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      Sedentary Behavior and Cardiovascular Disease Risk : Mediating Mechanisms

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          Abstract

          Sedentary behavior has a strong association with cardiovascular disease (CVD) risk, which may be independent of physical activity. To date, the mechanism(s) that mediate this relationship are poorly understood. We hypothesize that sedentary behavior modifies key hemodynamic, inflammatory, and metabolic processes resulting in impaired arterial health. Subsequently, these vascular impairments directly and indirectly contribute to the development of CVD.

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          Most cited references25

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          Endothelial dysfunction - a major mediator of diabetic vascular disease.

          The vascular endothelium is a multifunctional organ and is critically involved in modulating vascular tone and structure. Endothelial cells produce a wide range of factors that also regulate cellular adhesion, thromboresistance, smooth muscle cell proliferation, and vessel wall inflammation. Thus, endothelial function is important for the homeostasis of the body and its dysfunction is associated with several pathophysiological conditions, including atherosclerosis, hypertension and diabetes. Patients with diabetes invariably show an impairment of endothelium-dependent vasodilation. Therefore, understanding and treating endothelial dysfunction is a major focus in the prevention of vascular complications associated with all forms of diabetes mellitus. The mechanisms of endothelial dysfunction in diabetes may point to new management strategies for the prevention of cardiovascular disease in diabetes. This review will focus on the mechanisms and therapeutics that specifically target endothelial dysfunction in the context of a diabetic setting. Mechanisms including altered glucose metabolism, impaired insulin signaling, low-grade inflammatory state, and increased reactive oxygen species generation will be discussed. The importance of developing new pharmacological approaches that upregulate endothelium-derived nitric oxide synthesis and target key vascular ROS-producing enzymes will be highlighted and new strategies that might prove clinically relevant in preventing the development and/or retarding the progression of diabetes associated vascular complications. © 2013.
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            Television viewing time and mortality: the Australian Diabetes, Obesity and Lifestyle Study (AusDiab).

            Television viewing time, the predominant leisure-time sedentary behavior, is associated with biomarkers of cardiometabolic risk, but its relationship with mortality has not been studied. We examined the associations of prolonged television viewing time with all-cause, cardiovascular disease (CVD), cancer, and non-CVD/noncancer mortality in Australian adults. Television viewing time in relation to subsequent all-cause, CVD, and cancer mortality (median follow-up, 6.6 years) was examined among 8800 adults > or =25 years of age in the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). During 58 087 person-years of follow-up, there were 284 deaths (87 CVD deaths, 125 cancer deaths). After adjustment for age, sex, waist circumference, and exercise, the hazard ratios for each 1-hour increment in television viewing time per day were 1.11 (95% confidence interval [CI], 1.03 to 1.20) for all-cause mortality, 1.18 (95% CI, 1.03 to 1.35) for CVD mortality, and 1.09 (95% CI, 0.96 to 1.23) for cancer mortality. Compared with a television viewing time of or =2 to or =4 h/d. For CVD mortality, corresponding hazard ratios were 1.19 (95% CI, 0.72 to 1.99) and 1.80 (95% CI, 1.00 to 3.25). The associations with both cancer mortality and non-CVD/noncancer mortality were not significant. Television viewing time was associated with increased risk of all-cause and CVD mortality. In addition to the promotion of exercise, chronic disease prevention strategies could focus on reducing sitting time, particularly prolonged television viewing.
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              Breaking prolonged sitting reduces postprandial glycemia in healthy, normal-weight adults: a randomized crossover trial.

              Sedentary behavior is a risk factor for cardiometabolic disease. Regularly interrupting sedentary behavior with activity breaks may lower this risk. We compared the effects of prolonged sitting, continuous physical activity combined with prolonged sitting, and regular activity breaks on postprandial metabolism. Seventy adults participated in a randomized crossover study. The prolonged sitting intervention involved sitting for 9 h, the physical activity intervention involved walking for 30 min and then sitting, and the regular-activity-break intervention involved walking for 1 min 40 s every 30 min. Participants consumed a meal-replacement beverage at 60, 240, and 420 min. The plasma incremental area under the curve (iAUC) for insulin differed between interventions (overall P < 0.001). Regular activity breaks lowered values by 866.7 IU · L(-1) · 9 h(-1) (95% CI: 506.0, 1227.5 IU · L(-1) · 9 h(-1); P < 0.001) when compared with prolonged sitting and by 542.0 IU · L(-1) · 9 h(-1) (95% CI: 179.9, 904.2 IU · L(-1) · 9 h(-1); P = 0.003) when compared with physical activity. Plasma glucose iAUC also differed between interventions (overall P < 0.001). Regular activity breaks lowered values by 18.9 mmol · L(-1) · 9 h(-1) (95% CI: 10.0, 28.0 mmol · L(-1) · 9 h(-1); P < 0.001) when compared with prolonged sitting and by 17.4 mmol · L(-1) · 9 h(-1) (95% CI: 8.4, 26.3 mmol · L(-1) · 9 h(-1); P < 0.001) when compared with physical activity. Plasma triglyceride iAUC differed between interventions (overall P = 0.023). Physical activity lowered values by 6.3 mmol · L(-1) · 9 h(-1) (95% CI: 1.8, 10.7 mmol · L(-1) · 9 h(-1); P = 0.006) when compared with regular activity breaks. Regular activity breaks were more effective than continuous physical activity at decreasing postprandial glycemia and insulinemia in healthy, normal-weight adults. This trial was registered with the Australian New Zealand Clinical Trials registry as ACTRN12610000953033.
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                Author and article information

                Journal
                Exercise and Sport Sciences Reviews
                Exercise and Sport Sciences Reviews
                Ovid Technologies (Wolters Kluwer Health)
                0091-6331
                2017
                April 2017
                : 45
                : 2
                : 80-86
                Article
                10.1249/JES.0000000000000106
                28118158
                18be4472-03ec-4c2c-941f-e3d4a17bbc07
                © 2017
                History

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