Exercise Blood Pressure Research Articles

Peripheral revascularization attenuates the exercise pressor reflex and increases coronary exercise hyperemia in peripheral arterial disease.

Peripheral arterial disease (PAD) is associated with augmented blood pressure (BP) and impaired coronary blood flow responses to exercise, which may increase cardiovascular risk. We investigated the effects of leg revascularization on the BP and coronary blood flow responses to exercise in PAD. Seventeen PAD patients (11 men, 66 ± 2 yr) performed single-leg plantar flexion exercise 24 h before and 1 mo following leg revascularization. BP and heart rate (HR) were measured continuously, and rate pressure product (systolic BP × HR) was calculated as an index of myocardial oxygen demand. Coronary blood velocity was obtained by transthoracic Doppler echocardiography in 8/17 subjects. The mean BP response to plantar flexion exercise was attenuated by leg revascularization (pre-revascularization: 15 ± 4 vs. post-revascularization: 7 ± 3 mmHg, P = 0.025). The HR response to plantar flexion was also attenuated following leg revascularization (pre-revascularization: 9 ± 1 vs. post-revascularization: 6 ± 1 beats/min, P = 0.006). The change in coronary blood velocity with exercise was greater at the post-revascularization visit: 4 ± 1 vs. pre-revascularization: -1 ± 2 cm/s ( P = 0.038), even though the change in rate pressure product was not greater following revascularization in these subjects (pre-revascularization: 2,796 ± 871 vs. post-revascularization: 1,766 ± 378 mmHg·beats/min, P = 0.082). These data suggest that leg revascularization alters reflex control of BP, HR, and coronary blood flow in response to exercise in patients with PAD. NEW & NOTEWORTHY We found that peripheral revascularization procedures lowered exercise blood pressure and improved coronary blood flow in patients with peripheral arterial disease.

The Effects of Aerobic Fitness on Blood Pressure Reactivity During Controlled Low and High Sodium Diets

PurposeIncreased blood pressure (BP) reactivity to acute exercise is predictive of future cardiovascular events. Excess dietary sodium exaggerates centrally‐mediated BP reactivity in salt‐resistant rodents. Regular exercise attenuates BP reactivity in rodents, presumably through increased fitness. However, the influence of dietary sodium on BP reactivity has not been investigated in humans. Furthermore, the interaction between dietary sodium and aerobic fitness on neurovascular regulation has not been investigated in humans. Therefore, we sought to test the hypotheses that 1) high dietary sodium exaggerates BP reactivity to acute hand‐grip exercise in humans; and 2) high aerobic fitness modulates high dietary sodium‐induced alterations in BP reactivity in healthy, young adults.MethodsThirteen healthy, young adults (8F/5M, age: 28±2 yrs, BMI: 24.1±0.9 kg/m2; BP: 109±2/63±2mmHg; Mean±SEM) completed randomized, controlled 10‐day diets of high (7 g/day) and low (1 g/day) dietary sodium separated by ≥ four weeks. Beat‐to‐beat laboratory BP was measured via photoplethysmography on day 10 of both diets. BP reactivity was assessed as ΔBP (mmHg) during the final minute of a two‐minute static hand‐grip exercise trial at 40% maximal voluntary contraction compared to a preceding 10‐minute baseline. Aerobic fitness was assessed as VO2Peak using a progressive‐intensity treadmill exercise protocol and indirect calorimetry. Differences in high‐ vs. low‐sodium BP reactivity (high – low sodium ΔBP reactivity; using the final minute of hand‐grip exercise BP data) was compared by splitting the participants into two categories of fitness (low vs. high) and completing an independent‐samples t‐test. Low aerobic fitness was defined as a relative VO2Peak of ≤40 ml*kg−1*min−1. Using this criterion, seven participants were classified as having “low aerobic fitness” and six were classified as having “high aerobic fitness”. Twenty four‐hour urinary sodium excretion was measured to ensure dietary compliance.ResultsUrinary Na+ excretion increased on the high‐ vs. low‐sodium diet (259.7±18.4 vs. 33.2±6.6 mmol/24 hours; p < 0.01). There was no difference in 24‐hr mean arterial BP on the high‐ vs. low‐sodium diet (82.9±2.1 vs. 79.8±2.4 mmHg, p > 0.05). The high sodium diet augmented systolic (24.2±2.6 vs. 17.4±3.1; p = 0.03), but not diastolic (18.7±1.8 vs. 15.5±2.5; p = 0.19) BP reactivity during acute hand‐grip exercise in all participants. There was a trend (p = 0.06) for the low aerobic fitness participants to demonstrate greater Δ systolic BP reactivity compared to the high aerobic fitness participants (11.5±4.3 vs. 1.1±2.4 ΔBP reactivity). However, there was not a statistically significant difference (p = 0.32) between the low and high aerobic fitness participants regarding Δ diastolic BP reactivity between diets (5.5±3.5 vs. 0.7±2.9 ΔBP reactivity).ConclusionThese preliminary data suggest that 1) high dietary sodium exaggerates systolic BP reactivity to acute hand‐grip exercise in humans; and 2) high aerobic fitness may modulate some of the neurovascular effects of high dietary sodium in healthy young adults, although more data is needed.Support or Funding InformationNIH Grant 1RO1HL128388This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

A Cross-Sectional Study of the Prevalence of Exercise-Induced Hypertension in Childhood Following Repair of Coarctation of the Aorta

Exercise-testing may be a more tolerable method of detecting hypertension in children after coarctation repair compared to gold-standard 24-hour ambulatory blood pressure (BP) monitoring (ABPM). This study aims to determine the prevalence of exercise-induced hypertension and end-organ damage in children after coarctation repair, and the effectiveness of exercise-testing compared to 24-hour ABPM in this population. Exercise-testing (Bruce protocol), transthoracic echocardiogram, 24-hour ABPM, and pulse wave velocity were performed in 41 patients aged 8 to 18 years with previous coarctation repair. Median age at repair was 13 days. Exercise-testing data were compared to healthy paediatric controls. Hypertension was defined as BP >95th percentile on 24-hour ABPM compared to normalised data, and systolic BP (SBP) arbitrarily >200mmHg on exercise-testing. After 13±3years, 39% (14/36) were hypertensive on 24-hour ABPM and 12% (5/41) on exercise-testing. Coarctation patients had a higher peak exercise SBP and reduced endurance compared to controls (164±26mmHg vs. 148±19mmHg, p=0.003; and 13.0±1.7mins vs. 14.2±2.4mins, p=0.007; respectively). All patients with a peak exercise SBP >190mmHg were hypertensive on 24-hour ABPM. Pulse wave velocity was higher in hypertensive patients on exercise-testing and 24-hour ABPM compared to normotensive patients (p=0.004 and p=0.06; respectively). Exercise-testing may be a useful tool to detect hypertension in children and young adults after coarctation repair, particularly in those who do not tolerate 24-hour ABPM. Normative peak exercise BP data for age should be obtained to improve the accuracy of exercise-testing in detecting hypertension.

Exercise Blood Pressure Guidelines: Time to Re-evaluate What is Normal and Exaggerated?

Blood pressure responses to graded exercise testing can provide important diagnostic and prognostic information. While published guidelines outline what constitutes a "normal" and "abnormal" (i.e., exaggerated) blood pressure response to exercise testing, the widespread use of exaggerated blood pressure responses as a clinical tool is limited due to sparse and inconsistent data. A review of the original sources from these guidelines reveals an overall lack of empirical evidence to support both the normal blood pressure responses and their upper limits. In this current opinion, we critically evaluate the current exercise blood pressure guidelines including (1) the normal blood pressure responses to graded exercise testing; (2) the upper limits of this normal response; (3) the blood pressure criteria for test termination; and (4) the thresholds for exaggerated blood pressure responses. We provide evidence that exercise blood pressure responses vary according to subject characteristics, and subsequently a re-evaluation of what constitutes normal and abnormal responses is necessary to strengthen the clinical utility of this assessment.

Influence of dietary nitrate supplementation on lung function and exercise gas exchange in COPD patients

BackgroundDuring exercise as pulmonary blood flow rises, pulmonary capillary blood volume increases and gas exchange surface area expands through distention and recruitment. We have previously demonstrated that pulmonary capillary recruitment is limited in COPD patients with poorer exercise tolerance. Hypoxia and endothelial dysfunction lead to pulmonary vascular dysregulation possibly in part related to nitric oxide related pathways. PurposeTo determine if increasing dietary nitrate might influence lung surface area for gas exchange and subsequently impact exercise performance. MethodsSubjects had stable, medically treated COPD (n = 25), gave informed consent, filled out the St George Respiratory Questionnaire (SGRQ), had a baseline blood draw for Hgb, performed spirometry, and had exhaled nitric oxide (exNO) measured. Then they performed the intra-breath (IB) technique for lung diffusing capacity for carbon monoxide (DLCO) as well as pulmonary blood flow (Qc). Subsequently they completed a progressive semi-recumbent cycle ergometry test to exhaustion with measures of oxygen saturation (SpO2) and expired gases along with DLCO and Qc measured during the 1st work load only. Subjects were randomized to nitrate supplement group (beetroot juice) or placebo group (black currant juice) for 8 days and returned for repeat of the above protocol. ResultsExhaled nitric oxide levels rose >200% in the nitrate group (p < 0.05) with minimal change in placebo group. The SGRQ suggested a small fall in perceived symptom limitation in the nitrate group, but no measure of resting pulmonary function differed post nitrate supplementation. With exercise, there was no influence of nitrate supplementation on peak VO2 or other measures of respiratory gas exchange. There was a tendency for the exercise DLCO to increase slightly in the nitrate group with a trend towards a rise in the DLCO/Qc relationship (p = 0.08) but not in the placebo group. The only other significant finding was a fall in the exercise blood pressure in the nitrate group, but not placebo group (p < 0.05). ConclusionDespite evidence of a rise in exhaled nitric oxide levels with nitrate supplementation, there was minimal evidence for improvement in exercise performance or pulmonary gas exchange surface area in a stable medically treated COPD population.

Effects of 12-week brisk walking training on exercise blood pressure in elderly patients with essential hypertension: a pilot study

ABSTRACTBackground: Essential hypertension (EP) is characterized by blood pressure (BP) elevations, which often lead to target organ damage and cardiovascular illness. The following study investigates whether aerobic exercise programs with different intensities could reduce the magnitude of BP rise. Methods: Patients with essential hypertension were recruited from the Baoshan Community Health Service Center. A total of 46 patients were finally selected and randomly assigned into two groups: control group (CON) included patients who did not participate in exercise intervention training; treatment group (TRG) included patients who participated in 12-week brisk walking training (60-min of brisk walking, three times a week for a total of 12 weeks). 3-minute step tests of low and high intensity were conducted pre- and post-intervention. To compare the effects of exercise intervention, 23 subjects with normal blood pressure (NBP) who did not participate in 12-week brisk walking training, were recruited. Results: After 12 weeks of brisk walking, SBP of TRG during resting, low and high-intensity exercise was significantly reduced by 8.3mmHg, 15.6mmHg, and 22.6mmHg, respectively; while HR of TRG’s during resting, low and high intensity was significantly reduced by 3.6beats/minute, 8.7beats/minute and 11.3beats/minute, respectively. Meanwhile, after 12 weeks of brisk walking, TRG’s steps per day, o2max, moderate physical activity time and physical activity energy expenditure significantly increased by 6000 steps, 2.4 ml/kg/m, 40 minutes and 113 kcal, respectively. At the same time, TRG’s body fat rate and sedentary time significantly reduced by 2% and 60 minutes per day. Conclusion: Brisk walking can reduce the magnitude of BP rise during exercise of different intensities and may be reduced the risk of acute cardiovascular incidents in elderly patients with essential hypertension.Abbreviations: EP: Essential hypertension; BP: blood pressure; CON: control group; TRG: treatment group; NBP: normal blood pressure; PA: physical activity

The exaggerated blood pressure response to exercise in the sub-acute phase after stroke is not affected by aerobic exercise.

The prevalence of an exaggerated exercise blood pressure (BP) response is unknown in patients with subacute stroke, and it is not known whether an aerobic exercise program modulates this response. The authors randomized 53 patients (27 women) with subacute stroke to 12weeks of twice-weekly aerobic exercise (n=29) or to usual care without scheduled physical exercise (n=24). At baseline, 66% of the patients exhibited an exaggerated exercise BP response (peak systolic BP ≥210mmHg in men and ≥190mmHg in women) during a symptom-limited ergometer exercise test. At follow-up, patients who had been randomized to the exercise program achieved higher peak work rate, but peak systolic BP remained unaltered. Among patients with a recent stroke, it was common to have an exaggerated systolic BP response during exercise. This response was not altered by participation in a 12-week program of aerobic exercise.

The Effect of the Motivational Interview Method on the Lifestyle of Hypertensive Individuals

This study aims to analyse the effect of motivational interviews on the lifestyle of hypertensive individuals. This study was conducted with hypertensive individuals between the ages of 24 and 45, registered in seven family health centres in Aksehir, Konya, Turkey. The 75 individuals who agreed to participate were allocated into two groups: experimental and control. Both the groups were administered the pre-test, then the experimental group was visited for a total of 5 times: four visits at threeweek intervals and one visit after one month. The study was completed by administering the post-test to both groups and data were analysed using SPSS 17.0. Statistically significant differences were found between the pre-test and post-test scores of the experimental group in terms of blood pressure and BMI. In conclusion, motivational interviews can be used in ensuring healthy nutrition and regulation of their exercise level and blood pressure for hypertensive individuals. Keywords: Hypertension, lifestyle, blood pressure, body mass index, nursing

Impaired baroreflex sensitivity, carotid stiffness, and exaggerated exercise blood pressure: a community-based analysis from the Paris Prospective Study III.

People with exaggerated exercise blood pressure (BP) have adverse cardiovascular outcomes. Mechanisms are unknown but could be explained through impaired neural baroreflex sensitivity (BRS) and/or large artery stiffness. This study aimed to determine the associations of carotid BRS and carotid stiffness with exaggerated exercise BP. Blood pressure was recorded at rest and following an exercise step-test among 8976 adults aged 50 to 75 years from the Paris Prospective Study III. Resting carotid BRS (low frequency gain, from carotid distension rate, and heart rate) and stiffness were measured by high-precision echotracking. A systolic BP threshold of ≥ 150mmHg defined exaggerated exercise BP and ≥140/90mmHg defined resting hypertension (±antihypertensive treatment). Participants with exaggerated exercise BP had significantly lower BRS [median (Q1; Q3) 0.10 (0.06; 0.16) vs. 0.12 (0.08; 0.19) (ms2/mm) 2×108; P < 0.001] but higher stiffness [mean ± standard deviation (SD); 7.34 ± 1.37 vs. 6.76 ± 1.25 m/s; P < 0.001) compared to those with non-exaggerated exercise BP. However, only lower BRS (per 1SD decrement) was associated with exaggerated exercise BP among people without hypertension at rest {specifically among those with optimal BP; odds ratio (OR) 1.16 [95% confidence intervals (95% CI) 1.01; 1.33], P = 0.04 and high-normal BP; OR, 1.19 (95% CI 1.07; 1.32), P = 0.001} after adjustment for age, sex, body mass index, smoking, alcohol, total cholesterol, high-density lipoprotein cholesterol, resting heart rate, and antihypertensive medications. Impaired BRS, but not carotid stiffness, is independently associated with exaggerated exercise BP even among those with well controlled resting BP. This indicates a potential pathway from depressed neural baroreflex function to abnormal exercise BP and clinical outcomes.

The clinical importance of exercise blood pressure

Clinical exercise stress testing is a common medical test performed in cardiology and exercise physiology clinics the world over. Measurement of blood pressure (BP) during testing is mandated. Whilst systolic BP should normally rise with incremental exercise, and diastolic BP remains relatively stable, abnormal responses can occur. Low BP or ‘exercise hypotension’ is a known signal of underlying cardiovascular disease and sign of poor prognosis. On the other hand, observational evidence suggests an exaggerated BP response is also associated with heightened cardiovascular disease risk. Historically, research has focused on the BP response to peak or maximum exercise intensities. However, exaggerated BP during submaximal exercise (light-to-moderate intensity) may expose the presence of high BP otherwise not detected by traditional resting measurement in the clinic. Exaggerated exercise BP is related to subclinical cardiovascular disease risk markers such as raised arterial stiffness and impaired cardiac structure and function. The mechanisms underlying such associations are complex, but physiological insight has been gained from studying changes in arterial haemodynamics in response to dynamic exercise. Similarly, there are several known modifiers of the exercise BP response, including age, disease status and aerobic capacity. An area of continued focus is to establish if modifiers, such as aerobic capacity, also modify associations between exercise BP and clinical outcomes throughout the life-course. Future work is also directed towards filling a crucial evidence gap, providing population-based thresholds of exercise BP that are associated with acute and longer-term outcomes. This should pave the way for pragmatic research aimed towards enhancing the clinical use of exercise BP.

Exaggerated blood pressure response to exercise and late-onset hypertension in young adults.

Exaggerated blood pressure response (EBPR) during exercise has been associated with an increased risk of incidental systemic hypertension and cardiovascular morbidity; however, there is no consensus definition of EBPR. We aimed to determine which marker best defines EBPR during exercise and to predict the long-term development of hypertension in individuals younger than 50 years. We reviewed 107 exercise tests performed in 1992, applied several reported methods to define EBPR at moderate and maximum exercise, and contacted the patients by telephone 20 years after the test to verify hypertension status. Finally, we determined which definition best predicted incidental hypertension at 20-year follow-up. The mean age of the participants at the time of exercise testing was 25.7±11.1 years. Logistic regression showed a significant association of diastolic blood pressure of more than 95 mmHg at peak exercise and systolic pressure more than 180 mmHg at moderate exercise with new-onset hypertension at 20-year follow-up [odds ratio: 6.3 (2.09-18.9) and odds ratio: 7.09 (2.31-21.7), respectively]. If EBPR was present, as defined by at least one of these parameters, the probability of incidental later onset hypertension was 70%. In our population, diastolic blood pressure of more than 95 mmHg at maximum exercise or systolic blood pressure more than 180 mmHg at moderate-intensity exercise (100 W) were the best predictors of new-onset hypertension at long-term follow-up. Individuals with EBPR according to these criteria should be monitored closely to detect the early development of hypertension.

The clinical importance of exercise blood pressure

Clinical exercise stress testing is a common medical test performed in cardiology and exercise physiology clinics the world over. Measurement of blood pressure (BP) during testing is mandated. Whilst systolic BP should normally rise with incremental exercise, and diastolic BP remains relatively stable, abnormal responses can occur. Low BP or ‘exercise hypotension’ is a known signal of underlying cardiovascular disease and sign of poor prognosis. On the other hand, observational evidence suggests an exaggerated BP response is also associated with heightened cardiovascular disease risk. Historically, research has focused on the BP response to peak or maximum exercise intensities. However, exaggerated BP during submaximal exercise (light-to-moderate intensity) may expose the presence of high BP otherwise not detected by traditional resting measurement in the clinic. Exaggerated exercise BP is related to subclinical cardiovascular disease risk markers such as raised arterial stiffness and impaired cardiac structure and function. The mechanisms underlying such associations are complex, but physiological insight has been gained from studying changes in arterial haemodynamics in response to dynamic exercise. Similarly, there are several known modifiers of the exercise BP response, including age, disease status and aerobic capacity. An area of continued focus is to establish if modifiers, such as aerobic capacity, also modify associations between exercise BP and clinical outcomes throughout the life-course. Future work is also directed towards filling a crucial evidence gap, providing population-based thresholds of exercise BP that are associated with acute and longer-term outcomes. This should pave the way for pragmatic research aimed towards enhancing the clinical use of exercise BP.

Masked hypertension is revealed by exaggerated submaximal exercise blood pressure among adolescents from the Avon longitudinal study of parents and children (ALSPAC)

ObjectivesMasked hypertension (MH) is associated with hypertension-related markers of organ damage, but is undetectable by clinic (resting) BP. Exaggerated systolic BP response to submaximal exercise reveals MH in adults, but it is unknown whether this is the case during adolescence. We aimed to determine if exercise BP was raised in adolescents with MH, and associations with markers of organ damage.Methods585 adolescents (aged 17.7 ± 0.3 years; 41.9% male) from the Avon longitudinal study of parents and children (ALSPAC), completed a step-exercise test with post-exercise BP, resting (clinic) BP and 24-hour ambulatory BP (ABP). MH was defined on the basis of guideline adult thresholds as clinic BP ≤ 140/90 mmHg and 24 h ABP ≥ 130/80 mmHg, or paediatric thresholds (age, sex and height percentiles). Assessment of markers of organ damage including left-ventricular mass (LVM) and carotid-femoral pulse wave velocity (PWV) was also undertaken.Results45 (7.7%) participants were classified with MH. Resting and post-exercise SBP were higher in those with MH vs. normotensives (126.1 ± 7.3 mmHg vs. 114.7 ± 10.0 mmHg, p < 0.001; 152.2±17.3 vs 141.1 ± 15.1 mmHg, p = 0.001). A post-exercise SBP threshold of 150 mmHg revealed MH (AUC = 0.69, 95% CI: 0.61–0.76, p < 0.001) and was associated with greater LVM index (30.2 ± 6.5 vs. 27.6 ± 5.8 g/m2.7, p < 0.001) and PWV (5.9 ± 0.6 vs. 5.7 ± 0.7 m/s, p = 0.01).ConclusionsThis is the first study within adolescents demonstrating post-exercise SBP can reveal MH and an association with markers of organ damage. Exaggerated exercise BP might be a warning signal of underlying high BP and increased cardiovascular risk undetected by clinic BP.

Blood Pressure Response to Exercise and Cardiovascular Disease.

This review aimed to provide a clinical update on exercise blood pressure (BP) and its relationship to cardiovascular disease (CVD), outlining key determinants of abnormal exercise BP responses. We also highlight current evidence gaps that need addressing in order to optimise the relevance of exercise BP as clinical CVD risk factor. Abnormal exercise BP manifests as either exercise hypotension (low BP response) or as exaggerated exercise BP (high BP response). Exercise hypotension is an established sign of existing and likely severe CVD, but exaggerated exercise BP also carries elevated CVD risk due to its association with sub-clinical hypertension. Although exaggerated exercise BP is related to heightened CVD risk at any exercise intensity, recent data suggest that the BP response to submaximal intensity exercise holds greater prognostic and clinical significance than BP achieved at peak/maximal intensity exercise. Cardiorespiratory fitness is a strong modifier of the exercise BP response, and should be taken into consideration when assessing the association with CVD. Both exercise hypotension and exaggerated exercise BP serve as markers that should prompt evaluation for potential underlying CVD. However, the clinical utility of these markers is currently inhibited by the lack of consensus informing the definitions and thresholds for abnormalities in exercise BP.

Abstract P408: Waist-to-height Ratio Index For Predicting The Incidence Of Hypertension

Background: Several anthropometric indices such as body mass index (BMI) and waist circumference (WC) have been examined as indicators of cardiovascular diseases in both adults and children. Waist-to-height ratio (WHtR) has been considered a superior predictor for detecting cardiovascular risk factors than BMI. We investigated the association between WHtR and incident hypertension in prospective study. Methods: A total of 1,718 subjects aged 39-72 years in a longitudinal study were recruited. Participants were divided into two groups according to development of hypertension during 2005-2008 (baseline) and 2008-2011 (follow-up). Logistic regression models were used to evaluate WHtR as a significant predictor of the hypertension. Results: During 2.8 years of follow-up, 185 new cases of hypertension (10.8%) were diagnosed with an incidence rate of approximately four percent per year. The WHtR was significantly higher in the subjects who had developed hypertension than in those who had not (0.54±0.05 vs. 0.51±0.05, p &lt;0.001). After adjusted for baseline age, gender, smoking status, alcohol intake, regular exercise, total cholesterol (LDL), and systolic blood pressure (SBP), logistic regression analysis indicated participants with the highest quartile of WHtR (WHtR≥0.54) were 4.51 times more likely to have hypertension than those with the lowest quartile (OR 4.51; 95% CI 2.41-8.43; p&lt;.0001). The area under the curve (AUC) for WHtR in identifying hypertension risk was significantly greater than BMI (p=0.0233). Conclusion: A positive association between WHtR and the incidence of hypertension was found in Korean adults. We assumed the WHtR may be a better predictor of incident hypertension in a community-based prospective study.

Exercise capacity and haemodynamic response among 12,327 individuals with cardio-metabolic risk factors undergoing treadmill exercise

Aims Haemodynamic parameters during and after exercise test seem to have a role in predicting cardiovascular events. We sought to evaluate the potential different responses in exercise capacity, heart rate and blood pressure levels in relation to major cardiovascular disease risk factors, among individuals undergoing exercise tolerance testing. Methods and results Consecutive individuals ( N = 12,327), aged 55 ± 11.8 years, underwent exercise tolerance testing, using the Bruce protocol. Obese participants showed higher values of peak systolic and diastolic blood pressure ( p < 0.01), with no heart rate differences. Diabetic patients presented increased systolic blood pressure across the test ( p = 0.02) and decreased tolerance to exercise ( p = 0.05), but without differences in diastolic blood pressure or heart rate. Hypertensives showed exaggerated blood pressure, chronotropic response and decreased capacity to exercise ( p < 0.001 for all). Smokers had increased baseline systolic blood pressure, peak diastolic blood pressure and recovery heart rate and decreased tolerance to exercise ( p < 0.001 for all). For all high-risk subgroups, exercise testing was more often positive. Age-stratified analysis revealed different patterns: all four risk factors significantly decreased peak metabolic equivalent in subjects <50 years old ( p < 0.05 for all), while in participants between 50 and 69 years old, diabetes mellitus ( p = 0.03), hypertension ( p = 0.04) and smoking ( p = 0.01) predicted achieved metabolic equivalent. For patients of ≥ 70 years old, obesity ( p = 0.006) and hypertension ( p = 0.02) decreased peak metabolic equivalent and systolic blood pressure recovery. In subjects without pre-existing cardiovascular disease and negative exercise tolerance testing (7064 subjects, mean age: 52.4 ± 12.1 years, 62.9% males), age, obesity, hypertension and female gender inversely and independently predicted peak metabolic equivalent. Conclusions High-risk individuals showed different haemodynamic responses when undergoing exercise tolerance testing, reflecting independent pathophysiological pathways.

Impaired Muscle Oxygenation and Elevated Exercise Blood Pressure in Hypertensive Patients: Links With Vascular Stiffness.

This study examined in vivo (1) skeletal muscle oxygenation and microvascular function, at rest and during handgrip exercise, and (2) their association with macrovascular function and exercise blood pressure (BP), in newly diagnosed, never-treated patients with hypertension and normotensive individuals. Ninety-one individuals (51 hypertensives and 40 normotensives) underwent office and 24-hour ambulatory BP, arterial stiffness, and central aortic BP assessment, followed by a 5-minute arterial occlusion and a 3-minute submaximal handgrip exercise. Changes in muscle oxygenated and deoxygenated hemoglobin and tissue oxygen saturation were continuously monitored by near-infrared spectroscopy and beat-by-beat BP by Finapres. Hypertensives had higher (P<0.001) central aortic BP and pulse wave velocity versus normotensives and exhibited (1) a blunted tissue oxygen saturation response during occlusion, with slower (P=0.006) deoxygenation rate, suggesting reduced muscle oxidative capacity, and (2) a slower reoxygenation rate and blunted hyperemic response (P<0.05), showing reduced microvascular reactivity. Muscle oxygenation responses were correlated with aortic systolic and pulse pressure and augmentation index (P<0.05; age and body mass index (BMI) adjusted). When exercising at the same submaximal intensity, hypertensives required a significantly greater (P<0.001) increase in BP for achieving similar muscle oxygenation levels as normotensives. This response was correlated with the magnitude of microvascular hyperemia and aortic BP. In conclusion, nontreated patients with hypertension exhibit prominent reductions in in vivo indices of skeletal muscle oxidative capacity, suggestive of mitochondrial dysfunction, and blunted muscle microvascular reactivity. These dysfunctions were associated with higher aortic systolic BP and arterial stiffness. Dysregulations in muscle oxygen delivery/utilization and microvascular stiffness, in hypertensive patients, partially contribute to their exaggerated BP during exercise.

1238Impaired baroreflex sensitivity, carotid stiffness and exaggerated exercise blood pressure: a community-based analysis from the Paris Prospective Study 3

1238Impaired baroreflex sensitivity, carotid stiffness and exaggerated exercise blood pressure: a community-based analysis from the Paris Prospective Study 3

P648Exaggerated exercise blood pressure response is accompanied by increased sympathetic activity and arterial stiffness in subjects with high normal blood pressure

P648Exaggerated exercise blood pressure response is accompanied by increased sympathetic activity and arterial stiffness in subjects with high normal blood pressure

Absence of resting cardiovascular dysfunction in middle-aged endurance-trained athletes with exaggerated exercise blood pressure responses.

Untrained individuals with exaggerated blood pressure (EBP) responses to graded exercise testing are characterized as having resting dysfunction of the sympathetic and cardiovascular systems. The purpose of this study was to determine the resting cardiovascular state of endurance-trained individuals with EBP through a comparison of normotensive athletes with and without EBP. EBP was defined as a maximal systolic blood pressure (SBP) at least 190 mmHg and at least 210 mmHg for women and men respectively, in response to a graded exercise test. Twenty-two life-long endurance-trained athletes (56 ± 5 years, 16 men) with EBP (EBP+) and 11 age and sex-matched athletes (55 ± 5 years, eight men) without EBP (EBP-) participated in the study. Sympathetic reactivity was assessed using BP responses to a cold pressor test, isometric handgrip exercise, and postexercise muscle ischemia. Resting left ventricular structure and function was assessed using two-dimensional echocardiography, whereas central arterial stiffness was assessed using carotid-to-femoral pulse wave velocity. Calf vascular conductance was measured at rest and peak postexercise using strain-gauge plethysmography. All sympathetic reactivity, left ventricular, and arterial stiffness indices were similar between groups. There was no between-group difference in resting vascular conductance, whereas peak vascular conductance was higher in EBP+ relative to EBP- (1.81 ± 0.65 vs. 1.45 ± 0.32 ml/100 ml/min/mmHg, P < 0.05). Findings from this study suggest that athletes with EBP do not display the resting cardiovascular state typically observed in untrained individuals with EBP. This response in athletes, therefore, is likely a compensatory mechanism to satisfy peripheral blood-flow demands rather than indicative of latent dysfunction.