induced changes in hemorheology and hemorheological changes were assessed by measuring plasma viscosity, calculated plasma volume, and total plasma protein. Cardiovascular, hemorheologic, and hematologic variables were assessed in 29 healthy men during a 30-min baseline period and a 5-min speech task. Results indicated that the speech task produced a significant increase in plasma viscosity and total plasma protein and a significant decrease in calculated plasma volume. Significant correlations were observed between changes in blood pressure and heart rate and changes in plasma viscosity, total plasma protein, and calculated plasma volume. These results provide direct evidence that acute psychological stress can produce significant changes in hemorheology and hemoconcentration. The most likely mechanism for the stress-induced hemoconcentration effect is a fluid shift from the vascular to the interstitial spaces through increased blood pressure.

Postural effects on hemodynamic response to interpersonal interaction

Laboratory studies of stress-induced cardiovascular reactivity have been conducted predominantly with participants in a seated posture. This procedure may contribute to limited laboratory-field generalization of cardiovascular response. The present study examined hemodynamic adjustments underlying pressor responses, in addition to heart rate and systolic time intervals, during seated and standing role-played, interpersonal interaction in 60 young adults. Irrespective of gender or race, blood pressure responses to the seated and standing interactions were comparable. However, seated interactions yielded a significantly greater increase in heart rate, shortened preejection period and decreased stroke index as compared to standing. Alternatively, interacting while standing yielded a significantly increased left ventricular ejection time and total peripheral resistance in comparison to sitting. These results suggest that hemodynamic adjustments during stressful interpersonal interaction vary as a function of posture, with somewhat greater cardiac influences apparent while seated and a more pronounced vascular response while standing.

The influence of dietary cholesterol on cardiac and hepatic beta-adrenergic receptors in egyptian sand rats

We examined the effects of dietary cholesterol on cardiac and hepatic beta-adrenergic receptor functioning. Age-matched adult desert rodents (Psammomys obesus) were randomized to either a 5% cholesterol diet (CD, n = 20), or normal rabbit chow (RC, n = 18). After a 2-month exposure to the diets, animals were sacrificed and tissue from both heart and liver were retained for radioligand bindings studies. In heart tissue, cholesterol fed animals, relative to controls, showed an increased production of adenosine 3,5>-cyclic monophosphate (cAMP) in response to isoproterenol. Cholesterol supplementation was not associated with an increase in heart beta-adrenergic receptor number. Animals fed the 5% cholesterol diet showed significant increases in the number of beta-adrenergic receptor sites in hepatic tissue (M = 13.2 vs. 10.4 pmol/mg protein, CD and RC, respectively). The increased number of receptor sites in the liver was accompanied by a significant increase in isoproterenol-stimulated cAMP production. Results are supportive of the hypothesis that dietary cholesterol contributes to an upregulation of beta-adrenergic receptor function in cardiac, as well as hepatic tissue. These findings may be relevant to the observations of excessive stress-induced cardiovascular reactivity in persons with high cholesterol levels.

An overview of the role of cardiovascular reactivity to stressful challenges in the etiology of hypertension.

There is significant variability among individuals in the cardiovascular responses to both physical and psychologic stimuli, a phenomenon called cardiovascular reactivity. The magnitude of cardiovascular reactivity may distinguish those prone to develop cardiovascular disease or differentiate pathophysiologic states among individuals who have existing pathologies such as hypertension. This article describes the cardiovascular reactivity hypothesis as a proposed mechanism of hypertension development. Furthermore, proposed mechanisms underlying the pathophysiology of hyperreactivity are also discussed. The value of assessing stress-induced cardiovascular reactivity is evaluated with special regard to hypertension, and future avenues for nursing research are presented.

Does cardiovascular reactivity to mental stress have prognostic value in postinfarction patients? A pilot study.

The possible relationship between mental stress-induced cardiovascular reactivity and clinical prognosis was examined in a pilot study of 13 postinfarction patients. All patients had previously participated in the placebo condition of a secondary intervention trial. On completion of the trial, blood pressure, heart rate, and venous plasma catecholamines were evaluated at rest and in response to a modified Stroop test on two occasions. At follow-up 39 to 64 months later, five patients had suffered a new clinical event (reinfarction and/or stroke). These patients had shown significantly larger systolic and diastolic blood pressure responses to the Stroop test than had patients who remained event-free at follow-up. Catecholamine concentrations also differed between groups during mental stress, but on only one of the two test days. Groups did not differ on baseline measurements, cardiovascular response to exercise testing, fasting serum lipid and glucose concentrations, age, or duration of follow-up.

Interaction of sodium sensitivity and stress in young adults.

The interaction of sodium sensitivity and stress-induced cardiovascular reactivity was studied in white and black young adults aged 18-23 years. The cardiovascular response to difficult mental arithmetic was measured before and after 14 days of oral sodium loading (10 g NaCl/day added to the usual diet). A sodium-sensitive blood pressure response occurred in 18.4% of whites and 37.3% of blacks. A significant correlation between blood pressure change and sodium excretion occurred in the sodium-sensitive group (r = - 0.28, p less than 0.01). High sodium intake did not augment blood pressure or heart rate response to the beta-adrenergic-mediated stimulus of mental arithmetic in the population, which was grouped by blood pressure, race, or sodium sensitivity.

Racial differences in stress-induced cardiovascular reactivity and hypertension: current status and substantive issues.

Essential hypertension is perhaps the number-one health problem of Black Americans. Research has indicated that stress-induced cardiovascular hyperreactivity may be a significant contributor to essential hypertension. The high prevalence of hypertension among Blacks suggests that this group, in comparison with Whites, may be particularly susceptible to cardiovascular hyperreactivity. The first portion of this article reviews research to date that has examined racial differences in resting and stressor-induced cardiovascular activity. The second half of this article overviews some critical methodological and conceptual issues involved in the study of racial differences in reactivity. These issues include the effects of Black-White differences in plasma renin levels and sodium excretion, the effects of experimenter race, and differences in perceptions of the laboratory environment. Additionally, the issue of racial group classification and the implications this has for interpreting Black-White differences in reactivity is discussed. Two perspectives on racial group classification, the genetic and the sociocultural, are addressed in some detail, and the relevance of each to research on racial differences in stress reactivity is presented.