Exaggerated Exercise Blood Pressure Research Articles

Exercise systolic blood pressures are unaffected by time of day in healthy young adults.

Blood pressure (BP) assessment during exercise testing has the capacity to identify exaggerated exercise BP (EEBP). BP has a circadian rhythm; therefore, exercise BPs may change throughout the day complicating EEBP identification. The purpose of this study was to determine the effect of time of day on exercise BP in healthy young adults. Thirty-one participants [48% female; 23(4) years] completed a modified Bruce treadmill protocol in the morning (M), afternoon (A), and evening (E). Submaximal (stage 4) and peak (highest value) systolic BP (SBP) were determined and ΔSBP was calculated (peak SBP-pre-exercise SBP). Repeated-measures tests were used to compare SBP data. EEBP was defined as a submaximal SBP ≥ 170 mmHg. Chronotype was assessed using the Morning-Eveningness Questionnaire (MEQ) and Pearson correlations were used to determine the relationship between MEQ score and ΔSBP during all tests. Significance was set at P < 0.05. Submaximal SBP (M:159(25); A:156(16); E:162(24) mmHg; P = 0.295), peak SBP (M:177(32); A:184(25); E:185(26) mmHg; P = 0.087) and ΔSBP (M:62(29); A:67(23); 65(20) mmHg; P = 0.546) were similar across time points. Eight participants had an EEBP on at least two tests. MEQ scores were correlated with ΔSBP during the A test (r = 0.357, P = 0.049) and E test (r = 0.363, P = 0.045). In conclusion, time of day had no effect on SBP responses to exercise, but our correlational analysis suggests changes in SBP may differ between chronotypes depending on the time of day of exercise. Given the clinical value of EEBP, it is notable that 26% of our healthy young sample had EEBP.

Exploring the direct and indirect effects of cardiovascular disease risk factors on exercise blood pressure.

Exaggerated exercise blood pressure (BP) is independently associated with cardiovascular disease (CVD) outcomes. However, it is unknown how individual CVD risk factors may interact with one another to influence exercise BP. The aim of this study was to quantify direct and indirect associations between CVD risk factors and exercise BP, to determine what CVD risk factor/s most-strongly relate to exercise BP. In a cross-sectional design, 660 participants (44 ± 2.6 years, 54% male) from the population-based Childhood Determinants of Adult Health Study had BP measured during low-intensity fixed-workload cycling. CVD risk factors were measured, including body composition, clinic (rest) BP, blood biomarkers, and cardiorespiratory fitness. Associations between CVD risk factors and exercise BP were assessed using linear regression, with direct and indirect pathways of association assessed via structural equation model. Sex, waist-to-hip ratio, fitness, and clinic BP were independently associated with exercise systolic BP (SBP), and along with age, had direct associations with exercise SBP (p < 0.05 all). Most CVD risk factors were indirectly associated with exercise SBP via a relation with clinic BP (p < 0.05 all). Clinic BP, waist-to-hip ratio, and fitness were most-strongly associated (direct and indirect association) with exercise SBP (β[95% CI]: 9.35 [8.04, 10.67], 4.91 [2.56, 7.26], and -2.88 [-4.25, -1.51] mm Hg/SD, respectively). Many CVD risk factors are associated with exercise BP, mostly with indirect effects via clinic BP. Clinic BP, body composition, and fitness were most-strongly associated with exercise BP. These results may elucidate how lifestyle modification could be a primary strategy to decrease exaggerated exercise BP-related CVD risk.

Type-2 Diabetes and the Clinical Importance of Exaggerated Exercise Blood Pressure.

Exaggerated exercise blood pressure (EEBP) during clinical exercise testing is associated with poor blood pressure (BP) control and cardiovascular disease (CVD). Type-2 diabetes (T2DM) is thought to be associated with increased prevalence of EEBP, but this has never been definitively determined and was the aim of this study. Clinical exercise test records were analyzed from 13 268 people (aged 53±13 years, 59% male) who completed the Bruce treadmill protocol (stages 1-4, and peak) at 4 Australian public hospitals. Records (including BP) were linked to administrative health datasets (hospital and emergency admissions) to define clinical characteristics and classify T2DM (n=1199) versus no T2DM (n=12 069). EEBP was defined as systolic BP ≥90th percentile at each test stage. Exercise BP was regressed on T2DM history and adjusted for CVD and risk factors. Prevalence of EEBP (age, sex, preexercise BP, hypertension history, CVD history and aerobic capacity adjusted) was 12% to 51% greater in T2DM versus no T2DM (prevalence ratio [95% CI], stage 1, 1.12 [1.02-1.24]; stage 2, 1.51 [1.41-1.61]; stage 3, 1.25 [1.10-1.42]; peak, 1.18 [1.09-1.29]). At stages 1 to 3, 8.6% to 15.8% (4.8%-9.7% T2DM versus 3.5% to 6.1% no-T2DM) of people with 'normal' preexercise BP (<140/90 mm Hg) were identified with EEBP. Exercise systolic BP relative to aerobic capacity (stages 1-4 and peak) was higher in T2DM with adjustment for all CVD risk factors. People with T2DM have higher prevalence of EEBP and exercise systolic BP independent of CVD and many of its known risk factors. Clinicians supervising exercise testing should be alerted to increased likelihood of EEBP and thus poor BP control warranting follow-up care in people with T2DM.

Antihypertensive treatment effect on exercise blood pressure and exercise capacity in older adults.

An exaggerated blood pressure (BP) response to exercise and low exercise capacity are risk factors for cardiovascular disease (CVD). The effect of pharmacological antihypertensive treatment on exercise BP in older adults is largely unknown. This study investigates these effects accounting for differences in exercise capacity. Participants enrolled in the Southall and Brent Revisited (SABRE) study undertook a 6-min stepper test with expired gas analysis and BP measured throughout exercise. Participants were stratified by antihypertensive treatment status and resting BP control. Exercise systolic and diastolic BP (exSBP and exDBP) were compared between groups using potential outcome means [95% confidence intervals (CIs)] adjusted for exercise capacity. Exercise capacity was also compared by group. In total, 659 participants were included (mean age ± SD: 73 ± 6.6 years, 57% male). 31% of normotensive and 23% of hypertensive older adults with controlled resting BP had an exaggerated exercise BP. ExSBP was similar between normotensive and treated/controlled individuals [mean (95%CI): 180 (176 184) mmHg vs. 177 (173 181) mmHg, respectively] but was higher in treated/uncontrolled and untreated/uncontrolled individuals [mean (95% CI): 194 (190 197) mmHg, P < 0.001 and 199 (194 204) mmHg, P < 0.001, respectively]; these differences persisted after adjustment for exercise capacity and other confounders. Exercise capacity was lower in treated vs. normotensive individuals [mean (95% CI) normotensive: 16.7 (16.0,17.4) ml/kg/min]; treated/controlled: 15.5 (14.8,16.1) ml/kg/min, P = 0.009; treated/uncontrolled: [15.1 (14.5,15.7) ml/kg per min, P = 0.001] but was not reduced in untreated/uncontrolled individuals [mean (95% CI): 17.0 (16.1,17.8) ml/kg per min, P = 0.621]. Irrespective of resting BP control and despite performing less exercise, antihypertensive treatment does not fully mitigate an exaggerated BP response to exercise suggesting residual CVD risk in older adults.

The Identification and Management of High Blood Pressure Using Exercise Blood Pressure: Current Evidence and Practical Guidance.

High blood pressure (BP) is a leading risk factor for cardiovascular disease (CVD). The identification of high BP is conventionally based on in-clinic (resting) BP measures, performed within primary health care settings. However, many cases of high BP go unrecognised or remain inadequately controlled. Thus, there is a need for complementary settings and methods for BP assessment to identify and control high BP more effectively. Exaggerated exercise BP is associated with increased CVD risk and may be a medium to improve identification and control of high BP because it is suggestive of high BP gone undetected on the basis of standard in-clinic BP measures at rest. This paper provides the evidence to support a pathway to aid identification and control of high BP in clinical exercise settings via the measurement of exercise BP. It is recommended that exercise professionals conducting exercise testing should measure BP at a fixed submaximal exercise workload at moderate intensity (e.g., ~70% age-predicted heart rate maximum, stage 1–2 of a standard Bruce treadmill protocol). If exercise systolic BP is raised (≥170 mmHg), uncontrolled high BP should be assumed and should trigger correspondence with a primary care physician to encourage follow-up care to ascertain true BP control (i.e., home, or ambulatory BP) alongside a hypertension-guided exercise and lifestyle intervention to lower CVD risk related to high BP.

Cardiorespiratory Fitness, Workload, and the Blood Pressure Response to Exercise Testing

We propose that for correct clinical interpretation of exaggerated exercise blood pressure (EEBP), both cardiorespiratory fitness and exercise workload must be considered. A key recommendation toward achieving the correct clinical interpretation of EEBP is that exercise BP should be measured during submaximal exercise with a fixed external workload.

The association of elevated blood pressure during ischaemic exercise with sport performance in Master athletes with and without morbidity

BackgroundAn exaggerated exercise blood pressure (BP) is associated with a reduced exercise capacity. However, its connection to physical performance during competition is unknown.AimTo examine BP responses to ischaemic handgrip exercise in Master athletes (MA) with and without underlying morbidities and to assess their association with athletic performance during the World Master Track Cycling Championships 2019.MethodsForty-eight Master cyclists [age 59 ± 13yrs; weekly training volume 10.4 ± 4.1 h/week; handgrip maximum voluntary contraction (MVC) 46.3 ± 11.5 kg] divided into 2 matched groups (24 healthy MA and 24 MA with morbidity) and 10 healthy middle-aged non-athlete controls (age 48.3 ± 8.3 years; MVC 40.4 ± 14.8 kg) performed 5 min of forearm occlusion including 1 min handgrip isometric contraction (40%MVC) followed by 5 min recovery. Continuous beat-by-beat BP was recorded using finger plethysmography. Age-graded performance (AGP) was calculated to compare race performances among MA. Healthy Master cyclists were further grouped into middle-age (age 46.2 ± 6.4 years; N:12) and old-age (age 65.0 ± 7.7 years; N:12) for comparison with middle-aged non-athlete controls.ResultsHealthy and morbidity MA groups showed similar BP responses during forearm occlusion and AGP (90.1 ± 4.3% and 91.0 ± 5.3%, p > 0.05, respectively). Healthy and morbidity MA showed modest correlation between the BP rising slope for 40%MVC ischaemic exercise and AGP (r = 0.5, p < 0.05). MA showed accelerated SBP recovery after cessation of ischaemic handgrip exercise compared to healthy non-athlete controls.ConclusionOur findings associate long-term athletic training with improved BP recovery following ischaemic exercise regardless of age or reported morbidity. Exaggerated BP in Master cyclists during ischaemic exercise was associated with lower AGP during the World Master Cycling Championships.

Exaggerated Exercise Blood Pressure as a Marker of Baroreflex Dysfunction in Normotensive Metabolic Syndrome Patients

IntroductionExaggerated blood pressure response to exercise (EEBP = SBP ≥ 190 mmHg for women and ≥210 mmHg for men) during cardiopulmonary exercise test (CPET) is a predictor of cardiovascular risk. Sympathetic hyperactivation and decreased baroreflex sensitivity (BRS) seem to be involved in the progression of metabolic syndrome (MetS) to cardiovascular disease.ObjectiveTo test the hypotheses: (1) MetS patients within normal clinical blood pressure (BP) may present EEBP response to maximal exercise and (2) increased muscle sympathetic nerve activity (MSNA) and reduced BRS are associated with this impairment.MethodsWe selected MetS (ATP III) patients with normal BP (MetS_NT, n = 27, 59.3% males, 46.1 ± 7.2 years) and a control group without MetS (C, n = 19, 48.4 ± 7.4 years). We evaluated BRS for increases (BRS+) and decreases (BRS−) in spontaneous BP and HR fluctuations, MSNA (microneurography), BP from ambulatory blood pressure monitoring (ABPM), and auscultatory BP during CPET.ResultsNormotensive MetS (MetS_NT) had higher body mass index and impairment in all MetS risk factors when compared to the C group. MetS_NT had higher peak systolic BP (SBP) (195 ± 17 vs. 177 ± 24 mmHg, P = 0.007) and diastolic BP (91 ± 11 vs. 79 ± 10 mmHg, P = 0.001) during CPET than C. Additionally, we found that MetS patients with normal BP had lower spontaneous BRS− (9.6 ± 3.3 vs. 12.2 ± 4.9 ms/mmHg, P = 0.044) and higher levels of MSNA (29 ± 6 vs. 18 ± 4 bursts/min, P < 0.001) compared to C. Interestingly, 10 out of 27 MetS_NT (37%) showed EEBP (MetS_NT+), whereas 2 out of 19 C (10.5%) presented (P = 0.044). The subgroup of MetS_NT with EEBP (MetS_NT+, n = 10) had similar MSNA (P = 0.437), but lower BRS+ (P = 0.039) and BRS− (P = 0.039) compared with the subgroup without EEBP (MetS_NT−, n = 17). Either office BP or BP from ABPM was similar between subgroups MetS_NT+ and MetS_NT−, regardless of EEBP response. In the MetS_NT+ subgroup, there was an association of peak SBP with BRS− (R = −0.70; P = 0.02), triglycerides with peak SBP during CPET (R = 0.66; P = 0.039), and of triglycerides with BRS− (R = 0.71; P = 0.022).ConclusionNormotensive MetS patients already presented higher peak systolic and diastolic BP during maximal exercise, in addition to sympathetic hyperactivation and decreased baroreflex sensitivity. The EEBP in MetS_NT with apparent well-controlled BP may indicate a potential depressed neural baroreflex function, predisposing these patients to increased cardiovascular risk.

Cardiorespiratory fitness, fatness, and the acute blood pressure response to exercise in adolescence.

Exaggerated exercise blood pressure (BP) is associated with cardiovascular risk factors in adolescence. Cardiorespiratory fitness and adiposity (fatness) are independent contributors to cardiovascular risk, but their interrelated associations with exercise BP are unknown. This study aimed to determine the relationships between fitness, fatness, and the acute BP response to exercise in a large birth cohort of adolescents. 2292 adolescents from the Avon Longitudinal Study of Parents and Children (aged 17.8±0.4years, 38.5% male) completed a sub-maximal exercise step test that allowed fitness (VO2 max ) to be determined from workload and heart rate using a validated equation. Exercise BP was measured immediately on test cessation and fatness calculated as the ratio of total fat mass to total body mass measured by DXA. Post-exercise systolic BP decreased stepwise with tertile of fitness (146 (18); 142 (17); 141 (16) mmHg) but increased with tertile of fatness (138 (15); 142 (16); 149 (18) mmHg). In separate models, fitness and fatness were associated with post-exercise systolic BP adjusted for sex, age, height, smoking, and socioeconomic status (standardized β: -1.80, 95%CI: -2.64, -0.95mmHg/SD and 4.31, 95%CI: 3.49, 5.13mmHg/SD). However, when fitness and fatness were included in the same model, only fatness remained associated with exercise BP (4.65, 95%CI: 3.69, 5.61mmHg/SD). Both fitness and fatness are associated with the acute BP response to exercise in adolescence. The fitness-exercise BP association was not independent of fatness, implying the cardiovascular protective effects of cardiorespiratory fitness may only be realized with more favorable body composition.

HIGHER PREVALENCE OF EXAGGERATED EXERCISE BLOOD PRESSURE IN PEOPLE WITH TYPE 2 DIABETES CAN BE EXPLAINED BY CARDIOVASCULAR RISK FACTORS: THE EXERCISE STRESS TEST COLLABORATION (EXERTION)

Objective: Exaggerated exercise blood pressure (EEBP) during clinical exercise testing is associated with elevated cardiovascular disease (CVD) risk. Type-2 diabetes (T2DM) is thought to be associated with higher prevalence of EEBP, but this has never been determined in a large clinical population, which was the aim of this study. Design and method: Clinical exercise test records were analysed from 15,994 people (mean age 53 ± 13 years, 59% male) referred for the Bruce treadmill protocol (stages 1–4 + peak) at 4 Australian public hospitals. Exercise records including blood pressure (BP) were linked to administrative datasets (hospital and emergency admissions) to define clinical characteristics and classify prior history of T2DM (n = 1,345) vs. no-T2DM (n = 14,649). EEBP was defined &gt; 90th centile for each exercise stage. Exercise BP was regressed on T2DM history, adjusted to consider CVD risk factors. Results: EEBP prevalence (stage-1: + 4.1%; stage-2: + 4.4%; stage-3: + 4.9%; stage-4: + 4.8%; peak: + 1.9%, P &lt; 0.05 respectively) and exercise systolic BP (stage-1: + 4.25, stage-2: + 4.52, stage-3: + 4.43, stage-4: + 3.08, peak: + 0.75 mmHg, P &lt; 0.05 respectively) were higher across all exercise stages in T2DM vs. no-T2DM. However, all differences were abolished by adjustment for either: age, sex, peak workload, CVD history, or pre-exercise BP. Restricting analyses to those with normal pre-exercise BP (&lt;140/90 or &lt; 130/90 mmHg) revealed no differences in exercise BP or EEBP prevalence between T2DM and no-T2DM. Conclusions: This is the first study to confirm higher prevalence of EEBP in T2DM, but this is explained by accompanying CVD risk factors. Identification of EEBP should prompt aggressive CVD risk factor modification in T2DM.

Attenuation of exaggerated blood pressure responses to exercise: a byproduct of improved vascular function with passive heat therapy?

Attenuation of exaggerated blood pressure responses to exercise: a byproduct of improved vascular function with passive heat therapy?

Pulse wave velocity is related to exercise blood pressure response in young adults. The Cardiovascular Risk in Young Finns Study

Purpose: High pulse wave velocity (PWV), a marker of increased arterial stiffness, and an exaggerated exercise blood pressure (EEBP) response during an exercise test have both been related to an increased risk of hypertension and cardiovascular events. Contradictory results have been published about the association between these two parameters, and their relation in healthy young adults is unknown.Materials and methods: This study consisted of 209 young adults (mean age 38 years) who participated in the ongoing Cardiovascular Risk in Young Finns Study between 2007 and 2009. We measured resting PWV with impedance cardiography in 2007, and participants performed a maximal cardiopulmonary exercise test with blood pressure (BP) measurements at rest, during exercise and during recovery in 2008–2009.Results: High PWV (≥age- and sex-specific median) at baseline was associated with EEBP (SBP >210 mmHg for men and >190 mmHg for women) an average of 14 months later and with systolic BP during different stages of exercise from rest to peak and recovery (during peak exercise, β ± SE was 4.1 ± 1.1, p < 0.001). The association between high PWV and systolic BP remained after adjustment for traditional cardiovascular risk factors and other exercise parameters (during peak exercise, β ± SE was 2.3 ± 1.1, p = 0.04).Conclusions: Increased arterial stiffness predicts EEBP during a maximal exercise test in young adults during all stages of exercise from rest to peak and recovery. PWV could provide an additional tool for EEBP risk evaluation.

The influence of fitness on exercise blood pressure and its association with cardiac structure in adolescence.

Exaggerated exercise blood pressure (BP) is associated with altered cardiac structure and increased cardiovascular risk. Fitness modifies these associations, but the effect in healthy adolescents is unknown. We performed an observational study to determine the influence of fitness on post-exercise BP, and on its relationship with cardiac structure in adolescents. 4835 adolescents from the Avon Longitudinal Study of Parents and Children, (15.4 (0.3) years, 49% male) completed a submaximal cycle test. Fitness was estimated as physical work capacity 170 adjusted for lean body mass and post-exercise BP measured immediately posttest. Cardiovascular structure and function, including left ventricular (LV) mass (n=1589), left atrium (LA) size (n=1466), cardiac output (CO, n=1610), and total peripheral resistance (TPR, n=1610) were measured at rest by echocardiography 2.4 (0.4) years later. Post-exercise systolic BP increased stepwise by fitness tertile (131.2mmHg [130.4, 132.1]; 137.3mmHg [136.5, 138.0]; 142.3mmHg [141.5, 143.1]). Each 5mmHg of post-exercise systolic BP was associated with 2.46g [1.91, 3.01] greater LV mass, 0.02cm [0.02, 0.03] greater LA size, and 0.25g/m2.7 [0.14, 0.36] greater LV mass index. Adjustment for fitness abolished associations (0.29g [-0.16, 0.74]; 0.01cm [-0.001, 0.014] and 0.08g/m2.7 [-0.001, 0.002]). Similar associations between post-exercise systolic BP and each outcome were found between the lowest and highest fitness thirds. CO increased with fitness third (difference 0.06 L/min [-0.05, 0.17]; 0.23 L/min [0.12, 0.34]) while TPR decreased (difference -0.13mmHg·min/L [-0.84,0.59]; -1.08mmHg·min/L [-0.1.80, 0.35]). Post-exercise systolic BP increased with fitness, which modified its association with cardiac structure. Higher CO, but lower TPR suggests a physiologically adapted cardiovascular system with greater fitness, highlighting the importance of fitness in adolescence.

Body Silhouette Trajectories Across the Lifespan and Vascular Aging.

Vascular aging is a major contributor to cardiovascular disease and can be quantified by higher carotid stiffness, intima-media thickness and diameter, and hypertension. Weight gain across the lifetime may be an important, modifiable determinant of vascular aging. We therefore aimed to assess lifetime body silhouette trajectories (a marker of weight change across the lifespan) in relation to vascular aging in late adulthood. We used cross-sectional data from a community-based cohort study (n=8243; age, 59.4; 38.7% women). A linear mixed model was used to assess trajectories of recalled body silhouettes from age 8 to 45 years. We assessed carotid artery properties (ultrasonography), resting hypertension (blood pressure ≥140/90 mm Hg or use of antihypertensives), and exaggerated exercise blood pressure, a marker of masked hypertension (systolic blood pressure ≥150 mm Hg during submaximal exercise) at study recruitment when the participants were 50 to 75 years of age. We identified 5 distinct body silhouette trajectories: lean stable (32.0%), lean increase (11.1%), moderate stable (32.5%), lean-marked increase (16.3%), and heavy stable (8.1%). Compared with individuals in the lean-stable trajectory, those in the moderate-stable, lean-marked increase, and heavy-stable trajectories had higher carotid stiffness, intima-media thickness and diameter (odds ratios between 1.23 and 2.10 for highest quartile versus lowest quartile of manifestations of vascular aging; P<0.05) and were more likely to have resting hypertension and exaggerated exercise blood pressure, after adjustment for potential confounders (odds ratios between 1.31 and 1.60; P<0.05). Vascular aging was most prominent among individuals who were lean in early life but markedly gained weight during young adulthood and among those who were heavy in early life and maintained weight.

Abstract P194: Body Silhouette Trajectories Across the Lifespan and Vascular Aging: The Paris Prospective Study 3

Background: Vascular aging, i.e. accumulation of functional and structural changes of vessels throughout life, is a major contributor to cardiovascular disease. It can be quantified by higher carotid stiffness, intima-media thickness and diameter, and hypertension. Weight gain across the lifetime may be an important, modifiable determinant of vascular aging. Aim: To assess lifetime body silhouette trajectories (a marker of weight change across the lifespan) in relation to vascular aging in late adulthood. Methods: We used cross-sectional data from a community-based study (n=8,083; age 59.4; 38.6% women). A linear mixed model was used to assess trajectories of recalled body silhouettes from age 8 to 45. We assessed carotid stiffness, IMT and diameter (ultrasonography), resting hypertension (blood pressure ≥140/90 mmHg or use of antihypertensives), and exaggerated exercise blood pressure, a marker of masked hypertension (systolic blood pressure ≥150 mmHg during submaximal exercise). Results: We identified 5 trajectories: lean-stable (32%), lean-increase (11%), moderate-stable (33%), lean-marked increase (16%) and heavy-stable (8%). Compared to those in the lean-stable trajectory, individuals in the moderate-stable, lean-marked increase and heavy-stable trajectories had more evidence of vascular aging (Figure). Conclusions: Vascular aging was most prominent among individuals who were lean in early life but gained weight during young adulthood, and among those who were heavy in early life and maintained weight. This suggests that prevention of weight gain across the life course, especially during young adulthood, is important to promote healthy vascular aging.

Abstract P171: Occupational, Sport and Leisure Physical Activity Have Contrasting Effects on Neural Baroreflex Sensitivity. The Paris Prospective Study III

Background: Physical activity (PA) is beneficial for baroreflex sensitivity (BRS), but it is unclear whether the type of PA has similar effects on the neural (nBRS) or vascular (carotid stiffness) components of BRS. We sought to determine this in healthy adults from a community- based study via assessment of occupational (OPA), sport (SPA), leisure (LPA) and total PA (TPA). Methods: In 8649 adults aged 50 to 75 years, resting nBRS (estimated by low frequency gain, from carotid distension rate and heart rate) and carotid stiffness were measured by high-precision carotid echotracking. PA was self-reported using the Baecke questionnaire, which distinguishes OPA, SPA, LPA and TPA. The associations between PA and nBRS and carotid stiffness were quantified using multivariate linear regression analysis. Analyses were conducted separately in the working and non- working population. Results: In working adults (n=5039), OPA was associated with lower nBRS function (p=0.026) and borderline higher carotid stiffness (p=0.08). The associations between OPA and nBRS remained independent after additionally adjusting for SPA (p=0.03) and exaggerated exercise blood pressure (p=0.005), a predictor of future hypertension and cardiovascular events. When examining the type of OPA separately (i.e. lifting heavy loads, standing or walking at work) lifting heavy loads only was associated with impaired nBRS (p=0.048). When stratified by education, this association remained only in those with less than tertiary education. SPA was associated with higher nBRS (p=0.0005) and borderline lower carotid stiffness (p=0.052). Neither LPA nor TPA was associated with nBRS or carotid stiffness. In non-working adults (n=3610), SPA and TPA were both associated with lower carotid stiffness (p=0.012 and p=0.020), but not nBRS. LPA was not associated with either parameter. Conclusion: Occupation-related PA, in particular lifting heavy loads, is associated with lower nBRS function, especially in those with lower education. Higher amounts of sport-related PA are associated with higher nBRS and lower carotid stiffness.

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.

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.

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.