Exercise Systolic Blood Pressure Response Research Articles

Exercise Systolic Blood Pressure Response During Cycle Ergometry is Associated with Future Hypertension in Normotensive Individuals.

We aimed to investigate the association between the exercise systolic blood pressure (SBP) response and future hypertension (HTN) in normotensive individuals referred for cycle ergometry, with special regard to reference exercise SBP values, and exercise capacity. In this longitudinal cohort study, data from 14,428 exercise tests were cross-linked with Swedish national registries on diagnoses and medications. We excluded individuals with a baseline diagnosis of cardiovascular disease or HTN. The peak exercise SBP (SBPpeak) was recorded and compared to the upper limit of normal (ULN) derived from SBPpeak reference equations incorporating age, sex, resting SBP and exercise capacity. To evaluate the impact of exercise capacity, three SBP to work rate slopes (SBP/W-slopes), were calculated, relative to either supine or seated SBP at rest or to the first exercise SBP. Adjusted hazard ratios (HRadjusted [95% Confidence interval, CI]) for incident HTN during follow-up, in relation to SBP response metrics, were calculated. We included 3,895 normotensive individuals (49±14 years, 45% females) with maximal cycle ergometer tests. During follow-up (median 7.5 years) 22% developed HTN. Higher SBPpeak and SBPpeak>ULN were associated with incident HTN (HRadjusted 1.19 [1.14-1.23] per 10 mmHg, and 1.95 [1.54-2.47], respectively). All three SBP/W-slopes were positively associated to incident HTN, particularly the SBP/W-slope calculated as supine-to-peak SBP (HRadjusted 1.25 [1.19-1.31] per 1 mmHg/10W). Both SBPpeak>ULN based on reference values and high SBP/W-slopes were associated with incident HTN in normotensive individuals and should be considered in the evaluation of the cycle ergometry SBP response.

Exercise systolic blood pressure indexed to work rate predicts future risk of incident stroke

Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): 1) The CircM network, Linköping University 2) The Swedish Stroke Association. Background Hypertension is a major risk factor for stroke. Exaggerated peak systolic blood pressure (SBP) during exercise is associated with increased risk of hypertension in normotensive subjects, whereas low, rather than high, peak exercise SBP predicts cardiovascular and all-cause mortality. Purpose We aimed to study the risk of incident fatal and non-fatal stroke in relation to absolute and work rate indexed exercise SBP, in patients referred for exercise testing. Methods We cross-linked clinical data from 14,428 bicycle ergometer exercise tests with data from the National Patient Registry and the Registry of Prescribed Medications up until December 2019. Subjects with a history of cerebrovascular disease were excluded, as well as subjects with submaximal tests, a drop in SBP during exercise, or with missing SBP data at the end of exercise. Baseline comorbidity was defined as diagnosis of, or treatment for, hypertension, diabetes, hyperlipidemia, and coronary artery disease (CAD). Work rate indexed SBP response (SBP/Watt-slope) was calculated as the increase in SBP during exercise divided by the increase in work rate. We applied Cox regression to calculate hazard ratios (HR) with 95% confidence intervals (95% CI) for the risk of incident stroke in association to peak SBP and the SBP/Watt-slope. We used absolute values as well the upper limit of normal (≥2 Z scores) of a recently published reference population, with reference equation including age, sex, SBP at rest, Wmax (for SBP peak only) and height (for SBP/W-slope only). Analyses were adjusted for age, sex, and baseline comorbidity. Results In total, 7,946 subjects (54% male, age 55±13 years) were included, with baseline comorbidity of hypertension (28%), diabetes (7%), hyperlipidemia (16%), and CAD (13%). During a median follow-up of 8.4 years (inter quartile range 5.8-11.5), 3.1% developed ischemic (2.2%) or hemorrhagic (1.0%) stroke. There were positive associations to future stroke with absolute peak exercise SBP (HR: 1.08 [1.03 – 1.13] per 10 mmHg increase) and with SBP/Watt-slope (HR: 1.09 [1.05 – 1.14] per 1 mmHg/10 Watt increase), but not after adjustment for sex, age and baseline comorbidity. However, having a SBP/Watt-slope ≥2 Z scores was associated with an increased risk for stroke (HR: 1.56 [1.08 – 2.25)] after adjustment for baseline comorbidity, whereas an adjusted SBP peak ≥2 Z scores was not (HR: 0.62 [0.32 – 1.21]). Conclusion A workload-indexed SBP response (SBP/Watt-slope) above the upper limit of normal may help to identify subjects with no history of cerebrovascular disease at risk of future stroke. In contrast, the absolute exercise SBP response to exercise does not add substantial information to the risk estimation above age, sex, and baseline comorbidity.

Physical Activity and Cardiac Morphologic Adaptations

Chronic and intense exercise programs lead to cardiac adaptations, followed by increased left ventricular wall thickness and cavity diameter, at times meeting the criteria for left ventricular hypertrophy (LVH), commonly referred to as “athlete’s heart”. Recent studies have also reported that extremely vigorous exercise practices have been associated with heightened left ventricular trabeculation extent, fulfilling noncompaction cardiomyopathy criteria, as part of exercise-induced structural adaptation. These changes are specific to the exercise type, intensity, duration, and volume and workload demands imposed on the myocardium. They are considered physiologic adaptations not associated with a negative prognosis. Conversely, hypertrophic cardiac adaptations resulting from chronic elevations in blood pressure (BP) or chronic volume overload due to valvular regurgitation, lead to compromised cardiac function, increased cardiovascular events, and even death. In younger athletes, hypertrophic cardiomyopathy (HCM) is the usual cause of non-traumatic, exercise-triggered sudden cardiac death. Thus, an extended cardiac examination should be performed, to differentiate between HCM and non-pathological exercise-related LVH or athlete’s heart. The exercise-related cardiac structural and functional adaptations are normal physiologic responses designed to accommodate the increased workload imposed by exercise. Thus, we propose that such adaptations are defined as “eutrophic” hypertrophy and that LVH is reserved for pathologic cardiac adaptations. Systolic BP during daily activities may be the strongest predictor of cardiac adaptations. The metabolic demand of most daily activities is approximately 3–5 metabolic equivalents (METs) (1 MET = 3.5 mL of O2 kg of body weight per minute). This is similar to the metabolic demand of treadmill exercise at the first stage of the Bruce protocol. Some evidence supports that an exercise systolic BP response ≥150 mmHg at the end of that stage is a strong predictor of left ventricular hypertrophy, as this BP reflects the hemodynamic burden of most daily physical tasks. Aerobic training of moderate intensity lowers resting and exercise systolic BP at absolute workloads, leading to a lower hemodynamic burden during daily activities, and ultimately reducing the stimulus for LVH. This mechanism explains the significant LVH regression addressed by aerobic exercise intervention clinical studies.

Systolic Blood Pressure Response to Exercise in Endurance Athletes in Relation to Oxygen Uptake, Work Rate and Normative Values.

Work rate has a direct impact on the systolic blood pressure (SBP) during aerobic exercise, which may be challenging in the evaluation of the SBP response in athletes reaching high work rates. We aimed to investigate the exercise SBP response in endurance athletes in relation to oxygen uptake (VO2), work rate and to recent reference equations for exercise SBP in the general population. Endurance athletes with a left-ventricular end-diastolic diameter above the reference one performed a maximal bicycle cardiopulmonary exercise test. The increase in SBP during exercise was divided by the increase in VO2 (SBP/VO2 slope) and in Watts, respectively (SBP/W slope). The maximum SBP (SBPmax) and the SBP/W slope were compared to the predicted values. In total, 27 athletes (59% men) were included; mean age, 40 ± 10 years; mean VO2max, 50 ± 5 mL/kg/min. The mean SBP/VO2 slope was 29.8 ± 10.2 mm Hg/L/min, and the mean SBP/W slope was 0.27 ± 0.08 mm Hg/W. Compared to the predicted normative values, athletes had, on average, a 12.2 ± 17.6 mm Hg higher SBPmax and a 0.12 ± 0.08 mm Hg/W less steep SBP/W slope (p < 0.01 and p < 0.001, respectively). In conclusion, the higher SBPmax values and the less steep SBP/W slope highlight the importance of considering work rate when interpreting the SBP response in endurance athletes and suggest a need for specific normative values in athletes to help clinicians distinguish physiologically high maximal blood pressure from a pathological blood pressure response.

Blood Pressure and Arterial Stiffness after a Maximal Aerobic Exercise in Young Adult Binge Drinkers and Moderate Drinkers

Exaggerated systolic blood pressure (SBP) response to exercise predicts the development of hypertension. In normotensive young adults, alcohol consumption is associated with increased arterial stiffness, which potentially influence exercise SBP response. Young adults who have alcohol drinking habits usually exercise regularly, but their exercise SBP response has received little attention. Whether alcoholic drinking pattern influences exercise SBP response remains to be determined. The purpose of this study is two‐fold: 1) to investigate SBP and arterial stiffness in response to maximal aerobic exercise; and 2) to examine if alcoholic drinking pattern influences the response. Twenty healthy young adults (9 women; age: 27±3 years; BMI: 24.1±2.1 kg/m2; mean±SD) with a history of alcohol consumption over the past year were included in this study. Based on the self‐reported alcoholic drinking pattern, participants were categorized as binge drinkers (n=10; BD) or moderate drinkers (n=10; MOD). Brachial SBP and central SBP and arterial stiffness (carotid to femoral pulse wave velocity; cfPWV) were measured before and after a maximal graded exercise test on a cycle ergometer. At the end of maximal exercise, brachial SBP increased (BD: 110±13 vs. 172±15 mmHg; pre‐ vs. post‐ex; P&lt;0.0005 and MOD: 110±9 vs. 158±22 mmHg; P&lt;0.0005), regardless of drinking pattern (P=0.1 for BD vs. MOD). Central systolic BP (BD: 101±10 vs. 113±7 mmHg and MOD: 102±8 vs. 112±8 mmHg; P≤0.01 for both groups) increased in all participants after exercise (obtained ~ 4min post‐ex), regardless of drinking pattern (P=0.5 for BD vs. MOD). After exercise (~15 min), cfPWV did not increase in MOD (5.6±0.8 vs. 5.7±1.1 m/s; P=0.8), while cfPWV increased in BD (5.5±0.5 vs. 6.3±0.9 m/s; P=0.02). In conclusion, our study found that SBP response to maximal aerobic exercise was similar between BD and MOD. However, arterial stiffness was higher following maximal aerobic exercise in BD, suggesting a negative adaptation in vasculature associated with binge drinking. Future studies with larger sample sizes and a group of alcohol abstainers are needed to confirm our findings.

Effect Of Vitamin D At Rest And In Response To Maximal Exercise

Conflicting evidence suggests insufficient vitamin D (VitD) levels are associated with high resting blood pressure (BP). However the relationship between VitD and the peak systolic BP (SBP) response to exercise, a predictor of future hypertension, has yet to be investigated. PURPOSE: We sought to examine the relationship among serum 25-hydroxy VitD (25[OH]D), resting BP, and the peak SBP response to a graded exercise stress test among a large sample (n=417) of healthy men (49%) and women (51%) over a broad age range (20-76 yr; mean age 44.1±0.8y). We hypothesized that individuals with clinically sub-optimal VitD would have higher resting BP and a peak SBP response to a graded exercise stress test compared to individuals with optimal VitD levels. METHODS: Fasting serum VitD, anthropometrics, resting BP, and peak exercise SBP were obtained at the baseline visit of a larger clinical trial (STOMP; NCT01140308). RESULTS: Mean VitD levels were 36.1±0.7ng/mL, with 41.2% of individuals classified as sub-optimal (<32ng/mL). Average resting BP was 118.9±0.6/75.3±0.5mmHg, with 41% of individuals having high BP (n=174) consisting of those with pre-hypertension (32.5%) and established hypertension (8.5%). Individuals with optimal VitD had higher resting SBP (120.6±13.4mmHg vs. 116.4±12.7mmHg; p=0.002) and DBP (76.0±9.9mmHg vs. 74.1±9.1mmHg; p=0.048) than individuals with sub-optimal VitD, respectively. Similarly, individuals with optimal VitD tended to have a greater peak exercise SBP response than individuals with sub-optimal VitD (p=0.114). CONCLUSION: In contrast to our hypothesis, VitD was positively associated with resting BP levels, but was not associated with peak SBP under maximal exercise conditions. Additional studies are needed to confirm our findings and to provide insight into mechanisms underlying these associations among individuals with high BP. TRIAL REGISTRATION: NCT01140308

Exaggerated exercise blood pressure response in middle-aged men as a predictor of future blood pressure: a 10-year follow-up

ABSTRACTObjective: The prognostic value of an exaggerated exercise systolic blood pressure response (EESBPR) remains controversial. This study was designed to assess whether an EESBPR is associated with the predictor of future blood pressure. Methods: From an initial population of 1,534 male-subjects with normal BP or no medication who underwent ergometric exercise, 733 subjects (mean age: 41 years old) at baseline to follow-up BP after an average of 10 years were selected. A 12-min exercise tolerance test with three phases of estimated load from predictive maximum oxygen intake was performed at baseline, and exercise BP was measured. Results: Exercise BP response was classified by three group: Low group (G) (exercise SBP < 180 mmHg), Middle G (exercise BP:180–199 mmHg), High G (exercise BP:200 mmHg ≦). BP after 10 years in Low G was 123 ± 12/79 ± 7 mmHg, in Middle G:127 ± 13/81 ± 8 mmHg, in High G :134 ± 15/84 ± 10 mmHg. Compared with in Low G, BP after 10 years in High G significantly increased (p < 0.05). Multiple regression analysis was carried out to clarify the relationship of exercise SBP at baseline to BP after 10 years. In multivariate-adjusted models, the relationship of SBP at follow-up was stronger to exercise SBP (β = 0.271, P < 0.001) than to resting SBP (β = 0.148, P < 0.001). Maximum oxygen intake (β = −0.193, P = 0.003) and resting SBP correlated with SBP after 10 years. Conclusions: In middle-aged men, exercise SBP would be a stronger predictor of future SBP, DBP rather than BP at rest. In optimal of classification of BP (SBP < 120 mmHg), exercise BP response was clearly associated with BP after 10 years.

Relation of Risk of Atrial Fibrillation With Systolic Blood Pressure Response During Exercise Stress Testing (from the Henry Ford ExercIse Testing Project)

Decreases in systolic blood pressure during exercise may predispose to arrhythmias such as atrial fibrillation (AF) because of underlying abnormal autonomic tone. We examined the association between systolic blood pressure response and incident AF in 57,442 (mean age 54 ± 13 years, 47% women, and 29% black) patients free of baseline AF who underwent exercise treadmill stress testing from the Henry Ford ExercIse Testing project. Exercise systolic blood pressure response was examined as a categorical variable across clinically relevant categories (>20 mm Hg: referent; 1 to 20 mm Hg, and ≤0 mm Hg) and per 1-SD decrease. Cox regression, adjusting for demographics, cardiovascular risk factors, medications, history of coronary heart disease, history of heart failure, and metabolic equivalent of task achieved, was used to compute hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between systolic blood pressure response and incident AF. Over a median follow-up of 5.0 years, a total of 3,381 cases (5.9%) of AF were identified. An increased risk of AF was observed with decreasing systolic blood pressure response (>20 mm Hg: HR 1.0, referent; 1 to 20 mm Hg: HR 1.09, 95% CI 0.99, 1.20; ≤0 mm Hg: HR 1.22, 95% CI 1.06 to 1.40). Similar results were obtained per 1-SD decrease in systolic blood pressure response (HR 1.08, 95% CI 1.04 to 1.12). The results were consistent when stratified by age, sex, race, hypertension, and coronary heart disease. In conclusion, our results suggest that a decreased systolic blood pressure response during exercise may identify subjects who are at risk for developing AF.

Systolic Blood Pressure Response During Exercise Stress Testing: The Henry Ford ExercIse Testing (FIT) Project.

BackgroundThe prognostic significance of modest elevations in exercise systolic blood pressure response has not been extensively examined.Methods and ResultsWe examined the association between systolic blood pressure response and all-cause death and incident myocardial infarction (MI) in 44 089 (mean age 53±13 years, 45% female, 26% black) patients who underwent exercise treadmill stress testing from the Henry Ford ExercIse Testing (FIT) Project (1991–2010). Exercise systolic blood pressure response was examined as a categorical variable (>20 mm Hg: referent; 1 to 20 mm Hg, and ≤0 mm Hg) and per 1 SD decrease. Cox regression was used to compute hazard ratios (HR) and 95% CI for the association between systolic blood pressure response and all-cause death and incident MI. Over a median follow-up of 10 years, a total of 4782 (11%) deaths occurred and over 5.2 years, a total of 1188 (2.7%) MIs occurred. In a Cox regression analysis adjusted for demographics, physical fitness, and cardiovascular risk factors, an increased risk of death was observed with decreasing systolic blood pressure response (>20 mm Hg: HR=1.0, referent; 1 to 20 mm Hg: HR=1.13, 95% CI=1.05, 1.22; ≤0 mm Hg: HR=1.21, 95% CI=1.09, 1.34). A trend for increased MI risk was observed (>20 mm Hg: HR=1.0, referent; 1 to 20 mm Hg: HR=1.09, 95% CI=0.93, 1.27; ≤0 mm Hg: HR=1.19, 95% CI=0.95, 1.50). Decreases in systolic blood pressure response per 1 SD were associated with an increased risk for all-cause death (HR=1.08, 95% CI=1.05, 1.11) and incident MI (HR=1.09, 95% CI=1.03, 1.16).ConclusionsOur results suggest that modest increases in exercise systolic blood pressure response are associated with adverse outcomes.

Exaggerated exercise blood pressure response and risk of stroke in patients referred for stress testing

Background/objectivesThere is some evidence to suggest that exercise systolic blood pressure (SBP) may be associated with future risk of stroke in subjects without a history of coronary artery disease (CAD). However, the value of an exaggerated exercise SBP response (EESBPR) for predicting stroke in patients referred for stress testing for clinical reasons has not been investigated. MethodsWe evaluated a community-based sample of 10,047 patients with known or suspected CAD who underwent treadmill exercise echocardiography. An EESBPR was defined as a peak exercise SBP of >220mmHg. The ratio of the increase in SBP during exercise to exercise workload (ΔSBPeEW) was also estimated. The endpoints were stroke of any type, ischemic stroke and hemorrhagic stroke. Median follow-up was 3.5years. ResultsAnnualized rates of stroke of any type, ischemic stroke and hemorrhagic stroke were 0.6% (95% CI 0.53–0.67), 0.49% (95% CI 0.42–0.56) and 0.12% (95% CI 0.09–0.15) in patients without EESBPR vs. 0.69% (95% CI 0.37–1), 0.49% (95% CI 0.23–0.76) and 0.19% (95% CI 0.02–0.35) in those with EESBPR (p=0.68, 0.90 and 0.39, respectively). Similarly, there was no significant univariate association between ΔSBPeEW and the occurrence of any endpoint. In multivariate analysis, hypertension, male sex, age, diabetes mellitus and resting SBP remained predictors of stroke of any type. EESBPR and ΔSBPeEW were not predictors of any of the endpoints evaluated. ConclusionWe did not observe any significant association between exercise SBP and the future occurrence of stroke in patients with known or suspected CAD referred for exercise echocardiography.

Exaggerated exercise systolic blood pressure response and risk of stroke in patients with known or suspected coronary artery disease

Exaggerated exercise systolic blood pressure response and risk of stroke in patients with known or suspected coronary artery disease

Exercise Testing in Nonatherosclerotic Heart Disease

Exercise testing first appeared in the medical literature in 1938.1 Since then, exercise testing has achieved an established place in the armamentarium of tests available to the physician for evaluating patients with known or suspected cardiac disease. In clinical practice, the application of exercise testing is often combined with cardiac imaging. This is reflected in recently available appropriate use criteria for myocardial perfusion imaging and stress echocardiography.2,3 However, exercise testing as a standalone test without imaging still has value in properly selected patients. The latest iteration of guidelines from the American College of Cardiology/American Heart Association (ACC/AHA) concerning exercise testing is dominated by diagnostic or prognostic assessments of atherosclerotic coronary artery disease applications.4 Less prominent are those applications that pertain to hypertrophic cardiomyopathy (HCM), valvular heart disease, and arrhythmias including pacemakers, all of which are the subject of this review. In the latest version of the ACC/AHA guidelines for exercise testing published in 2002,4 HCM is listed as a relative contraindication. However, in the ACC/European Society of Cardiology (ESC) expert consensus document on hypertrophic cardiomyopathy published in 2003,5 an abnormal exercise systolic blood pressure response is listed as a risk factor for sudden cardiac death in HCM. The exercise testing guidelines raise the issue of safety. Several reported series address this issue. The University of Minnesota group6 has exercised >3000 HCM patients over a period of 10 years with only 1 potentially fatal event, ie, exercise-induced sustained ventricular tachycardia that was successfully terminated with electric cardioversion. In addition, the Cleveland Clinic7 reported on 263 consecutive HCM patients who underwent exercise stress testing. Major complications occurred in 0.04% and minor events occurred in 23%. Major complications consisted of sustained ventricular tachycardia requiring direct-current cardioversion in 1 patient. Minor complications consisted of mild …

Prognostic Value of an Exaggerated Exercise Blood Pressure Response in Patients With Diabetes Mellitus and Known or Suspected Coronary Artery Disease

The prognostic value of an exaggerated exercise systolic blood pressure response (EESBPR) remains controversial. Our aim was to assess whether an EESBPR is associated with the long-term outcome in patients with diabetes mellitus and known or suspected coronary artery disease (CAD). From an initial population of 22,262 patients with known or suspected CAD who underwent treadmill exercise electrocardiography or exercise echocardiography at our institution, 2,591 patients with a history of diabetes mellitus were selected for the present study. EESBPR was defined as systolic blood pressure >220 mm Hg during exercise. The end points were all-cause mortality and hard events (ie, death or myocardial infarction). A total of 236 patients (9.1%) developed an EESBPR during the tests. During a mean follow-up of 6.5 +/- 3.9 years, 484 patients died and 646 experienced hard events. The 10-year mortality rate was 16.6% in patients with an EESBPR compared to 30.9% in those without an EESBPR (p <0.001). The 10-year hard event rate was also lower in patients with an EESBPR (23.2% vs 38.9% in patients without an EESBPR; p <0.001). On multivariate analysis, an EESBPR remained independently associated with a lower risk of all-cause mortality (hazard ratio 0.53, 95% confidence interval 0.36 to 0.78, p = 0.001) and hard events (hazard ratio 0.57, 95% confidence interval 0.41 to 0.79; p <0.001). These results remained consistent in the subgroup of patients without a known history of CAD. In conclusion, an EESBPR was associated with improved survival and a lower rate of death or myocardial infarction in patients with diabetes mellitus and known or suspected CAD.

Abstract 6057: Elevated LDL-Cholesterol Causes a Higher Exercise Blood Pressure Response

Background: Increased blood pressure (BP) response during exercise has been associated with an increased cardiovascular risk. It is unknown how LDL-cholesterol (LDL-c) is related to the exercise-induced BP response as well as to the large (LAE) and small artery (SAE) elasticity in subjects free from overt cardiovascular disease (CVD). We examined the relationship between serum LDL-c and the BP response during a moderate exercise treadmill test in subjects with no overt CVD and also the relationship between LDL-c and LAE and SAE. Methods: 1229 Subjects (700 male, 529 female) free of overt CVD were recruited during a CVD prevention screening program. A fasting venous blood sample was taken for LDL-cholesterol determination. LAE and SAE were derived from radial pulse wave contour analysis. Resting BP was measured. Then they performed a treadmill exercise test for 3 minutes at a 5 METS (metabolic equivalents) workload. Systolic and diastolic BP were measured at the peak of the 3 min exercise test, The study population was divided in quartiles among distribution of LDL-cholesterol (LDL-c). Results: Table 1 summarizes the results. There was no significant difference in large artery elasticity. Conclusions: In asymptomatic subjects, LDL-c is not related with resting BP. Higher LDL-c is related with higher exercise systolic BP response. This higher BP response can be explained by a lower smaller artery elasticity which is a marker for endothelial dysfunction probably related to higher LDL-c. Further studies to examine the effect of lipid-lowering therapy on exercise BP response are warranted Table 1

Therapeutic Effect Of Physical Activity On Exaggerated Blood Pressure Response To Exercise In Black Women

0693 An exaggerated exercise blood pressure response (EEBPR) in normotensive individuals is an independent marker for developing future hypertension. In the Surgeon General's Report on Physical Activity and Health, lifestyle of regular physical activity is emphasized in playing an important role in the prevention pf hypertension. PURPOSE: To investigat the effects of aerobic physical activity on normotensive individuals exhibiting EEBPR. METHODS: Seven 18–26 year-old normotensive African-American women with an exaggerated exercise systolic blood pressure response were screened and subjected to an 8-week aerobic training regimen consisting of supervised exercise on a cycle ergometer at 70% OV2max, 3 times/week for 30 minutes/session. Cardiovascular measures of blood pressure, heart rate, cardiac output, stroke volume, total peripheral vascular resistance, pulse pressure, arterial compliance, and arteriovenous oxygen difference were recorded at baseline, and at work intensities of 30W and 50%OV2max. The statistical significance of pre- vs. post-training differences were evaluated using a paired t −test at P <0.05. RESULTS: A 8.8% post-training increase in OV2max were found. No significance differences were detected in the baseline pre- vs. post-training values. At an absolute work intensity of 30W significant decrements in heart rate, arteriovenous oxygen difference, systolic pressure, and mean arterial pressure were found after training. Submaximal exercise at 50% OV2max was associated with significant increments in the pre- vs. post-training stroke volume, cardiac output and arterial compliance, and with significant decrements in the pre- vs. post-training total peripheral vascular resistance, systolic pressure, mean arterial pressure, and pulse pressure. CONCLUSION: Moderate aerobic exercise attenuated an EEBPR in African-American women, which may be an effective antihypertensive therapy for African-American women at risk for hypertension. Supported by NIH Grant GM-S06018.

Relationship between exercise systolic blood pressure and left ventricular geometry in overweight, mildly hypertensive patients.

To examine the association between the graded exercise systolic blood pressure (SBP) response and left ventricular (LV) geometric structure in patients with untreated mild hypertension. The study included 80 sedentary, overweight patients (43 female and 37 male) with unmedicated high normal blood pressure or stage 1-2 hypertension. An echocardiogram was used to determine LV mass and the relative wall thickness (RWT) in relation to the chamber dimension. Participants performed a maximal graded exercise test, and the SBP was recorded at workloads of 2, 4 and 6 metabolic equivalents and at peak exercise. Separate statistical models were used to determine the influence of LV mass indexed for height(2.7) (LVMIh) and RWT on submaximal exercise SBP and peak exercise SBP, controlling for resting SBP, age, gender, ethnicity and body mass index. A greater RWT was associated with a higher submaximal SBP level (P = 0.038). Neither LVMIh (P = 0.989) nor the interaction of RWT and LVMIh (P = 0.787) were related to the submaximal SBP. None of the main or interaction effects of RWT and LVMIh were associated with the peak exercise SBP level. Increases in RWT were associated with higher submaximal exercise SBP responses in a sample of overweight, unmedicated hypertensives. These results suggest that RWT is an important determinant of the association between cardiac mass and exercise SBP response.

Angiographic and prognostic implications of an exaggerated exercise systolic blood pressure response and rest systolic blood pressure in adults undergoing evaluation for suspected coronary artery disease

This study was designed to assess the angiographic and prognostic implications of an exaggerated systolic blood pressure response to exercise ("exercise hypertension") in adults undergoing evaluation for suspected coronary artery disease. The clinical implications of exercise hypertension are unclear. Subjects for this prospective cohort study were derived from a consecutive sample of 9,608 adults who were referred for treadmill testing and who augmented their systolic blood pressure by at least 10 mm Hg. There were 594 subjects who underwent coronary angiography within 90 days of treadmill testing. Exercise hypertension was defined as a peak exercise systolic blood pressure > or = 210 mm Hg in men and > or = 190 mm Hg in women. Severe angiographic coronary disease was defined as left main coronary artery disease (> or = 50% diameter stenosis), three-vessel disease (> or = 70% diameter stenosis) or two-vessel disease with > or = 70% diameter stenosis of the proximal left anterior descending coronary artery. All-cause mortality was assessed during a follow-up period of approximately 2 years. Exercise hypertension was present in 196 subjects (33%). Severe coronary disease was less common in subjects with exercise hypertension (14% vs. 25%, odds ratio 0.51, 95% confidence interval [CI] 0.32 to 0.81, p = 0.004). Exercise hypertension remained associated with a lower rate of severe coronary disease even after adjusting for rest hypertension, age, gender, exercise capacity and other possible confounders. During the follow-up period, there were 23 deaths; only 2 occurred in the group with exercise hypertension. After adjusting for severity of coronary disease, exercise hypertension remained associated with a lower mortality rate (adjusted relative risk 0.20, 95% CI 0.05 to 0.84, p = 0.03). In adults evaluated for coronary artery disease, exercise hypertension is associated with a lower likelihood of angiographically severe disease and a lower adjusted mortality rate.

Is there a relationship between exercise systolic blood pressure response and left ventricular mass? The Framingham Heart Study

Is there a relationship between exercise systolic blood pressure response and left ventricular mass? The Framingham Heart Study

Is there a relationship between exercise systolic blood pressure response and left ventricular mass? The Framingham Heart Study.

To assess the association between an exaggerated exercise systolic blood pressure response and the occurrence of left ventricular hypertrophy in healthy, normotensive individuals. Cross-sectional survey using M-mode echocardiography to measure left ventricular mass and to detect left ventricular hypertrophy. The Framingham Heart Study. Eight-hundred sixty men and 1118 women were studied who were free of cardiovascular or pulmonary disease, who were not taking any antihypertensive or cardiovascular medications, and who successfully achieved at least 90% of their age-predicted maximum heart rate during a monitored exercise treadmill test. All subjects had normal baseline and exercise electrocardiograms. Men with a peak exercise systolic blood pressure of 210 or more and women with a peak exercise systolic blood pressure of 190 or more were considered to have an "exaggerated" blood pressure response; 122 men and 67 women met these criteria. Subjects with an exaggerated exercise systolic blood pressure response had 10% higher left ventricular mass than those with a normal exercise systolic blood pressure response (in men: 115 +/- 25 compared with 105 +/- 24 g/m, P less than 0.001; in women: 86 +/- 22 compared with 73 +/- 16 g/m, P less than 0.001); they also had a higher prevalence of left ventricular hypertrophy (in men: odds ratio, 1.34, 95% CI, 1.00 to 1.80; in women: odds ratio, 2.12, CI, 1.48 to 3.03). After adjusting for age, resting systolic blood pressure, and body mass index, however, subjects with an exaggerated exercise systolic blood pressure response had only 5% higher left ventricular mass (in men: 111 +/- 2.1 compared with 106 +/- 0.8 g/m, P = 0.02; in women: 80 +/- 1.8 compared with 74 +/- 0.4 g/m, P = 0.002), and they no longer had a statistically increased prevalence of left ventricular hypertrophy (in men: odds ratio, 1.21, CI, 0.87 to 1.67; in women: odds ratio, 1.30, CI, 0.84 to 2.01). The apparent relation between exercise systolic blood pressure response and left ventricular mass is confounded by age, resting systolic blood pressure, and body mass; the degree of confounding is such that the biologic significance of this relationship should be questioned.