Three hours of sitting resulted in a significant impairment in shear rate and SFA FMD. When light activity breaks were introduced hourly during sitting, the decline in FMD was prevented.

The effectiveness of a family-based cardiovascular disease risk reduction intervention was evaluated in two ethnic groups. Participants were 206 healthy, volunteer low-to-middle-income Mexican-American and non-Hispanic white (Anglo-American) families (623 individuals), each with a fifth or a sixth-grade child. Families were recruited through elementary schools. Half of the families were randomized to a year-long educational intervention designed to decrease the whole family's intake of high salt, high fat foods, and to increase their regular physical activity. Eighty-nine percent of the enrolled families were measured at the 24-month follow-up. Both Mexican- and Anglo-American families in the experimental groups gained significantly more knowledge of the skills required to change dietary and exercise habits than did those in the control groups. Experimental families in both ethnic groups reported improved eating habits on a food frequency index. Anglo families reported lower total fat and sodium intake. There were no significant group differences in reported physical activity or in tested cardiovascular fitness levels. Significant differences for Anglo-American experimental vs. control adult subjects were found for LDL cholesterol. Significant intervention-control differences ranging from 2.2 to 3.4 mmHg systolic and/or diastolic blood pressure were found in all subgroups. Direct observation of diet and physical activity behaviors in a structured environment suggested generalization of behavior changes. There was evidence that behavior change persisted one year beyond the completion of the intervention program. It is concluded that involvement of families utilizing school based resources is feasible and effective. Future studies should focus on the most cost-effective methods of family involvement, and the potential for additive effects when family strategies are combined with other school health education programs.

BackgroundNormalization of brachial artery flow-mediated dilation (FMD) to individual shear stress area under the curve (peak FMD:SSAUC ratio) has recently been proposed as an approach to control for the large inter-subject variability in reactive hyperemia-induced shear stress; however, the adoption of this approach among researchers has been slow. The present study was designed to further examine the efficacy of FMD normalization to shear stress in reducing measurement variability.MethodsFive different magnitudes of reactive hyperemia-induced shear stress were applied to 20 healthy, physically active young adults (25.3 ± 0. 6 yrs; 10 men, 10 women) by manipulating forearm cuff occlusion duration: 1, 2, 3, 4, and 5 min, in a randomized order. A venous blood draw was performed for determination of baseline whole blood viscosity and hematocrit. The magnitude of occlusion-induced forearm ischemia was quantified by dual-wavelength near-infrared spectrometry (NIRS). Brachial artery diameters and velocities were obtained via high-resolution ultrasound. The SSAUC was individually calculated for the duration of time-to-peak dilation.ResultsOne-way repeated measures ANOVA demonstrated distinct magnitudes of occlusion-induced ischemia (volume and peak), hyperemic shear stress, and peak FMD responses (all p < 0.0001) across forearm occlusion durations. Differences in peak FMD were abolished when normalizing FMD to SSAUC (p = 0.785).ConclusionOur data confirm that normalization of FMD to SSAUC eliminates the influences of variable shear stress and solidifies the utility of FMD:SSAUC ratio as an index of endothelial function.

This study examined the relationships among body fat, diet composition, energy intake, and exercise in adults. Male (n = 107) and female (n = 109) adults aged 18-71 y (36.6 +/- 1.0 y, means +/- SEM) were hydrostatically weighed to determine body fat (5.7-49.0% of total weight). Diet and exercise behaviors were determined by use of a questionnaire. As body fat increased, percent of energy intake derived from fat increased (p less than 0.001) whereas the percent from carbohydrate decreased (p less than 0.001). There was no relationship between energy intake and adiposity although leanness and exercise were related (p less than 0.001). When subgroups of lean and obese subjects were compared, the lean subjects derived approximately 29% of their energy from fat and 53% from carbohydrate vs 35% and 46%, respectively, for the obese subjects. No differences were found between groups for energy intake but the lean individuals exercised more often than did the obese individuals. These data suggest that diet composition may play as important a role in fat deposition as do energy intake and lack of exercise.

IntroductionIt is unknown if there are limb differences in vascular function during prolonged sitting.PurposeThis study was designed to test whether the effects of prolonged sitting on brachial artery (BA) and the superficial femoral artery (SFA) are similar.MethodsTwelve men (24.2 ± 4 yrs.) participated in a 3 hr prolonged sitting trial (SIT). SFA and BA flow mediated dilation (FMD) and respective flow patterns were measured at baseline, 1 hr, 2 hr and 3 hr.ResultsBy a one-way ANOVA there was a significant decline in SFA FMD during 3 hrs of SIT (p < 0.001). Simultaneously, there was a significant decline in antegrade (p = 0.04) and mean (0.037) shear rates. By a one way ANOVA there were no significant differences in BA FMD during 3 hrs of sitting. There were no changes in the shear rates in the BA except for a significant decrease in antegrade shear rate (p = 0.029) and a significant increase in oscillatory shear index (p = 0.034) during 3 hrs of sitting. Furthermore, there was no correlation between BA and SFA FMD measurements.ConclusionThree hours of sitting resulted in impaired SFA FMD but not BA FMD. Although 3 hours of sitting did not impair BA FMD, it impaired shear patterns in the BA.

Objective: Inflammation has been found to play a role in the etiology of cardiovascular disease as well as provoke endothelial dysfunction. Inflammatory cytokines associated with endothelial function are interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). IL-6 is exercise intensity dependent and has been shown to inhibit TNF-α expression directly. The aim of this study was to investigate the interaction of IL-6 and TNF-α on endothelial function in response to acute exercise in overweight men exhibiting different physical activity profiles. Methods and Procedures: Using a randomized mixed factorial design, 16 overweight men (8 active, maximal exercise capacity (VO 2 peak) = 34.2 ± 1.7, BMI = 27.4 ± 0.7 and 8 inactive, VO 2 peak = 30.9 ± 1.2, BMI = 29.3 ± 1.0) performed three different intensity acute exercise treatments. Brachial artery flow-mediated dilation (FMD) and subsequent blood samples were taken pre-exercise and 1 h following the cessation of exercise. Results: Independent of exercise intensity, the active group displayed a 24% increase (P = 0.034) in FMD following acute exercise compared to a 32% decrease (P = 0.010) in the inactive group. Elevated (P < 0.001) concentrations of IL-6 following moderate (50% VO 2 ) and high (75% VO 2 ) intensity acute exercise were observed in both groups; however, concentrations of TNF-α were unchanged in response to acute exercise (P = 0.584). Discussion: The FMD response to acute exercise is enhanced in active men who are overweight, whereas inactive men who are overweight exhibit an attenuated response. The interaction of IL-6 and TNF-α did not provide insight into the physiological mechanisms associated with the disparity of FMD observed between groups.

The endothelium plays an integral role in the development and progression of atherosclerosis. Hemodynamic forces, particularly shear stress, have a powerful influence on endothelial phenotype and function; however, there is no clear consensus on how endothelial cells sense shear. Nevertheless, multiple endothelial cell signal transduction pathways are activated when exposed to shear stress in vitro. The type of shear, laminar or oscillatory, impacts which signal transduction pathways are initiated as well as which subsequent genes are up- or down-regulated, thereby influencing endothelial phenotype and function. Recently, human studies have examined the impact of shear stress and different shear patterns at rest and during exercise on endothelial function. Current evidence supports the theory that augmented exercise-induced shear stress contributes to improved endothelial function following acute exercise and exercise training, whereas retrograde shear initiates vascular dysfunction. The purpose of this review is to examine the current theories on how endothelial cells sense shear stress, to provide an overview on shear stress-induced signal transduction pathways and subsequent gene expression, and to review the current literature pertaining to shear stress and shear patterns at rest as well as during exercise in humans and the related effects on endothelial function.

Atherosclerotic cardiovascular disease (CVD) was proposed to be a postprandial phenomenon as early as 1979 (1). Impairment of the vascular endothelium is now felt to be a key central component of the initiation and progression of atherogenesis (2). Oxidative stress is harmful at multiple steps in atherogenesis, including direct contributions to endothelial function. Through such mechanisms, oxidative stress appears to mediate postprandial vascular dysfunction (3-6).Platelet aggregation, coagulation, fibrinolysis and vascular tone are regulated by the endothelium in its role in the defence against atherogenesis and atherosclerosis. Nitric oxide (NO) is arguably the most important mediator of these functions. The left panel of Figure 1 illustrates NO synthesis and function. The synthesis of NO from l-arginine, molecular oxygen and electrons carried by NADPH is catalysed by the endothelial nitric oxide synthase (eNOS), and dependent on other cofactors [tetrahydrobiopterin (BH 4 ), flavin adenine dinucleotide and flavin mononucleotide]. eNOS can be activated by shear stress from arterial blood flow, insulin and small molecule agonists [i.e. acetylcholine (ACh)]. Insulin and shear stress work through calcium-independent signalling pathways mediated in part by phosphatidylinositol-3-kinase (PI-3 kinase), whereas ACh works through a calcium-dependent pathway (7).The right panel of Figure 1 illustrates how the NO role in protecting the endothelium is compromised in postprandial lipaemia. Superoxide radical (O 2 ) )accumulates as a result of excess mitochondrial lipid oxidation. NO is the kinetically preferred scavenger for O 2 ) (8) because scavenging by NO occurs at an extremely rapid rate; three times faster than the interaction with other antioxidants (i.e. superoxide dismutase) (9). The reaction between O 2 ) and NO S U M M A R YAims: Postprandial lipaemia-induced endothelial dysfunction is felt to be mediated by increases in oxidative stress. In this review, we have examined the cross-sectional relationships found among these three variables. Methods: We found 20 studies conducted by 16 independent investigative teams through a Medline search from 1980 to 2008; studies were required to report correlations between at least two of the three variables of interest in studies of humans. This review is divided into (i) discussions on the biomarkers and other measures of postprandial lipaemia, oxidative stress and endothelial function; (ii) associations reported among the three variables; and (iii) other considerations including alternative intervention studies.Results: Triglycerides and free fatty acids are robust and well-standardised biomarkers of lipaemia. Measures of oxidative stress ranged from electron spin techniques to measures of lipid peroxidation and are limited by lack of standardisation. Brachial artery flow-mediated dilatation is the most commonly used measure of endothelial function. The associations between postprandial lipaemia and oxidative stress and between postprandial lipaemia and endothelial functi...