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      Effects of acute exercise on endothelial function in patients with abdominal aortic aneurysm

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          Abstract

          Endothelial dysfunction is observed in patients with abdominal aortic aneurysm (AAA), who have increased risk of cardiovascular events and mortality. This study aimed to assess the acute effects of moderate- and higher-intensity exercise on endothelial function, as assessed by flow-mediated dilation (FMD), in AAA patients (74 ± 6 yr old, n = 22) and healthy adults (72 ± 5 yr old, n = 22). Participants undertook three randomized visits, including moderate-intensity continuous exercise [40% peak power output (PPO)], higher-intensity interval exercise (70% PPO), and a no-exercise control. Brachial artery FMD was assessed at baseline and at 10 and 60 min after each condition. Baseline FMD was lower [by 1.10% (95% confidence interval: 0.72−.81), P = 0.044] in AAA patients than in healthy adults. There were no group differences in FMD responses after each condition ( P = 0.397). FMD did not change after no-exercise control but increased by 1.21% (95% confidence interval: 0.69−1.73, P < 0.001) 10 min after moderate-intensity continuous exercise in both groups and returned to baseline after 60 min. Conversely, FMD decreased by 0.93% (95% confidence interval: 0.41−1.44, P < 0.001) 10 min after higher-intensity interval exercise in both groups and remained decreased after 60 min. We found that the acute response of endothelial function to exercise is intensity-dependent and similar between AAA patients and healthy adults. Our findings provide evidence that regular exercise may improve vascular function in AAA patients, as it does in healthy adults. Improved FMD after moderate-intensity exercise may provide short-term benefit. Whether the decrease in FMD after higher-intensity exercise represents an additional risk and/or a greater stimulus for vascular adaptation remains to be elucidated.

          NEW & NOTEWORTHY Abdominal aortic aneurysm patients have vascular dysfunction. We observed a short-term increase in vascular function after moderate-intensity exercise. Conversely, higher-intensity exercise induced a prolonged reduction in vascular function, which may be associated with both short-term increases in cardiovascular risk and signaling for longer-term vascular adaptation in abdominal aortic aneurysm patients.

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          Most cited references 84

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          Ultrasound assessment of flow-mediated dilation.

          Developed in 1992, the flow-mediated dilation test is now the most commonly used noninvasive assessment of vascular endothelial function in humans. Since its inception, scientists have refined their understanding of the physiology, analysis, and interpretation of this measurement. Recently, a significant growth of knowledge has added to our understanding and implementation of this clinically relevant research methodology. Therefore, this tutorial provides timely insight into recent advances and practical information related to the ultrasonic assessment of vascular endothelial function in humans.
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            Cardiorespiratory fitness and adiposity as mortality predictors in older adults.

            Although levels of physical activity and aerobic capacity decline with age and the prevalence of obesity tends to increase with age, the independent and joint associations among fitness, adiposity, and mortality in older adults have not been adequately examined. To determine the association among cardiorespiratory fitness ("fitness"), adiposity, and mortality in older adults. Cohort of 2603 adults aged 60 years or older (mean age, 64.4 [SD, 4.8] years; 19.8% women) enrolled in the Aerobics Center Longitudinal Study who completed a baseline health examination during 1979-2001. Fitness was assessed by a maximal exercise test, and adiposity was assessed by body mass index (BMI), waist circumference, and percent body fat. Low fitness was defined as the lowest fifth of the sex-specific distribution of maximal treadmill exercise test duration. The distributions of BMI, waist circumference, and percent body fat were grouped for analysis according to clinical guidelines. All-cause mortality through December 31, 2003. There were 450 deaths during a mean follow-up of 12 years and 31 236 person-years of exposure. Death rates per 1000 person-years, adjusted for age, sex, and examination year were 13.9, 13.3, 18.3, and 31.8 across BMI groups of 18.5-24.9, 25.0-29.9, 30.0-34.9, and > or =35.0, respectively (P = .01 for trend); 13.3 and 18.2 for normal and high waist circumference (> or =88 cm in women; > or =102 cm in men) (P = .004); 13.7 and 14.6 for normal and high percent body fat (> or =30% in women; > or =25% in men) (P = .51); and 32.6, 16.6, 12.8, 12.3, and 8.1 across incremental fifths of fitness (P < .001 for trend). The association between waist circumference and mortality persisted after further adjustment for smoking, baseline health status, and BMI (P = .02) but not after additional adjustment for fitness (P = .86). Fitness predicted mortality risk after further adjustment for smoking, baseline health, and either BMI, waist circumference, or percent body fat (P < .001 for trend). In this study population, fitness was a significant mortality predictor in older adults, independent of overall or abdominal adiposity. Clinicians should consider the importance of preserving functional capacity by recommending regular physical activity for older individuals, normal-weight and overweight alike.
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              The relationship between shear stress and flow-mediated dilatation: implications for the assessment of endothelial function.

              Endothelium-dependent flow-mediated dilatation (FMD) describes the vasodilatory response of a vessel to elevations in blood flow-associated shear stress. Nitric oxide (NO), one of many vasoactive substances released by the endothelium in response to shear stress, is of particular interest to researchers as it is an antiatherogenic molecule, and a reduction in its bioavailability may play a role in the pathogenesis of vascular disease. The goal of many human studies is to create a shear stress stimulus that produces an NO-dependent response in order to use the FMD measurements as an assay of NO bioavailability. The most common non-invasive technique is the 'reactive hyperaemia test' which produces a large, transient shear stress profile and a corresponding FMD. Importantly, not all FMD is NO mediated and the stimulus creation technique is a critical determinant of NO dependence. The purpose of this review is to (1) explain that the mechanisms of FMD depend on the nature of the shear stress stimulus (stimulus response specificity), (2) provide an update to the current guidelines for FMD assessment, and (3) summarize the issues that surround the clinical utility of measuring both NO- and non-NO-mediated FMD. Future research should include (1) the identification and partitioning of mechanisms responsible for FMD in response to various shear stress profiles, (2) investigation of stimulus response specificity in coronary arteries, and (3) investigation of non-NO FMD mechanisms and their connection to the development of vascular disease and occurrence of cardiovascular events.
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                Author and article information

                Journal
                American Journal of Physiology-Heart and Circulatory Physiology
                American Journal of Physiology-Heart and Circulatory Physiology
                American Physiological Society
                0363-6135
                1522-1539
                January 01 2018
                January 01 2018
                : 314
                : 1
                : H19-H30
                Affiliations
                [1 ]VasoActive Research Group, School of Health and Sport Sciences, University of the Sunshine Coast, Maroochydore, Queensland, Australia
                [2 ]Sunshine Vascular Clinic, Buderim, Queensland, Australia
                [3 ]Sunshine Coast University Hospital, Sunshine Coast Hospital and Health Service, Birtinya, Queensland, Australia
                [4 ]Sport and Exercise Science, James Cook University, Townville, Queensland, Australia
                [5 ]School of Sport Science, Exercise, and Health, University of Western Australia, Crawley, Western Australia, Australia
                [6 ]Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom
                [7 ]Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Townsville, Queensland, Australia
                [8 ]Department of Vascular and Endovascular Surgery, Townsville Hospital, Townsville, Queensland, Australia
                Article
                10.1152/ajpheart.00344.2017
                © 2018

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