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Objectives: A hypertensive response to exercise (HRE) is associated with cardiovascular disease and high blood pressure (BP). Sub-clinical changes to cardiac structure may underlie these associations, although this has not been systematically determined. Via systematic review and meta-analysis, we aimed to (1) assess the relationship between exercise BP and cardiac structure, and (2) determine if cardiac structure is altered in those with an HRE, across various study populations (including those with/without high BP at rest)., Design and Methods: Three online databases were searched for cross-sectional studies reporting exercise BP, HRE and cardiac structural variables. Random-effects meta-analyses and meta-regressions were used to calculate pooled correlations between exercise BP and cardiac structure, and pooled mean differences and relative risk between those with/without an HRE., Results: Forty-nine studies, (n=23,707 total; aged 44±4 years; 63% male) were included. Exercise systolic BP was associated with increased left ventricular (LV) mass, LV mass index, relative wall thickness, posterior wall thickness and interventricular septal thickness (p<0.05 all). Those with an HRE had higher risk of LV hypertrophy (relative risk: 2.6 [1.85-3.70]), increased LV mass (47±7g), LV mass index (7±2g/m 2 ), relative wall thickness (0.02±0.005), posterior wall thickness (0.78±0.20mm), interventricular septal thickness (0.78±0.17mm) and left atrial diameter (2±0.52mm) vs. those without an HRE (p<0.05 all). Results were broadly similar between studies with different population characteristics., Conclusions: Exercise systolic BP is associated with cardiac structure, and those with an HRE show evidence towards adverse remodelling. Results were similar across different study populations, highlighting the hypertension-related cardiovascular risk associated with an HRE., (Copyright © 2021 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.)

Objective: 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., Methods: 2292 adolescents from the Avon Longitudinal Study of Parents and Children (aged 17.8 ± 0.4 years, 38.5% male) completed a sub-maximal exercise step test that allowed fitness (VO 2 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., Results: 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, -0.95 mmHg/SD and 4.31, 95%CI: 3.49, 5.13 mmHg/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, 5.61 mmHg/SD)., Conclusion: 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., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Individuals with type 2 diabetes mellitus (T2DM) have a greater blood pressure (BP) response to acute maximal exercise compared to those without T2DM; however, whether they exhibit a different arterial stiffness response to maximal exercise has yet to be explored. Adults with (n=66) and without T2DM (n=61) underwent an arterial stress test: at rest and immediately postexercise, carotid-femoral pulse wave velocity, the gold standard measure of arterial stiffness, brachial BP, heart rate, and other hemodynamic measurements were assessed. Linear regression models were used to evaluate between-group differences at rest, and the response to exercise (postexercise value), adjusting for covariates including BP and heart rate when relevant, and the corresponding baseline value of each parameter. All participants (mean±SD: age 59.3±10.6 years; body mass index 31.2±3.9 kg/m 2 ) had hypertension (mean BP 130±14/80±9 mm Hg). At rest, participants with T2DM had significantly higher carotid-femoral pulse wave velocity (10.3±2.7 versus 9.1±1.9 m/s), heart rate (69±11 versus 66±10 beats/min), and lower diastolic BP (79±9 versus 83±9 mm Hg), but systolic BP (129±15 versus 131±13 mm Hg) was similar. In response to exercise, participants with T2DM showed greater increases in carotid-femoral pulse wave velocity (1.6 [95% CI, 0.4-2.9 m/s]) and systolic BP (9 [95% CI, 1-17 mm Hg]) than participants without T2DM. A greater proportion of participants with T2DM had a hypertensive response to exercise compared to participants without T2DM (n=23, 35% versus n=11, 18%; P =0.033). By incorporating exercise as a vascular stressor, we provide evidence of a greater increase in arterial stiffness in individuals with T2DM, independently of resting arterial stiffness, and the BP postexercise.

Purpose: 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., Methods: 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., Results: Post-exercise systolic BP increased stepwise by fitness tertile (131.2 mm Hg [130.4, 132.1]; 137.3 mm Hg [136.5, 138.0]; 142.3 mm Hg [141.5, 143.1]). Each 5 mm Hg of post-exercise systolic BP was associated with 2.46 g [1.91, 3.01] greater LV mass, 0.02 cm [0.02, 0.03] greater LA size, and 0.25 g/m 2.7 [0.14, 0.36] greater LV mass index. Adjustment for fitness abolished associations (0.29 g [-0.16, 0.74]; 0.01 cm [-0.001, 0.014] and 0.08 g/m 2.7 [-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 -0.13 mm Hg·min/L [-0.84,0.59]; -1.08 mm Hg·min/L [-0.1.80, 0.35])., Conclusions: 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., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Purpose: Masked hypertension is associated with increased cardiovascular risk but is undetectable by clinic blood pressure (BP). Elevated systolic BP responses to submaximal exercise reveal the presence of masked hypertension 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 masked hypertension, and its association with cardiovascular risk markers., Methods: A total of 657 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 pre-, post-, and recovery-exercise BP, clinic BP and 24-hour ambulatory BP. Masked hypertension was defined as clinic BP <140/90 mm Hg and 24-hour ambulatory BP ≥130/80 mm Hg. Assessment of left-ventricular (LV) mass index and carotid-femoral pulse wave velocity (aortic PWV) was also undertaken. Thresholds of clinic, pre-, post-, and recovery-exercise systolic BP were explored from ROC analysis to identify masked hypertension., Results: Fifty participants (7.8%) were classified with masked hypertension. Clinic, pre-, post-, and recovery-exercise systolic BP were associated with masked hypertension (AUC ≥ 0.69 for all, respectively), with the clinic systolic BP threshold of 115 mm Hg having high sensitivity and specificity and exercise BP thresholds of 126, 150, and 130 mm Hg, respectively, having high specificity and negative predictive value (individually or when combined) for ruling out the presence of masked hypertension. Additionally, this exercise systolic BP above the thresholds was associated with greater left-ventricular mass index and aortic PWV., Conclusions: Submaximal exercise systolic BP is associated with masked hypertension and adverse cardiovascular structure in adolescents. Exercise BP may be useful in addition to clinic BP for screening of high BP and cardiovascular risk in adolescents., (© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Hypertension is the most common circulatory system condition, accounting for >40% of the cardiovascular disease total burden. One-third of Australians aged over 18 years have hypertension and in 68% of these it is uncontrolled. Australian data show hypertension accounts for 6% of general practitioner (GP) consults. Recent evidence has confirmed exercise is an effective adjunct therapy for hypertension management and the objective of this document is to provide a contemporary, evidence-based guide for optimal delivery of an exercise programme for blood pressure management. This work is an update to the 2009 Exercise and Sport Science Australia (ESSA) position stand. In most cases, the first line treatment to reduce BP is initiation of lifestyle changes, of which regular aerobic exercise is a principal component. Aerobic and resistance activities remain the cornerstone of exercise-based management of blood pressure, but recent work has uncovered variations on traditional delivery of exercise, such as high intensity interval training (HIIT) and a new exercise modality, isometric resistance training (IRT) may offer alternative management regimens. Exercise Physiologists, as well as other health care professionals, play an important role in helping to achieve BP control in patients with hypertension by reinforcing healthy lifestyle habits and prescribing appropriate exercise.

Physical activity (PA) is a preventative behavior for noncommunicable disease. However, little consideration is given as to whether different domains of PA have differing associations with health outcomes. We sought to determine the association between occupational, sport, leisure, and total PA with baroreflex sensitivity (BRS), distinguishing between neural (nBRS) and mechanical (mBRS) BRS. In a cross-sectional analysis of 8649 adults aged 50 to 75 years, resting nBRS (estimated by low-frequency gain, from carotid distension rate and heart rate) and mBRS (carotid stiffness) were measured by high-precision carotid echo-tracking. PA was self-reported using the validated Baecke questionnaire. The associations between PA and nBRS and mBRS were quantified using multivariate linear regression analysis, separately in the working and nonworking population. In working adults (n=5039), occupational PA was associated with worse nBRS (unstandardized β=-0.02; [95% CI, -0.04 to -0.003]; P =0.022) whereas sport PA was associated with better nBRS (β=0.04; [95% CI, 0.02-0.07]; P =0.003) and mBRS (β=-0.05; [95% CI, -0.09 to -0.00001]; P =0.049). Neither leisure PA nor total PA was associated with nBRS or mBRS. In nonworking adults (n=3610), sport PA and total PA were associated with better mBRS (β=-0.08; [95% CI, -0.15 to 0.02]; P =0.012 and β=-0.05; [95% CI, -0.10 to 0.009]; P =0.018) but not nBRS. These findings suggest differential associations between domains of PA and BRS and may provide insights into the mechanisms underlying the association between occupational PA and cardiovascular disease.

Aims: 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., Methods and Results: 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 ≥ 150 mmHg defined exaggerated exercise BP and ≥140/90 mmHg 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., Conclusion: 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., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com.)

Purpose of Review: 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., Recent Findings: 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.

Objectives: Exaggerated exercise blood pressure (EEBP) recorded during exercise testing at moderate-intensity is independently associated with cardiovascular mortality. It is hypothesized that EEBP may be indicative of underlying hypertension unnoticed by standard clinic (resting) BP measures (thus explaining increased mortality risk), but this has never been confirmed by association with hypertension defined using ambulatory BP monitoring, which was the aim of this study., Design: Cross-sectional study., Methods: 100 consecutive patients free from coronary artery disease (aged 56±9 years, 72% male) underwent clinically indicated exercise stress testing. Exercise BP was recorded at each stage of the Bruce protocol. Presence of hypertension was defined as 24-hour systolic BP ≥130mmHg or daytime systolic BP ≥135mmHg., Results: Exercise systolic BP at stage 1 and 2 of the test was significantly associated with the presence of hypertension (P<0.05), with the strongest association observed between stage 1 exercise systolic BP and 24-h systolic BP >130mmHg (AUC=0.752, 95% CI's 0.649-0.846, P<0.001). 79% of participants achieving systolic BP ≥150mmHg at stage 1 of the test were classified as having hypertension, with systolic BP >150mmHg predicting hypertension independently of age, sex and in-clinic hypertension status (OR=4.83, 95% CI's 1.62-14.39, P=0.005)., Conclusions: Irrespective of resting BP, systolic BP ≥150mmHg during early stages of the Bruce exercise stress test is associated with presence of hypertension. EEBP should be a warning signal to health/exercise professionals on the presence of hypertension and the need to provide follow up care to reduce cardiovascular risk., (Copyright © 2016 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.)

Aims: People with type 2 diabetes mellitus (T2DM) have abnormal peripheral and central haemodynamics at rest and during exercise, probably due to metabolic perturbations, but mechanisms are unknown. We used untargeted metabolomics to determine the relationships between metabolic perturbations and haemodynamics (peripheral and central) measured at rest and during exercise., Methods: Serum samples from 39 participants with T2DM (62 ± 9 years; 46 % male) and 39 controls (52 ± 10 years; 51 % male) were analysed by liquid chromatography-mass spectrometry, nuclear magnetic resonance spectroscopy and principal component analysis. Scores on principal components (PC) were used to assess relationships with haemodynamics including peripheral and central BP, central augmentation index (AIx) and central augmentation pressure (AP)., Results: Participants with T2DM had higher resting and exercise haemodynamics (peripheral and central BP, central AIx and central AP) compared to controls (p < 0.05). PC that comprised of a signature metabolic pattern of T2DM was independently associated with resting and exercise central AIx and central AP (p < 0.05)., Conclusions: Serum metabolic profile was associated with central, but not peripheral, haemodynamics in T2DM participants, suggesting that metabolic irregularities may explain abnormal central haemodynamics in T2DM patients.

Blood pressure (BP) is a mandatory safety measure during graded intensity clinical exercise stress testing. While it is generally accepted that exercise hypotension is a poor prognostic sign linked to severe cardiac dysfunction, recent meta-analysis data also implicate excessive rises in submaximal exercise BP with adverse cardiovascular events and mortality, irrespective of resting BP. Although more data is needed to derive submaximal normative BP thresholds, the association of a hypertensive response to exercise with increased cardiovascular risk may be due to underlying hypertension that has gone unnoticed by conventional resting BP screening methods. Delayed BP decline during recovery is also associated with adverse clinical outcomes. Thus, above and beyond being used as a routine safety measure during stress testing, exercise (and recovery) BP may be useful for identifying high-risk individuals and also as an aid to optimise care through appropriate follow-up after exercise stress testing. Accordingly, careful attention should be paid to correct measurement of exercise stress test BP (before, during and after exercise) using a standardised approach with trained operators and validated BP monitoring equipment (manual or automated). Recommendations for exercise BP measurement based on consolidated international guidelines and expert consensus are presented in this review.

Exercise-induced albuminuria is common in patients with type 2 diabetes mellitus (T2DM) in response to maximal exercise, but the response to light-moderate exercise is unclear. Patients with T2DM have abnormal central hemodynamics and greater propensity for exercise hypertension. This study sought to determine the relationship between light-moderate exercise central hemodynamics (including aortic reservoir and excess pressure) and exercise-induced albuminuria. Thirty-nine T2DM (62 ± 9 yr; 49% male) and 39 nondiabetic controls (53 ± 9 yr; 51% male) were examined at rest and during 20 min of light-moderate cycle exercise (30 W; 50 revolutions/min). Albuminuria was assessed by the albumin-creatinine ratio (ACR) at rest and 30 min postexercise. Hemodynamics recorded included brachial and central blood pressure (BP), aortic stiffness, augmented pressure (AP), aortic reservoir pressure, and excess pressure integral (Pexcess). There was no difference in ACR between groups before exercise (P > 0.05). Exercise induced a significant rise in ACR in T2DM but not controls (1.73 ± 1.43 vs. 0.53 ± 1.0 mg/mol, P = 0.002). All central hemodynamic variables were significantly higher during exercise in T2DM (i.e., Pexcess, systolic BP and AP; P < 0.01 all). In T2DM (but not controls), exercise Pexcess was associated with postexercise ACR (r = 0.51, P = 0.002), and this relationship was independent of age, sex, body mass index, heart rate, aortic stiffness, antihypertensive medication, and ambulatory daytime systolic BP (β = 0.003, P = 0.003). Light-moderate exercise induced a significant rise in ACR in T2DM, and this was independently associated with Pexcess, a potential marker of vascular dysfunction. These novel findings suggest that Pexcess could be important for appropriate renal function in T2DM., (Copyright © 2015 the American Physiological Society.)

Although physical activity (PA) improves arterial distensibility, it is unclear which type of activity is most beneficial. We aimed to examine the association of different types of PA with carotid distensibility (CD) and the mechanisms involved. Data included 4503 Australians and Finns aged 26-45 years. Physical activity was measured by pedometers and was self-reported. CD was measured using ultrasound. Other measurements included resting heart rate (RHR), cardiorespiratory fitness (CRF), blood pressure, biomarkers and anthropometry. Steps/day were correlated with RHR (Australian men r = -0.10, women r = - 0.14; Finnish men r = -0.15, women r = -0.11; P<0.01), CRF and biochemical markers, but not with CD. Self-reported vigorous leisure-time activity was more strongly correlated with RHR (Australian men r = -0.23, women r = -0.19; Finnish men r = -0.20, women r = -0.13; P < 0.001) and CRF, and was correlated with CD (Australian men r = 0.07; Finnish men r = 0.07, women r = 0.08; P < 0.05). This relationship of vigorous leisure-time activity with CD was mediated by RHR independently of potential confounders. In summary, vigorous leisure-time PA but not total or less intensive PA was associated with arterial distensibility in young to mid-aged adults. Promotion of vigorous PA is therefore recommended among this population. RHR was a key intermediary factor explaining the relationship between vigorous PA and arterial distensibility.

Purpose: A hypertensive response to moderate intensity exercise (HRE) is associated with increased cardiovascular risk. The mechanisms of an HRE are unclear, although previous studies suggest this may be due to haemostatic and/or haemodynamic factors. We investigated the relationships between an HRE with haemostatic and hemodynamic indices., Methods: Sixty-four participants (57 ± 10 years, 71 % male) with indication for exercise stress testing underwent cardiovascular assessment at rest and during moderate intensity exercise, from which 20 participants developed an HRE (defined as moderate exercise systolic BP ≥ 170 mmHg/men and ≥ 160 mmHg/women). Rest, exercise and post-exercise blood samples were analysed for haemostatic markers, including von Willebrand factor (vWf), and haemodynamic measures of brachial and central blood pressure (BP), aortic stiffness and systemic vascular resistance index (SVRi)., Results: HRE participants had higher rest vWf compared with normotensive response to exercise (NRE) participants (1,927 mU/mL, 95 % CI 1,240-2,615, vs. 1,129 mU/mL, 95 % CI 871-1,386; p = 0.016). vWf levels significantly decreased from rest to post-exercise in HRE participants (p = 0.005), whereas vWf levels significantly increased from rest to exercise in NRE participants (p = 0.030). HRE participants also had increased triglycerides, rest BP, aortic stiffness and exercise SVRi (p < 0.05 for all). Rest vWf predicted exercise brachial systolic BP (β = 0.220, p = 0.043; adjusted R (2) = 0.451, p < 0.001) independent of age, sex, body mass index, triglycerides, rest brachial systolic BP and aortic stiffness., Conclusions: Increased rest blood levels of vWf are independently associated with moderate intensity exercise systolic BP. These findings implicate abnormalities in haemostasis as a possible factor contributing to HRE at moderate intensity.

Evidence for the benefits of regular exercise is irrefutable and increasing physical activity levels should be a major goal at all levels of health care. People with hypertension are less physically active than those without hypertension and there is strong evidence supporting the blood pressure-lowering ability of regular exercise, especially in hypertensive individuals. This narrative review discusses evidence relating to exercise and cardiovascular (CV) risk in people with hypertension. Comparisons between aerobic, dynamic resistance, and static resistance exercise have been made along with the merit of different exercise volumes. High-intensity interval training and isometric resistance training appear to have strong CV protective effects, but with limited data in hypertensive people, more work is needed in this area. Screening recommendations, exercise prescriptions, and special considerations are provided as a guide to decrease CV risk among hypertensive people who exercise or wish to begin. It is recommended that hypertensive individuals should aim to perform moderate intensity aerobic exercise activity for at least 30 minutes on most (preferably all) days of the week in addition to resistance exercises on 2-3 days/week. Professionals with expertise in exercise prescription may provide additional benefit to patients with high CV risk or in whom more intense exercise training is planned. Despite lay and media perceptions, CV events associated with exercise are rare and the benefits of regular exercise far outweigh the risks. In summary, current evidence supports the assertion of exercise being a cornerstone therapy in reducing CV risk and in the prevention, treatment, and control of hypertension., (© American Journal of Hypertension, Ltd 2014. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Objectives: Physical activity is negatively associated with arterial stiffness. However, the relationship between sedentary behaviour and arterial stiffness is poorly understood. In this study, we aimed to investigate the association of sedentary behaviour with arterial stiffness among young adults., Design: Cross-sectional., Setting: 34 study clinics across Australia during 2004-2006., Participants: 2328 participants (49.4% male) aged 26-36 years who were followed up from a nationally representative sample of Australian schoolchildren in 1985., Measurements: Arterial stiffness was measured by carotid ultrasound. Sitting time per weekday and weekend day, and physical activity were self-reported by questionnaire. Cardiorespiratory fitness was estimated as physical work capacity at a heart rate of 170 bpm. Anthropometry, blood pressure, resting heart rate and blood biochemistry were measured. Potential confounders, including strength training, education, smoking, diet, alcohol consumption and parity, were self-reported. Rank correlation was used for analysis., Results: Sitting time per weekend day, but not per weekday, was correlated with arterial stiffness (males r=0.11 p<0.01, females r=0.08, p<0.05) and cardiorespiratory fitness (males r = -0.14, females r = -0.08, p<0.05), and also with fatness and resting heart rate. One additional hour of sitting per weekend day was associated with 5.6% (males p=0.046) and 8.6% (females p=0.05) higher risk of having metabolic syndrome. These associations were independent of physical activity and other potential confounders. The association of sitting time per weekend day with arterial stiffness was not mediated by resting heart rate, fatness or metabolic syndrome., Conclusions: Our study demonstrates a positive association of sitting time with arterial stiffness. The greater role of sitting time per weekend day in prediction of arterial stiffness and cardiometabolic risk than that of sitting time per weekday may be due to better reflection of discretionary sitting behaviour.

Exercise hypertension independently predicts cardiovascular mortality, although little is known about exercise central hemodynamics. This study aimed to determine the contribution of arterial wave travel and aortic reservoir characteristics to central blood pressure (BP) during exercise. We hypothesized that exercise central BP would be principally related to forward wave travel and aortic reservoir function. After routine diagnostic coronary angiography, invasive pressure and flow velocity were recorded in the ascending aorta via sensor-tipped intra-arterial wires in 10 participants (age, 55±10 years; 70% men) free of coronary artery disease with normal left ventricular function. Measures were recorded at baseline and during supine cycle ergometry. Using wave intensity analysis, dominant wave types throughout the cardiac cycle were identified (forward and backward, compression, and decompression), and aortic reservoir and excess pressure were calculated. Central systolic BP increased significantly with exercise (Δ=19±12 mm Hg; P<0.001). This was associated with increases in systolic forward compression waves (Δ=12×10(6)±17×10(6) W·m(-2)·s(-1); P=0.045) and forward decompression waves in late systole (Δ=9×10(6)±6×10(6) W·m(-2)·s(-1); P<0.001). Despite significant augmentation in BP (Δ=9±6 mm Hg; P=0.002), reflected waves did not increase in magnitude (Δ=-1×10(6)±3×10(6) W·m(-2)·s(-1); P=0.2). Excess pressure rose significantly with exercise (Δ=16±9 mm Hg; P<0.001), and reservoir pressure integral fell (Δ=-5×10(5)±5×10(5) Pa·s; P=0.010). Change in reflection coefficient negatively correlated with change in central systolic BP (r=-0.68; P=0.03). We conclude that elevation of exercise central BP is principally because of increases in aortic forward traveling waves generated by left ventricular ejection. These findings have relevance to understanding central BP waveform morphology and pathophysiology of exercise hypertension.

Background: Although a hypertensive response to exercise (HRE) is associated with cardiac risk and masked hypertension (MHT), its mechanisms and appropriate treatment remain unclear. We investigated spironolactone as a treatment for abnormal vascular and myocardial stiffness in HRE., Methods: In this randomized, double-blind, placebo-controlled study of 115 patients (54 ± 9 years, 57% men) with an HRE (≥210/105 mm Hg in men; ≥190/105 mm Hg in women) but no prior history of hypertension or myocardial ischemia, MHT prevalence was 40%. Patients were randomized to spironolactone 25mg daily (n = 58) or placebo (n = 57) and underwent evaluation at baseline and 3 months with exercise echocardiography, VO2max, pulse wave velocity (PWV), exercise and central blood pressure (BP), and 24-hour ambulatory BP. Changes in left ventricular mass index (LVMI), Doppler-derived E/em ratio (LV filling pressure), and myocardial strain were assessed., Results: Baseline 24-hour systolic BP (SBP) was 133 ± 10 mm Hg and peak-exercise SBP was 219 ± 16 mm Hg. Peak systolic strain (0.3 ± 3.6% vs. -0.1 ± 3.2, P = 0.56), E/em (-1.1 ± 2.3 vs. -0.6 ± 1.7, P = 0.30), VO(2max) (0.4 ± 4.9 vs. -0.9 ± 4.1 ml/kg/min, P = 0.15), and adjusted PWV did not significantly change with treatment, despite reduction in exercise SBP, 24-hour SBP, and LVMI. The change in exercise E/em was of borderline significance (-0.3 ± 2.4 vs. 0.8 ± 2.8, P = 0.06) and became significant after adjustment for baseline differences (P = 0.01). Patients with higher LVMI significantly increased VO(2max) (1.1 ± 5.6 vs. -2.4 ± 4.4 ml/kg/min, P < 0.05) and reduced exercise E/e(m) (-0.7 ± 2.7 vs. 1.9 ± 2.8, P < 0.05)., Conclusions: In HRE patients without previous hypertension, short-term spironolactone reduced exercise BP, 24-hour ambulatory BP, LVMI, and E/e(m) but did not significantly alter exercise capacity or myocardial strain.

Objective: Exaggerated exercise blood pressure (BP) predicts mortality. Some studies suggest this could be explained by chronic hyperlipidemia, but whether acute-hyperlipidemia effects exercise BP has never been tested, and was the aim of this study., Methods: Intravenous infusion of saline (control) and Intralipid were administered over 60 min in 15 healthy men by double-blind, randomized, cross-over design. Brachial and central BP (including, pulse pressure, augmentation pressure and augmentation index), cardiac output and systemic vascular resistance were recorded at rest and during exercise., Results: Compared with control, Intralipid caused significant increases in serum triglycerides, very low density lipoproteins and free fatty acids (p < 0.001 for all). However, there was no significant difference for any exercise hemodynamic variable (p > 0.05 for all)., Conclusion: Acute-hyperlipidemia does not significantly change exercise hemodynamics in healthy males. Therefore, the association between raised lipids and increased exercise BP is likely due to the chronic effects of hyperlipidemia., (Crown Copyright © 2012. Published by Elsevier Ireland Ltd. All rights reserved.)

Introduction: Patients with type 2 diabetes mellitus (T2DM) have exaggerated brachial and central (ascending aortic) blood pressure (BP) during exercise, which is associated with adverse outcomes. Central systolic loading, represented by the augmentation index (AIx), may contribute to exaggerated exercise central BP. This study sought to compare the central AIx response to peak exercise in T2DM and control patients and to identify mechanisms of altered exercise central AIx., Methods: Central BP and AIx were quantified by radial tonometry at rest and immediately after peak treadmill exercise in 106 patients with T2DM and 106 nondiabetic controls, pair-matched by age, gender, peak exercise brachial BP, and postexercise HR corresponding to tonometry acquisition. Cardiac volumes (by echocardiography) were assessed in a subgroup (22 T2DM and 22 controls) to derive rest and postexercise arterial-ventricular coupling parameters, including cardiac index (stroke volume index × HR), peripheral vascular resistance index (cardiac index / mean BP), and effective arterial elastance index (end-systolic pressure / stroke volume index). Reserve parameters (exercise--rest) were also defined., Results: Patients with T2DM had lower postexercise central AIx (-1% ± 13% vs 3% ± 14%, P = 0.038) and greater central AIx reserve (-24% ± 13% vs -20% ± 11%, P = 0.002) compared with controls, despite raised postexercise peripheral vascular resistance index (P = 0.013) and effective arterial elastance index (P = 0.011); these parameters independently predicted higher central AIx at rest (P < 0.01) but not after exercise. Moreover, T2DM was independently associated with lower postexercise central AIx (β = -0.21, P = 0.006). Cardiac index reserve, which was blunted in T2DM (P = 0.004), represented the only independent correlate of central AIx reserve (r = 0.39, P = 0.01)., Conclusions: Patients with T2DM have significantly (and paradoxically) lower postexercise central AIx and greater central AIx reserve, which may be explained by an impaired cardiac functional reserve.

Background: A hypertensive response to exercise (HRE; defined as normal clinic blood pressure (BP) and exercise systolic BP (SBP) ≥210 mm Hg in men or ≥190 mm Hg in women, or diastolic BP (DBP) ≥105 mm Hg) independently predicts mortality. The mechanisms remain unclear but may be related to masked hypertension. This study aimed to assess the prevalence of masked hypertension and its association with cardiovascular risk factors, including left ventricular (LV) mass, in patients with a HRE., Methods: Comprehensive clinical and echocardiographic evaluation (including central BP, aortic pulse wave velocity by tonometry) and 24-h ambulatory BP monitoring (ABPM) were performed in 72 untreated patients with HRE (aged 54 ± 9 years; 60% male; free from coronary artery disease confirmed by exercise stress echocardiography). Masked hypertension was defined according to guidelines as daytime ABPM ≥135/85 mm Hg and clinic BP <140/90 mm Hg., Results: Masked hypertension was present in 42 patients (58%). These patients had higher LV mass index (41.5 ± 8.7 g/m(2.7) vs. 35.9 ± 8.5 g/m(2.7); P = 0.01), LV relative wall thickness (RWT; 0.42 ± 0.09 vs. 0.37 ± 0.06; P = 0.004) and exercise SBP (222 ± 17 mm Hg vs. 212 ± 14 mm Hg; P = 0.01), but no significant difference in aortic pulse wave velocity or central pulse pressure (P > 0.05 for both). The strongest independent determinant of LV mass index was the presence of masked hypertension (unstandardized β = 5.6; P = 0.007), which was also independently related to LV RWT (unstandardized β = 0.04; P = 0.03)., Conclusions: Masked hypertension is highly prevalent in HRE patients with a normal resting office BP and is associated with increased LV mass index and RWT. Clinicians should consider measuring ABPM or home BP in HRE patients.

Background: Hypertension is ubiquitous in patients with heart failure and preserved ejection fraction (HFpEF) and contributes to arterial and ventricular stiffening. Exertional dyspnea may result from diastolic dysfunction with exercise; however, the association of central blood pressure (BP) to left ventricular filling pressure during exercise has not been assessed in this population and was the aim of this study., Methods: Fifteen patients with HFpEF and 15 age-matched and sex-matched controls were studied at rest, during submaximal and immediately after maximal exercise. Simultaneous echocardiography and radial tonometry was performed to measure E/e' and central BP, defined by central augmented pressure (C&#95;AP) and augmentation index (AIx)., Results: Patients with HFpEF had higher E/e' (P = 0.020) and peripheral and central BP (P < 0.001) at rest, yet similar C&#95;AP and AIx to controls (P > 0.05). There was a large increase in E/e' with exercise in patients (P = 0.012) but no change in C&#95;AP or AIx. Importantly, the change in E/e' from rest to submaximal exercise was significantly and independently associated with ΔC&#95;AP (r = 0.559; P = 0.030) and ΔAIx (r = 0.654; P = 0.008) in patients with HFpEF. In contrast with the controls, E/e', C&#95;AP and AIx decreased with exercise and there were no associations between exercise E/e' and central or peripheral BP (P > 0.05 for all)., Conclusion: Indices of central BP are associated with the left ventricular diastolic response to exercise in patients with HFpEF. Arterial function and central hemodynamics may be important targets for treating symptoms associated with raised left ventricular filling pressure with exertion.

Purpose: A hypertensive response to exercise (HRE) is common in patients with type 2 diabetes and is associated with increased left ventricular (LV) mass and mortality. This study aimed to determine whether lifestyle modification would improve exercise blood pressure (BP) and reduce LV mass in patients with type 2 diabetes., Methods: One hundred and eighty-five patients with type 2 diabetes were randomized to 1 yr of lifestyle intervention (n=97, mean ± SD age=54.7 ± 11.3 yr, 51% men) or usual care (control; n=88, age=53.8 ± 8.1 yr, 61% men). Brachial BP was measured at rest and during a graded maximal exercise test at baseline and 1 yr. Patients also underwent two-dimensional echocardiography to determine LV dimensions. A subgroup of 61 patients had resting and exercise central BP estimated from radial tonometry. An HRE was defined as a maximal exercise systolic BP of ≥210 mm Hg for men and ≥190 mm Hg for women., Results: At study entry, there were 101 patients (55%) with an HRE (n=51 controls). Compared with controls, lifestyle intervention significantly reduced the propensity to develop an HRE in those participants who did not have HRE at baseline (29.8% vs 59.5%, P=0.006). However, absolute values of exercise and resting (brachial and central) BP and LV mass were not significantly changed (all P values >0.05). There were significant (all P values <0.05) improvements in V˙O2max, body mass index, plasma glucose, insulin resistance, and HDL cholesterol after lifestyle intervention compared with control., Conclusions: Lifestyle intervention significantly attenuates the development of an HRE but does not reduce cardiac size after 1 yr in patients with type 2 diabetes., (© 2011 by the American College of Sports Medicine)

An exaggerated blood pressure (BP) response to exercise predicts future cardiovascular risk. The mechanisms underlying exercise-induced hypertension remain unclear, although endothelial dysfunction and elevated arterial stiffness may contribute. Given the association between reductions in nitric oxide (NO) and vascular dysfunction, we sought to determine whether acute inhibition of NO synthase with N(G)-monomethyl-L-arginine (L-NMMA) would lead to exaggerated BP responses to maximal exercise and attenuate exercise-induced reductions in arterial stiffness. In 10 healthy subjects (31±5 years), BP and heart rate (HR) were measured before, during and after an incremental cycling exercise test to determine maximal oxygen consumption (VO(2)max). Trials were performed with placebo (saline) or intravenous infusion of L-NMMA on separate days in a randomized, double-blind, crossover design. Central (aortic) and peripheral (femoral) arterial stiffness were assessed using pulse wave velocity (PWV). BP was increased with L-NMMA at rest and during sub-maximal exercise, but not at maximal exercise (mean BP 117±5 vs 118±8 mm Hg, saline vs L-NMMA, P>0.05). Furthermore, L-NMMA had no influence on exercising HR or VO(2)max (P<0.05). Notably, aortic PWV was similarly increased after exercise with either saline or L-NMMA (P<0.05), whereas postexercise decreases in femoral PWV were attenuated with L-NMMA (P<0.05). Our findings suggest that NO is an important contributor to reductions in femoral artery stiffness after maximal exercise in healthy individuals. Furthermore, acute pharmacological inhibition of NO synthase causes augmented BP responses to sub-maximal exercise, but does not lead to exaggerated BP responses to maximal exercise or reduce maximal oxygen consumption.

Background: Adult patients with cystic fibrosis (CF) have resting abnormal large artery haemodynamics. Here, we obtain further insight in patients with CF by evaluating haemodynamic response to physiological stress., Methods: Thirty-six stable CF patients mean (SD) age 28.9 (9.0)years and 25 controls matched for age, gender and body mass index were studied. Central haemodynamic parameters; including augmentation index (AIx) and wasted left ventricular pressure energy (∆E(W)) were determined pre, during and post light intensity cycle ergometry., Results: During exercise, despite a similar heart rate and blood pressure, patients had comparatively greater ∆E(W) (P=0.03) and trend towards greater AIx (P=0.07) than controls. Exercise ∆E(W) was greatest in patients with CF related diabetes (n=11). In all subjects, exercise ∆E(W) was related to age (r=0.54, P<0.001) and FEV(1)% predicted (r=-0.32, P=0.01)., Conclusions: Adults with CF have an abnormal haemodynamic response to exercise. This finding has deleterious implications for myocardial performance., (Copyright © 2010 European Cystic Fibrosis Society. Published by Elsevier B.V. All rights reserved.)

Blood (or plasma) rheology is related to cardiovascular risk. Mechanisms of this association are unclear but may be partially related to impaired left ventricular (LV) function and increased central blood pressure (BP) during light activity. This study aimed to test these hypotheses. Twenty patients (14 men; aged 61+/-12 years) with polycythemia rubra vera (n=16) or hemochromatosis (n=4) were studied at rest and during exercise at approximately 50% of maximal heart rate before and after venesection (500 mL; volume replaced with saline) to elicit an acute decrease in plasma viscosity at stable BP. Controls (n=20) underwent the same protocol with 25-mL venesection. Central BP and augmentation index were determined by tonometry. Resting LV systolic (peak longitudinal systolic strain rate and strain) and diastolic functions were determined by tissue-Doppler echocardiography. Venesection with blood volume replacement decreased viscosity (1.46+/-0.10 to 1.41+/-0.11 centipoise), protein, and hemoglobin (P<0.05 for all) and increased strain rate and strain (P<0.001 for both) in patients but not in controls (P>0.10 for all). There was no change in LV diastolic function (P>0.12 for all). Exercise augmentation index in patients was reduced after venesection (24+/-12% to 17+/-9%; P=0.001) despite no significant change in other BP variables. Hemodynamics (resting or exercise) were not significantly changed in controls. Exercise central systolic BP correlated with triglycerides (r=0.59; P<0.001). However, neither exercise hemodynamic changes nor LV functional changes correlated with any biochemical changes after venesection (P>0.05). We conclude that an acute change in blood rheology improves ventricular-vascular interaction by enhanced LV systolic function and reduced light-exercise central BP.

Background: Central blood pressure (BP) and markers of wave reflection (augmentation index; AIx) measured by radial tonometry have prognostic value independent from brachial BP. The measurement of the central waveform is increasingly used during altered hemodynamics, including exercise, but reliability of the test has not been reported under changed loading conditions. This study aimed to test the technique's reproducibility during major hemodynamic perturbations induced by exercise., Methods: Radial waveforms were recorded (SphygmoCor) in 28 healthy subjects (aged 53 +/- 11 years) at rest, during submaximal exercise (cycling at 50, 60, and 70% of maximal age-predicted heart rate (HR)) and immediately after maximal treadmill exercise on two occasions separated by 9 +/- 5 days. Data were compared between testing days. Waveforms were calibrated with brachial BP measured using a mercury sphygmomanometer. Pulse pressure amplification (PPAmp) was defined as the ratio of brachial to central pulse pressure., Results: There was very good reproducibility between visits at all exercise intensities for all waveform measures, including AIx, central pulse pressure, and PPAmp (intraclass correlations at 50% exercise were 0.93, 0.89, and 0.89, respectively; P < 0.001). The mean difference between tests at this intensity was 0 +/- 4% for AIx, 4 +/- 6 mm Hg for central pulse pressure, and -0.02 +/- 0.09 for PPAmp. There were no significant differences between visits for HR, PPAmp, or AIx at rest or with exercise (P > 0.05 for all)., Conclusions: Radial tonometry is a reproducible technique for measurement of central waveform indices during perturbations induced by exercise. It should, therefore, be suitable for use in intervention studies in which hemodynamics are altered.

NO modulates resting blood pressure and wave reflection. The effect of NO on exercise central hemodynamics is unknown but has important implications relating to cardiovascular risk. The aim of this study was to determine the contribution of NO to pulse pressure (PP) amplification and wave reflection during exercise. Twelve healthy men aged 29+/-1 years (mean+/-SEM) undertook cycle exercise at 60% of their maximal heart rate. Noninvasive measures of central blood pressure, estimated aortic pulse wave velocity, and wave reflection (augmentation index) were obtained by pulse wave analysis during intravenous infusion of saline (control), N(G)-monomethyl-l-arginine (a NO-synthase inhibitor), or noradrenaline (control vasoconstrictor). PP amplification was defined as the ratio of peripheral to central PP. Cardiac output and stroke volume were determined by electric bioimpedance. Both N(G)-monomethyl-l-arginine and noradrenaline caused a significant increase in mean arterial pressure (P<0.01) and augmentation index (P<0.01), as well as reduced ratio of peripheral to central PP (P<0.05) at baseline. Exercise caused a significant increase in the ratio of peripheral to central PP (P<0.001), whereas augmentation index and estimated aortic pulse wave velocity declined (for both P<0.05) during all 3 of the infusion protocols. However, no significant differences were observed in augmentation index, ratio of peripheral to central PP, or estimated aortic pulse wave velocity between infusion procedures (P>0.50) during exercise. Also, heart rate, peripheral vascular resistance, and cardiac output did not differ during exercise between saline, N(G)-monomethyl-l-arginine, or noradrenaline. Although we cannot rule out other vasodilator mechanisms having adjusted for NO blockade, our results indicate that NO does not solely contribute to systemic arterial stiffness or altered blood pressure amplification during light exercise.

Objectives: Exercise brachial blood pressure (BP) is predictive of cardiovascular events. As a result of the amplification of pulse pressure, central BP (a stronger cardiovascular risk factor) differs significantly from peripheral measures. Pulse pressure amplification is reduced with increasing age and hypercholesterolemia at rest, but the effect of exercise on central pressure in these populations is unknown. This study aimed to assess the central and peripheral BP response to exercise with aging and hypercholesterolemia., Methods: Twenty healthy younger (aged 29 +/- 5 years; mean +/- SD), 20 healthy older (aged 57 +/- 5 years) and 12 matched older (aged 59 +/- 7 years) men with hypercholesterolemia exercised (bicycle ergometer) at 60% of their predicted maximal heart rate. Central BP and augmentation index (AIx), a marker of systemic arterial stiffness, were obtained non-invasively using pulse wave analysis. Pulse pressure amplification was defined as the ratio of peripheral to central pulse pressure., Results: The resting haemodynamics of the older men were not significantly different from those with hypercholesterolemia. During exercise, amplification was significantly lower (P < 0.001), and the augmentation index significantly higher (P < 0.001) in the hypercholesterolemic individuals. Younger men had significantly increased amplification (P < 0.01) and reduced AIx (P < 0.001) at rest and during exercise compared with older men. In multiple regression analysis, exercise pulse pressure amplification was independently predicted by age (beta = -0.48; P < 0.001) and total cholesterol (beta = -0.28; P = 0.03)., Conclusion: With increasing age, exercise pulse pressure amplification is significantly attenuated because of increased wave reflection. These effects are exacerbated by hypercholesterolemia and may contribute to cardiovascular risk by mechanisms associated with central hypertension.

Exercise brachial blood pressure (BP) predicts mortality, but because of wave reflection, central (ascending aortic) pressure differs from brachial pressure. Exercise central BP may be clinically important, and a noninvasive means to derive it would be useful. The purpose of this study was to test the validity of a noninvasive technique to derive exercise central BP. Ascending aortic pressure waveforms were recorded using a micromanometer-tipped 6F Millar catheter in 30 patients (56+/-9 years; 21 men) undergoing diagnostic coronary angiography. Simultaneous recordings of the derived central pressure waveform were acquired using servocontrolled radial tonometry at rest and during supine cycling. Pulse wave analysis of the direct and derived pressure signals was performed offline (SphygmoCor 7.01). From rest to exercise, mean arterial pressure and heart rate were increased by 20+/-10 mm Hg and 15+/-7 bpm, respectively, and central systolic BP ranged from 77 to 229 mm Hg. There was good agreement and high correlation between invasive and noninvasive techniques with a mean difference (+/-SD) for central systolic BP of -1.3+/-3.2 mm Hg at rest and -4.7+/-3.3 mm Hg at peak exercise (for both r=0.995; P<0.001). Conversely, systolic BP was significantly higher peripherally than centrally at rest (155+/-33 versus 138+/-32 mm Hg; mean difference, -16.3+/-9.4 mm Hg) and during exercise (180+/-34 versus 164+/-33 mm Hg; mean difference, -15.5+/-10.4 mm Hg; for both P<0.001). True myocardial afterload is not reliably estimated by peripheral systolic BP. Radial tonometry and pulse wave analysis is an accurate technique for the noninvasive determination of central BP at rest and during exercise.

Background: Brachial blood pressure predicts cardiovascular outcome at rest and during exercise. However, because of pulse pressure amplification, there is a marked difference between brachial pressure and central (aortic) pressure. Although central pressure is likely to have greater clinical importance, very little data exist regarding the central haemodynamic response to exercise. The aim of the present study was to determine the central and peripheral haemodynamic response to incremental aerobic exercise., Materials and Methods: Twelve healthy men aged 31 +/- 1 years (mean +/- SEM) exercised at 50%, 60%, 70% and 80% of their maximal heart rate (HRmax) on a bicycle ergometer. Central blood pressure and estimated aortic pulse wave velocity, assessed by timing of the reflected wave (T(R)), were obtained noninvasively using pulse wave analysis. Pulse pressure amplification was defined as the ratio of peripheral to central pulse pressure and, to assess the influence of wave reflection on amplification, the ratio of peripheral pulse pressure to nonaugmented central pulse pressure (PPP : CDBP-P1) was also calculated., Results: During exercise, there was a significant, intensity-related, increase in mean arterial pressure and heart rate (P < 0.001). There was also a significant increase in pulse pressure amplification and in PPP : CDBP-P(1) (P < 0.001), but both were independent of exercise intensity. Estimated aortic pulse wave velocity increased during exercise (P < 0.001), indicating increased aortic stiffness. There was also a positive association between aortic pulse wave velocity and mean arterial pressure (r = 0.54; P < 0.001)., Conclusions: Exercise significantly increases pulse pressure amplification and estimated aortic stiffness.

Regular aerobic exercise is recommended by physicians to improve health and longevity. However, individuals exercising in urban regions are often in contact with air pollution, which includes particles and gases associated with respiratory disease and cancer. We describe the recent evidence on the cardiovascular effects of air pollution, and the implications of exercising in polluted environments, with a view to informing clinicians and other health professionals. There is now strong evidence that fine and ultra fine particulate matter present in air pollution increases cardiovascular morbidity and mortality. The main mechanisms of disease appear to be related to an increase in the pathogenic processes associated with atherosclerosis. People exercising in environments pervaded by air contaminants are probably at increased risk, due to an exercise-induced amplification in respiratory uptake, lung deposition and toxicity of inhaled pollutants. We make evidence-based recommendations for minimizing exposure to air-borne toxins while exercising, and suggest that this advice be passed on to patients where appropriate.