Increased cardiovascular reactivity during laboratory stress has been predictive of elevated risk for the development of hypertension (e.g., 25–27), whereas cardiorespiratory fitness is associated with reduced risk (5). It has been hypothesized that cardiorespiratory fitness might protect against hypertension, in part, by an attenuation of cardiovascular reactivity or improved recovery in response to acute stress (11,36). However, the evidence that cardiorespiratory fitness blunts blood pressure responses during or after stress has been mixed and mainly limited to young, normotensive, white male subjects with unreported parental history of hypertension (11–12,20). Black Americans (2,17,19,31) and normotensive individuals with a parental history of hypertension (16,24,32,33) have an elevated risk of developing hypertension and are more likely to exhibit stress reactivity than are normotensive individuals who have a negative parental history of hypertension. Previous research reporting that stress reactivity among college-aged black women did not differ according to parental history of hypertension (e.g., 3) did not control cardiorespiratory fitness.
Studies of the effect of fitness level on stress reactivity among people with a positive family history of hypertension have been scarce and limited to white women (7,8). Among a normotensive sample of black American women with unreported history of parental hypertension, systolic and mean arterial pressure (MAP) reactivity to a foot cold pressor was reduced after 6 wk of moderate aerobic-exercise training, without significant changes in vascular resistance or blood flow estimates (6). Most investigations of fitness and stress reactivity have assessed blood pressure responses without attention to the underlying hemodynamic changes that might have been obscured by integrated blood pressure responses. Though the mechanisms explaining reduced blood pressure after exercise training are not fully known, reductions in total peripheral resistance (TPR) and cardiac output each can occur (16). Cardiorespiratory fitness might affect cardiac output and vascular responses to stress differently among people who differ in parental history of hypertension, especially black Americans who are more likely than whites to have elevated peripheral resistance at rest (31) and during stress (32,35). Also, such effects of fitness might differ according to stressors that predominantly increase stroke volume (e.g., mental arithmetic) or vascular resistance (e.g., hand cold pressor) (15).
The purpose of this study was to examine the relationship between cardiorespiratory fitness and stress reactivity in normotensive black women having positive or negative histories of parental hypertension. In addition to measures of heart rate and blood pressure, we included measures of calf vascular resistance (CVR), calf blood flow (CBF), and stroke volume. Our goals were to determine 1) whether fitness level would be associated with blunted blood pressure reactivity and enhanced recovery among women having a positive parental history of hypertension, and 2) whether the hemodynamic patterns underlying those expected blood pressure effects would differ according to standardized stressors that elicit different hemodynamic responses. We especially focused on vascular resistance because an exaggerated increase in vascular resistance during stress has been commonly reported among black Americans (17,32,35). Based on our prior findings (7,8,15), we hypothesized that cardiorespiratory fitness would be inversely related to blood pressure responses during and after the hand cold pressor but unrelated to blood pressure responses to the forehead cold pressor and mental arithmetic.
Normotensive (mean ± SD: 110.5 ± 6.8/70.3 ± 6.3 mm Hg) black women (19 ± 1.1 yr) having positive (+ PH) or negative (−PH) parental history of hypertension were recruited from a university population through advertisements posted in university housing. Women were recruited if they were healthy, between the ages of 18 and 40, eumenorrheic, and the blood pressure status of their parents could be verified. Participants were nonsmokers who reported no cardiovascular disease, psychological disorders, other major illnesses, or use of cardiovascular or psychotropic drugs. Three +PH and four −PH women reported using oral contraceptives. Before participation, the women read and signed the Institutional Review Board–approved consent form that explained the benefits and risk associated with the study.
Parental hypertension was defined as having at least one parent physician-diagnosed with high blood pressure. Parents were asked to complete a general medical history form that required them to also verify their hypertension status in writing, provide a recent blood pressure reading, and indicate whether they had ever been diagnosed with high blood pressure. Those with hypertension were also asked the age of onset, length of diagnosis, and type of hypertensive medication. Parents were diagnosed on average at 40.5 ± 7.1 yr of age, with a range of 24–49 yr. One participant had two hypertensive parents, and all other +PH women had one hypertensive parent. Hypertension was normalized (125 ± 12.9/73.8 ± 8.5 mm Hg) by beta-blockers, calcium channel blockers, diuretics, or ACE inhibitors in all but one hypertensive parent (180/93 mm Hg) who was noncompliant with medication. The average blood pressure for parents of −PH participants was 121.7 ± 6.1/73.8 ± 6.5 mm Hg. The response rate for parental medical history questionnaires was 80%, and hypertension status reported by participants agreed with information provided by parents.
During the first session, participants completed a medical history form and had resting auscultatory brachial blood pressure taken (mean of three trials). Additionally, inventories to obtain measures of trait anger and anger expression (37), hostility and cynicism (10), and trait anxiety (38) were completed because these characteristics have been related to increased reactivity and cardiovascular disease risk and might confound group comparisons (33). Contemporary physical activity level was assessed using the 7-Day Physical Activity Recall Interview (PAR;4). Instructions were given for charting the menstrual cycle (7) to schedule the laboratory stress session during the follicular phase.
Maximal exercise test.
The testing procedure was explained, and each participant was given the opportunity to ask questions before being fitted with a heart rate monitor, mouthpiece, and nose clip. V̇O2peak (mL·kg−1·min−1) was determined by open-circuit spirometry while participants cycled on a Mijnhardt model KEM-3 (Utrecht, The Netherlands) electronically braked cycle ergometer during a ramped protocol. After a 4-min warm-up at 25 W, the resistance increased continuously at a rate of 24 W·min−1 until volitional exhaustion. Heart rate and rating of perceived exertion (RPE), using the Borg 6–20 category scale with standard instructions, were taken every minute. Oxygen consumption was measured continuously with a SensorMedics Model 2900 (Yorba Linda, CA) metabolic cart. The metabolic cart was calibrated with standard gases analyzed using the micro-Scholander technique. V̇O2peak was defined as the highest attained oxygen consumption when at least two of the following criteria were met: a heart rate within 90% of the age predicted maximal heart rate, a respiratory exchange ratio above 1.1, and an RPE value greater than 18. A person certified in CPR was present at all testing sessions.
Body composition analysis.
Dual-energy x-ray absorptiometry (Hologic QDR-1000W, enhanced whole-body software version 5.71, Hologic, Inc., Waltham, MA) was used to obtain an estimate of percent body fat. Scanning was performed with the participant in the supine position.
Laboratory stress session.
The stress protocol was conducted during the follicular phase (days 5–13) because some research has suggested that cardiovascular stress reactivity is increased during the luteal phase of the cycle compared with the follicular phase in eumenorrheic women (28–29). Testing was conducted in the early afternoon for participants, typically between 14:30 and 16:30 h. Participants agreed to refrain from caffeine, nicotine, alcohol, and physical activity for at least 4 h before testing. The session involved participants completing two passive and one active coping stressor tasks while cardiovascular responses were assessed. One of the six possible task orders was randomly assigned to each participant such that the order was virtually counterbalanced between groups. The passive stressors were the hand and forehead cold pressors, and the active stressor was mental arithmetic. Each stressor was preceded by a 2-min baseline period and followed by a 2-min recovery period. Participants completed inventories to assess state anger (37) and state anxiety (38) after each recovery period.
Upon reporting to the lab, participants were prepared for the measurement of physiological variables, and resting values were sampled to verify that accurate readings were being obtained. Participants then were seated in a semirecumbent position (115°) within in a sound attenuated (∼65 db(A) below ambient), environmentally controlled chamber (21 ± 2°). They were told that they would be completing a series of three standard laboratory tasks that each would be preceded and followed by 2-min resting periods. Participants were not told the order of the stressors. There was an accommodation period of approximately 10 min before the start of the session. Participants were then informed via in intercom that equipment would be turned on again and the session was about to begin. Baseline data were collected for 5 min at the beginning of the session, and this initial baseline served as the baseline for the first stressor. There were approximately 5–7 min between completion of one task and the start of the baseline period of the next task, sufficient for recovery of the physiological variables to within 3% of the initial baseline values. The entire session lasted approximately 90 min.
Forehead and hand cold pressors.
Each cold pressor used a water temperature of 0–3°C and lasted 2 min. The hand cold pressor involved the participant placing her right hand to the level of the wrist in a bucket and removing it when instructed to do so. For the forehead cold pressor, the participant was instructed via intercom when to place an ice pack on her head and when to remove it. A towel was provided, and participants were instructed to only touch the ice pack using the towel. Participants were asked to rate their level of aversion to the cold pressors on a scale from one (not aversive) to 100 (extremely aversive), and their level of comfort on a Likert-type scale of one (very comfortable) to five (very uncomfortable) as a check of the manipulation (8).
The mental arithmetic task involved serial subtraction for about 5.5 min. The instructions and the task were presented by tape recorder. Participants were instructed to subtract 13 from a four-digit number without the aid of paper and pen or a calculator, and to continue subtracting from each answer until a new number was presented. The instructions informed participants that successful performance was important and that their answers were being recorded and scored. For the manipulation check, effort and difficulty associated with the mental arithmetic each were rated on five-point scales with one being no effort or not difficult and five being a lot of effort or very difficult (8). The number of answers per minute and percentage of correct responses were recorded as additional manipulation checks (8).
Heart rate and blood pressure.
Heart rate was measured using a Polar R-R recorder (Polar Electro Oy, Kempele, Finland). Finger arterial pressure was monitored continuously by photoplethysmography from the middle finger of the left hand by using an Omheda Finapres model 2300 Blood Pressure Monitor (Ohmeda Monitoring Systems, Englewood, CO). The hand rested at heart level, and the participant was instructed to keep her hand still during the testing session. Beat-to-beat blood pressure measures using the Finapres recorder have been validated against simultaneous intra-arterial monitoring and during tasks inducing fast and marked blood pressure changes. The method has accepted validity for measuring absolute blood pressure in the finger branch of the radial artery (34). Data from the Finapres for systolic (SBP), diastolic (DBP), and MAP were recorded on a beat-to-beat basis and stored using Data Acquisition Systems DATAQ version 3.50 (TJS Software, Durham, NC) on an IBM 286 computer. Data were averaged for each measurement period.
Stroke volume and cardiac output.
Estimates of stroke volume (SV) and cardiac output (𝑄̇) were made using a SORBA model CIC-1000 impedance electrocardiograph system (SORBA Medical Systems, Inc., Brookfield, WI). Participants were prepared with four patch electrodes placed on the forehead and on the left side of the body at the base of the neck, along the mid-axillary line at the level of the xiphoid process, and along the mid-axillary line on the upper thigh. A 500-μA signal at 500 kHz was passed between the outer electrodes, and stroke volume was calculated by estimating the change in impedance between the middle electrodes using the Kubicek equation. The Finapres was interfaced with the SORBA system and TPR (dyne·s·cm−5) was computed as [MAP/𝑄̇] × 80. The SORBA system samples continuously and performs an ensemble average for 40- to 50-s time periods. These blocks of data were averaged for each measurement period for SV, 𝑄̇, and TPR measures.
CBF and vascular resistance.
CBF (BF) was estimated using venous occlusion strain gauge plethysmography (Hokanson EC-4, Bellvue, WA) on the right leg. During each measurement period, a cuff around the ankle was inflated constantly to a pressure above SBP (∼230 mm Hg). Every 15 s, a cuff around the thigh was inflated to a pressure above venous pressure (∼50 mm Hg) for 7.5 s. The plethysmograph was connected to a chart recorder set at paper speed of 30 cm·min−1, and BF was estimated by calculating the slope of the curve during venous occlusion. CVR (CVR; peripheral resistance unit) was estimated by dividing MAP (one third of pulse pressure plus diastolic pressure) by BF.
All statistical analyses were performed using SPSS Windows version 10.0 software (SPSS, Inc., Chicago, IL). Changes in the dependent variables during the stressor tasks were tested for all participants using paired t-tests (two-tailed) to determine whether participants experienced a change from baseline. Group comparisons on participant characteristics and self-ratings after the stressor tasks were made using independent sample t-tests (two-tailed).
Change scores for each dependent variable were calculated for each participant to analyze reactivity and recovery measures; the mean during the baseline period preceding each stressor task was subtracted from the mean during exposure to stress. Recovery means were subtracted from the mean response during each stressor. To confirm that initial values of the dependent variables did not bias group comparisons, reactivity and recovery data also were analyzed using each pretask baseline value as a covariate (22). The analyses reported are based on change scores.
For hypothesis testing, a multiple linear regression analysis was used to examine the influence of fitness, parental history, and the fitness-by-parental history interaction on reactivity and recovery measures for each dependent variable (30). An interaction was considered significant when inclusion of the interaction term along with the two main effects significantly increased the adjusted R2. When the interaction was not significant, it was removed from the regression model and tests of the main effects were performed. The significance level was set at P < 0.05. A statistical power analysis indicated that groups of 15 +PH and 15 −PH participants would provide power of 0.80 at α = 0.05 when testing for the interaction and two main effects to detect a moderate effect of 0.5 SD with intertrial reliabilities of 0.80. Partial correlations are reported to describe the relationship between V̇O2peak and reactivity controlling for parental history.
Outliers and influential data points were identified using scores greater than 3 SDs from the mean and Cook’s distance statistic. Seven of 180 data points were judged influential and removed from the analyses. There were missing impedance data for four participants during the hand cold pressor, one participant during mental arithmetic, and one participant for the forehead cold pressor. CBF data were missing for three participants during mental arithmetic or recovery, three participants during the hand cold pressor and recovery, and two participants during or after the forehead cold pressor.
Means and SDs for participant characteristics are presented in Table 1. Women in the +PH group had significantly higher resting brachial DBP (P = 0.005) and MAP (P = 0.006) than women in the −PH group, but there were no other differences in baseline characteristics between +PH and −PH participants. V̇O2peak was inversely related (Pearson coefficient) to resting SBP (r = −0.52, P = 0.004) and MAP (r = −0.43, P = 0.02) but not significantly related to DBP (r = −0.27, P = 0.14) or self-reported physical activity assessed by the PAR (r = 0.21, P = 0.29).
There were significant increases in HR, 𝑄̇, SBP, DBP, and MAP during each stressor (P < 0.05). Also, SV decreased and BF increased during mental arithmetic (P < 0.05). Means and SDs for dependent variables during the initial baseline and each stressor for the +PH and −PH groups are presented in Table 2 for descriptive purposes.
Hand cold pressor.
V̇O2peak was inversely related to SBP changes in response to the hand cold pressor (t28 = −2.49, P = 0.02; r13.2 = −0.44) (Fig. 1). There was a significant fitness-by-parental history interaction for CVR reactivity (t23 = 2.32, P = 0.03). A positive relationship was obtained between V̇O2peak and CVR reactivity for all participants (r13.2 = 0.31), and the interaction was explained by a greater variation in scores among the −PH participants and a stronger relationship with V̇O2peak among the +PH participants (Fig. 2). There were no effects during recovery. Ratings of anger, anxiety, comfort, and aversion were similar between +PH and −PH participants (P > 0.05).
Forehead cold pressor.
There were significant main effects of V̇O2peak on responses to the forehead cold pressor for SBP, MAP, TPR and 𝑄̇. V̇O2peak was positively related to increases in SBP (t27 = 3.05, P = 0.01, r13.2 = 0.51), MAP (t28 = 2.28, P = 0.03; r13.2 = 0.40), and TPR (t27 = 2.36, P = 0.03; r13.2 = 0.42). Results for the TPR response are presented in Figure 3. There was an inverse relationship between V̇O2peak and increases in 𝑄̇ (t27 = −2.08, P = 0.047; r13.2 = −0.38). There also was a fitness-by-parental history interaction for changes in DBP (t28 = 2.04, P = 0.05). Fitness was positively associated with changes in DBP in +PH and −PH participants, but the relationship was stronger in the −PH women. There were no parental history main effects for any dependent variables (P > 0.05).
During recovery, there was a significant main effect of fitness on SBP such that V̇O2peak was positively associated with a reduction in SBP (t27 = 2.32, P = 0.03, r13.2 = 0.41). Other effects of fitness level, parental history status, or the fitness-by-parental history interaction were not significant (P > 0.05). Ratings of anger, anxiety, comfort, and aversion were similar between +PH and −PH participants (P > 0.05).
The fitness main effect for TPR reactivity during mental arithmetic was significant. V̇O2peak was positively related to increases in TPR (t = 2.30, P = 0.03; r13.2 = 0.43) (Fig. 4a). There was a significant fitness-by-parental history interaction for changes in CVR during mental arithmetic (t = −2.30, P = 0.04). CVR changes were not related to V̇O2peak in +PH participants, but there was a positive relationship with V̇O2peak in −PH participants. There were no other effects of fitness or parental history (P > 0.05).
During recovery, there were significant fitness-by-parental history interactions for heart rate, stroke volume, and TPR. The interaction for heart rate (t28 = 2.24, P = 0.03) was characterized by a positive relationship with V̇O2peak in the −PH participants and no relationship in the +PH participants. The interaction for stroke volume (t26 = 2.40, P = 0.03) was explained by an inverse relationship between V̇O2peak and stroke volume during recovery in −PH women and no relationship in +PH women. Reductions in TPR during recovery were positively related to V̇O2peak for −PH women but unrelated in +PH women (t26 = −2.86, P = 0.01) (Fig. 4b).
Also during recovery, there were significant fitness main effects with V̇O2peak inversely related to reductions in 𝑄̇ (t26 = −3.56, P = 0.002; r13.2 = −0.60) and positively related to reductions in MAP (t28 = 2.10, P = 0.046; r13.2 = 0.39). The fitness-by-parental history interaction effect for 𝑄̇ was nearly significant (t26 = 1.93, P = 0.07) with a stronger inverse relationship for the −PH women compared with the +PH women.
State anxiety scores were significantly higher in the −PH women (t28 = −2.20, P = 0.04) compared with +PH after mental arithmetic. However, results were unaffected when controlling for this group difference in a covariate analysis. The other self-ratings and performance measures were similar between +PH and −PH women (P > 0.05).
The primary findings of the study were: 1) Regardless of parental hypertension, fitter women had larger increases in CVR or TPR during the stressors, yet they had a blunted increase in systolic blood pressure during the hand cold pressor and enhanced recoveries of systolic blood pressure and MAP after mental arithmetic; 2) among fitter women, larger increases in blood pressure during the forehead cold pressor were explained by their larger increases in TPR despite smaller increases in cardiac output; and 3) despite their larger increases in CVR during mental arithmetic, fitter −PH women had enhanced recovery of TPR and stroke volume after mental arithmetic. These findings indicate that V̇O2peak has complex associations with blood pressure and hemodynamic responses during and after passive and active stressors. They encourage the measurement of stroke volume and vascular resistance in future studies designed to clarify the mixed positive and null findings in past studies of fitness and blood pressure reactivity.
The present results, obtained from young black normotensive women, are consistent with our previous findings among young white normotensive women that V̇O2peak level was associated with a reduction in blood pressure reactivity during the hand cold pressor (15) but unrelated to blood pressure responses during the forehead cold pressor or mental arithmetic, regardless of parental history of hypertension (7,8). The present results extend those findings by demonstrating that V̇O2peak is positively associated with enhanced blood pressure recovery after the forehead cold pressor and mental arithmetic, despite its association with measures of increased vascular resistance during those tasks and increased blood pressure during the forehead cold pressor.
Elevated vascular resistance has been reported at rest (17,31) and during stress (2,35) among hypertensive and normotensive black Americans, so our present findings of increased TPR and CVR during stress among the more fit participants might raise some concern. However, the increases in vascular resistance were not extreme and suggest a healthy vasculature system that can maintain normal blood flow during and after stress without exaggerated increases in blood pressure. Indeed, in several instances, the relationships between fitness and the measures of reactivity or recovery were stronger for the −PH women who had lower resting systolic and MAPs than the +PH women. Regardless of parental history, the enhanced recovery of TPR after mental arithmetic was large enough to explain the greater reductions in MAP observed among the fitter women despite their smaller decreases in cardiac output during recovery. In contrast to our previous findings among young white men and women (15), the cold pressor tests did not significantly increase the measures of vascular resistance independently of fitness levels; a null effect of the hand cold pressor on TPR has been observed elsewhere among college students (1).
We are aware of only a few other studies that have compared vascular resistance responses to stress according to different levels of fitness, and findings from those studies were mixed. Consistent with the present results, Claytor (9) reported that a 20% increase in V̇O2peak after 10 wk of exercise training was associated with an increase in TPR and a decrease in cardiac output during mental arithmetic and the Stroop color-word conflict task. In another study, TPR was greater during a reaction time stressor in participants who trained for 7 wk compared with those who remained inactive, despite a nonsignificant inverse relationship between V̇O2peak and TPR reactivity measured before the exercise training (13). In contrast, increases in TPR during a reaction time task were greater in sedentary men than in male runners (39). In a later study, de Geus et al. (14) reported that TPR reactivity to a reaction time task was not related to V̇O2peak before training in a sample of young, healthy men, but TPR reactivity was decreased after participants trained in aerobic exercise for 8 months; programs of other lengths did not alter TPR reactivity. Finally, in a sample of young black women, forearm vascular resistance and TPR reactivity were unchanged after 6 wk of aerobic exercise training (6).
It has been suggested that stress reactivity may be related to increased risk for cardiovascular disease because of a slower recovery from stress (23). Our findings of improved recovery are consistent with results of a recent meta-analysis that concluded that low levels of fitness were associated with slower cardiovascular recovery after active coping stressors (20). Additionally, Gerin and Pickering (18) reported that +PH individuals had slower recovery from stress compared with −PH individuals in the absence of differences in reactivity. The present results suggest that a moderate level of fitness may improve recovery from stress even in the absence of exaggerated responses during stress.
The cross-sectional design is a limitation of the present study. However, we were able to control several personal attributes or responses that have been related to cardiovascular responses during stress by equating the +PH and −PH groups or statistically determining that group differences did not influence the results. Prior studies of stress reactivity among Blacks have reported interactions between parental history of hypertension and stress emotions such as anger, but they did not control for V̇O2peak (2,3). The low fitness level of women in this study might be viewed as a limitation to the generalizability of our results, but it is consistent with population estimates of low physical activity among black American women compared with white women and the general population. The correlation between V̇O2peak and PAR was likely attenuated by the restricted ranges of fitness and PAR, but it was still within the range of prior observations (21).
The generally weaker effects of V̇O2peak on the participants who had hypertensive parents suggest that the level of fitness required to modify recovery after mental stress among black American women may differ according to parental history of hypertension. A randomized controlled trial designed to increase V̇O2peak is needed to clarify our findings. Such a trial should include a measure of central sympathetic neural outflow (e.g., muscle sympathetic nerve activity) or use adrenoreceptor antagonists to examine mechanisms that might explain the association of fitness with vascular responses to mental stress.
Address for correspondence: Erica M. Jackson, 2050 Beard-Eaves Memorial Coliseum, Auburn University, Auburn, AL 36849-5323; E-mail: email@example.com.
1. Allen, M. T., and M. D. Crowell. Patterns of autonomic response during laboratory stressors. Psychophysiology 26: 603–614, 1989.
2. Anderson, N. B. Racial differences in stressed-induced cardiovascular reactivity
and hypertension: current status and substantive issues. Psychol. Bull. 105: 89–105, 1989.
3. Anderson, N. B., J. D. Lane, F. Taguchi, R. B. Williams, Jr., and S. J. Houseworth. Race, parental history of hypertension, and patterns of cardiovascular reactivity
in women. Psychophysiology 26: 39–47, 1989.
4. Blair, S. N. How to assess exercise habits and physical fitness. In: Behavioral Health: A Handbook of Health Enhancement and Disease Prevention, J. D. Matarazzo (Ed.). New York: Wiley, 1984, pp. 424–447.
5. Blair, S. N., N. N. Goodyear, L. W. Gibbons, and K. H. Cooper. Physical fitness and incidence of hypertension in healthy normotensive men and women. JAMA 252: 487–490, 1984.
6. Bond, V., R. M. Mills, M. Caprarola, et al. Aerobic exercise attenuates blood pressure reactivity to cold pressor test in normotensive, young adult African-American
women. Ethn. Dis. 9: 104–110, 1999.
7. Buckworth, J., V. Convertino, K. J. Cureton, and R. K. Dishman. Increased finger arterial pressure after exercise de-training in women with a parental history of hypertension: autonomic tasks. Acta Physiol. Scand. 160: 29–41, 1997.
8. Buckworth, J., R. K. Dishman, and K. J. Cureton. Autonomic responses of women with parental hypertension: effects of physical activity
and fitness. Hypertension 24: 576–584, 1994.
9. Claytor, R. P. Stress reactivity: hemodynamic adjustments in trained and untrained humans. Med. Sci. Sports Exerc. 23: 873–881, 1991.
10. Cook, W. W., and D. M. Medley. Proposed hostility and pharisaic-virtue scales for the MMPI. J. Appl. Psychol. 38: 414–418, 1954.
11. Crews, D. J., and D. M. Landers. A meta-analytic review of aerobic fitness and reactivity to psychosocial stressors. Med. Sci. Sports Exerc. 19: S114–S120, 1987.
12. de Geus, E. J. C., and L. J. P. van Doornen. The effects of fitness training on the physiological stress response. Work Stress 7: 141–159, 1993.
13. de Geus, E. J. C., L. J. P. van Doornen, D. C. de Visser, and J. F. Orlebeke. Existing and training induced differences in aerobic fitness: their relationship to physiological response patterns during different types of stress. Psychophysiology 27: 457–478, 1990.
14. de Geus, E. J. C., L. J. P. van Doornen, and J. F. Orlebeke. Regular exercise and aerobic fitness in relation to psychological make-up and physiological stress reactivity. Psychosom. Med. 55: 347–363, 1993.
15. Dishman, R. K., E. M. Jackson, and Y. Nakamura. Influence of fitness and gender on blood pressure responses during active or passive stress. Psychophysiology 39: xxx, 2002.
16. Fagard, R. H., and C. M. Tipton. Physical activity
, fitness, and hypertension. In: Physical Activity
, Fitness, and Health: International Proceedings and Consensus Statement, C. Bouchard, R. J. Shephard, and T. Stephens (Eds.). Champaign, IL: Human Kinetics, 1994, pp. 633–668.
17. Falkner, B. The role of cardiovascular reactivity
as a mediator of hypertension in African-Americans. Semin. Nephrol. 16: 117–125, 1996.
18. Gerin, W., and T. G. Pickering. Association between delayed recovery of blood pressure after acute mental stress and parental hypertension. J. Hypertens. 13: 603–613, 1995.
19. Gillum, R. F. Epidemiology of hypertension in African American women. Am. Heart J. 131: 385–395, 1996.
20. Hocking Schuler, J. L., and W. H. O’Brien. Cardiovascular recovery from stress and hypertension risk factors: a meta-analytic review. Psychophysiology 34: 649–659, 1997.
21. Jacobs, D. R., B. E. Ainsworth, T. J. Hartman, and A. S. Leon. A simultaneous evaluation of 10 commonly used physical activity
questionnaires. Med. Sci. Sports Exerc. 25: 81–91, 1993.
22. Jennings, J. R., and L. A. Stine. Salient method, design, and analysis concerns. In:Handbook of Psychophysiology,
2nd Ed. J. T. Cacioppo, L. G. Tassinary, and G. G. Berntson (Eds.). New York: Cambridge University Press, 2000, pp. 870–899.
23. Krantz, D. S., and S. B. Manuck. Acute psychophysiologic reactivity and risk of cardiovascular disease: a review and methodologic critique. Psychol. Bull. 96: 435–464, 1984.
24. Lemne, C. E. Increased blood pressure reactivity in children of borderline hypertensive fathers. J. Hypertens. 16: 1243–1248, 1998.
25. Light, K. C., S. S. Girdler, A. Sherwood, et al. High stress responsivity predicts later blood pressure only in combination with positive family history and high life stress. Hypertension 33: 1458–1464, 1999.
26. Markovitz, J. H., J. M. Raczynski, D. Wallace, V. Chettur, and M. A. Chesney. Cardiovascular reactivity
to video game predicts subsequent blood pressure increases in young men: the CARDIA study. Psychosom. Med. 60: 186–191, 1997.
27. Menkes, M. S., K. A. Matthews, D. S. Krantz, et al. Cardiovascular reactivity
to the cold pressor as a predictor of hypertension. Hypertension 14: 524–530, 1989.
28. Miller, S. B., and A. Sita. Parental history of hypertension, menstrual cycle phase, and cardiovascular response to stress. Psychosom. Med. 56: 61–69, 1994.
29. Mills, P. J., and C. C. Berry. Menstrual cycle, race, and task effects on blood pressure recovery from acute stress. J. Psychosom. Res. 46: 445–454, 1999.
30. Pedhazur, E. J. Multiple regression in behavioral research: explanation and prediction, 2nd Ed. Fort Worth, TX: Holt, Rinehart, & Winston, 1982, pp. 436–471.
31. Pickering, T. G. Hypertension in Blacks. Curr. Opin. Nephrol. Hypertens. 3: 207–212, 1994.
32. Pickering, T. G., and W. Gerin. Cardiovascular reactivity
in the laboratory and the role of behavioral factors in hypertension: a critical review. Ann. Behav. Med. 12: 3–16, 1990.
33. Shapiro, D., I. B. Goldstein, and L. D. Jamner. Effects of anger/hostility, defensiveness, gender, and family history of hypertension on cardiovascular reactivity
. Psychophysiology 32: 425–435, 1995.
34. Shapiro, D., L. D. Jamner, J. D. Lane, et al. Blood pressure publication guidelines. Psychophysiology 33: 1–12, 1996.
35. Sherwood, A., C. W. May, W. C. Siegel, and J. A. Blumenthal. Ethnic differences in hemodynamic responses to stress in hypertensive men and women. Am. J. Hypertens. 8: 552–557, 1995.
36. Sinyor, D., S. Schwartz, F. Peronnet, G. Brisson, and P. Seraganian. Aerobic fitness level and reactivity to psychosocial stress: physiological, biochemical, and subjective measures. Psychosom. Med. 45: 205–217, 1983.
37. Spielberger, C. D. State-Trait Anger Expression Inventory: Revised Research Edition. Professional Manual. Odessa, FL: Psychological Assessment Resources, 1991, pp. 1–27.
38. Spielberger, C. D., R. L. Gorsach, R. Luschene, P. R. Vagg, and G. A. Jacobs. Manual for the State-Trait Anxiety Inventory (Self Evaluation Questionnaire). Palo Alto, CA: Consulting Psychologists Press, 1983, pp. 1–36.
39. van Doornen, L. J. P., and E. J. C. de Geus. Aerobic fitness and the cardiovascular response to stress. Psychophysiology 26: 17–28, 1989.
Keywords:©2002The American College of Sports Medicine
AFRICAN-AMERICAN; CARDIOVASCULAR REACTIVITY; PHYSICAL ACTIVITY; STRESS RECOVERY