Postprandial Arterial Stiffness Research Articles

A Low-Calorie Diet with or without Exercise Reduces Postprandial Aortic Waveform in Females with Obesity.

Arterial stiffness is considered a predictor of cardiovascular disease. Females have higher values of arterial stiffness than males, suggesting a greater risk of heart-related complications. Although a low-calorie diet (LCD) reduces fasting arterial stiffness, in part through weight loss, it is unknown if interval exercise (INT) adds to the benefit of LCD on fasting and postprandial arterial stiffness in females with obesity. Twenty-five females (47 ± 2.6 yr, 37.6 ± 1.3 kg·m-2) were randomized to 13 d of LCD (n = 12; mixed meals of ~1200 kcal·d-1) or LCD + INT (n = 13; 60 min·d-1 of supervised 3-min intervals at 90% HRpeak and 50% HRpeak). Arterial stiffness (augmentation index [AIx] and carotid-femoral pulse wave velocity [cfPWV]) and blood biochemistries were measured during a 75-g oral glucose tolerance test before and after the intervention to determine fasting and postprandial arterial stiffness as well as insulin sensitivity (simple index of insulin sensitivity [SIIS]) and inflammation (C-reactive protein, interleukin 8, and tumor necrosis factor alpha). Although LCD + INT increased V˙O2peak and HDL compared with LCD (P = 0.04 and P < 0.01, respectively), both interventions decreased body fat, LDL, total cholesterol, and triglycerides (all P < 0.01) and increased SIIS (P = 0.03). Despite no effect on fasting AIx (P = 0.27), LCD and LCD + INT decreased AIx60min (-7.4% ± 4.3% vs -7.0% ± 5.0%, P = 0.04) and tAUC120min (-663 ± 263 vs -457 ± 406, P = 0.03). There were no changes in fasting cfPWV (P = 0.91) or cfPWV120min (P = 0.62). Increased SIIS and decreased interleukin 8 were associated with reduced fasting AIx (r = -0.44, P = 0.03, and r = 0.40, P = 0.055), whereas decreased C-reactive protein correlated with reduced postprandial AIx60min (r = 0.43, P = 0.04). Independent of exercise, 13 d of LCD reduces postprandial AIx in females with obesity. Insulin sensitivity and inflammation correlated with improved arterial stiffness, suggesting unique mechanisms regulate fasted versus postprandial arterial stiffness.

Postprandial augmentation index is reduced in adults with prediabetes following continuous and interval exercise training.

What is the central question of this study? We compared high-intensity interval versus continuous training on fasting and postprandial arterial stiffness in people with prediabetes. What is the main finding and its importance? We show, for the first time, that exercise improves the augmentation index during the postprandial state, but not the fasted state, in adults with prediabetes. However, the fasted augmentation index improved in relationship to exercise dose, as assessed by kilocalories per session. Collectively, these findings suggest that short-term exercise can improve arterial compliance in adults with prediabetes. Therefore, lifestyle interventions designed to reduce arterial stiffness could have considerable clinical impact. People with prediabetes have elevated risk for cardiovascular disease, in part, owing to arterial stiffness mediated by low insulin sensitivity. However, the effect the intensity and/or amount (i.e. kilocalories per session) of short-term exercise training on fasting and postprandial arterial stiffness is unknown. We tested the hypothesis that increased intensity and dose (i.e. amount) of exercise would be correlated with reduced fasting and postprandial arterial stiffness in obese adults with prediabetes. After randomization, 31 adults (age 61.4± 8.3years, body mass index 32.1± 5.4kgm-2 ) with prediabetes performed supervised continuous (CONT; n= 17; 70% of peak heart rate) or interval (INT; n= 14; 3min at 50% of peak heart rate and 3min at 90% of peak heart rate) cycling training for 60minday-1 over 2weeks. The amount of exercise was calculated using regression equations derived from oxygen uptake ( ) and heart rate. Arterial stiffness [augmentation index (AI) and cartoid-femoral pulse wave velocity], insulin and glucose were determined during a 180 min 75g oral glucose tolerance test (OGTT) and analysed by the total area under the curve (tAUC) pre- versus post-training. The simple index of insulin sensitivity, (SIIS )OGTT, was calculated; aerobic fitness (peak ) and body mass were also assessed. Short-term training had no effect on weight but did improve peak (P= 0.003), glucose tAUC180min (P= 0.01) and insulin sensitivity (P= 0.002), independent of intensity. The CONT and INT exercise significantly reduced AI 2h postprandial (P= 0.008) and tAUC180min (P= 0.03). Reductions in fasted AI were related to exercise dose (trend: r= -0.37, P= 0.055). Increased peak was linked to reduced fasted (r= -0.47, P= 0.01) and tAUC180min AI (r= -0.39, P= 0.05). Decreased AI tAUC180min was correlated with increased insulin sensitivity (r= -0.50, P= 0.009). Short-term CONT and INT training reduced postprandial arterial stiffness comparably in adults with prediabetes.

Effect of a Single Dose of Vitamin D3 on Postprandial Arterial Stiffness and Inflammation in Vitamin D-Deficient Women.

Cholecalciferol (vitamin D3) improves vascular function and inflammation, potentially providing an explanation for the proposed cardiovascular protection of vitamin D. We investigated whether cholecalciferol supplementation reduces postprandial arterial dysfunction and inflammation. Randomized, 1:1, double-blind trial. Diabetes and Vascular Center, Franciscus Gasthuis, Rotterdam, The Netherlands. Twenty-four healthy, premenopausal, overweight or obese, vitamin D-deficient women. A single high (300,000 IU) or low dose (75,000 IU) of cholecalciferol. The effect of low- and high-dose cholecalciferol on postprandial leukocyte activation markers, pulse wave velocity (PWV), and augmentation index (AIx) during an oral fat loading test, expressed as area under the curve (AUC). High- and low-dose supplementation increased vitamin D by 163% ± 134% (P < 0.001) and 66% ± 59% (P < 0.001), respectively. Monocyte CD11b-AUC slightly increased after low but not high dose (6% ± 2%, P = 0.012, and 4% ± 1%, P = 0.339, respectively). There were no significant effects on postprandial PWV or AIx by high- or low-dose vitamin D. Fasting complement component 3 (C3) levels decreased by 5.9% (P = 0.004) in the high-dose group and by 4.0% (P = 0.018) in the low-dose group. A single dose of vitamin D does not seem to reduce arterial stiffness and leukocyte activation in overweight, vitamin D-deficient women. Vitamin D may decrease fasting C3. Possibly, higher vitamin D concentrations may be needed to decrease inflammation and improve vascular function in overweight or obese vitamin D-deficient women.

Differential effects of EPA versus DHA on postprandial vascular function and the plasma oxylipin profile in men

Our objective was to investigate the impact of EPA versus DHA on arterial stiffness and reactivity and underlying mechanisms (with a focus on plasma oxylipins) in the postprandial state. In a three-arm crossover acute test meal trial, men (n = 26, 35–55 years) at increased CVD risk received a high-fat (42.4 g) test meal providing 4.16 g of EPA or DHA or control oil in random order. At 0 h and 4 h, blood samples were collected to quantify plasma fatty acids, long chain n-3 PUFA-derived oxylipins, nitrite and hydrogen sulfide, and serum lipids and glucose. Vascular function was assessed using blood pressure, reactive hyperemia index, pulse wave velocity, and augmentation index (AIx). The DHA-rich oil significantly reduced AIx by 13% (P = 0.047) with the decrease following EPA-rich oil intervention not reaching statistical significance. Both interventions increased EPA- and DHA-derived oxylipins in the acute postprandial state, with an (1.3-fold) increase in 19,20-dihydroxydocosapentaenoic acid evident after DHA intervention (P < 0.001). In conclusion, a single dose of DHA significantly improved postprandial arterial stiffness as assessed by AIx, which if sustained would be associated with a significant decrease in CVD risk. The observed increases in oxylipins provide a mechanistic insight into the AIx effect.

Effects of typical Western meal on postprandial arterial stiffness and vasoactive chemicals in patients with chronic kidney disease and Type II Diabetes

The purpose was to evaluate the effect of an 800 kcal meal (carbohydrate:fat:protein = 41:46:13) on postprandial arterial stiffness in patients with CKD and Type II Diabetes (CKD&amp;T2DM) (n=7). Comparisons were made to patients with T2DM only (n=7) and healthy controls (CON) (n=8).MethodsUnder fasting conditions, arterial stiffness was measured, then an indwelling catheter was inserted and a blood sample was collected. Stiffness was measured/blood collected immediately after the meal and every hour (h) for 4h. Augmentation index normalized to 75 heart beats per minute (Aix75) was used to estimate arterial stiffness.ResultsAix75: Decreased from baseline (bl) (17.3 ± 2.5) to 1h (9.3 ± 2.3) returned at h4 p &lt; .05 (pooled time effect). CKD&amp;T2DM and T2DM differed from the CON (26.7 ± 4.1; 17.7± 9.7 vs. −3.65 ± 3.6) p &lt; .05 but not each other (pooled group effect). SBP: CKD&amp;T2DM (131.5 ± 4.8) differed from the CON (114.5 + 3.4) p &lt; .05. The CON and T2DM (121.8 ± 3.7) did not differ, nor did CKD&amp;T2DM and T2DM. DBP: Decreased from bl (74.8 ± 2.2) in h1 and 2 (67.5 ± 2.5; 68.0 ± 2.5) and returned at h4 (73.0 + 2.4) p &lt; .05 in all groups. Nitric oxide: No time or group effect. Endothelin: Was lower in all groups at h3 than at h0, h1, and 2 p &lt; .05.DiscussionCKD&amp;T2DM and T2DM patients experience a smaller postprandial reduction in arterial stiffness when compared to healthy CON. Hemodyamics may be a main contributor as illustrated by the trend seen in DBP.

Postprandial Vascular Responses to a High Fat Meal in Centrally Obese Adults

High fat meals have been implicated as a contributor to obesity and associated cardiovascular disease risk. Such meals may adversely affect vascular properties for hours after ingestion, which presumably leads to long-term vascular impairment. PURPOSE:Examine pre and postprandial arterial stiffness and endothelial function in response to a high fat meal and the effects of fitness and body composition on these responses. METHODS:Sixty-six subjects (age: 48 ± 9 yrs; 51 F, 13 M; BMI: 34.8 ± 3.8; waist circumference: 102 ± 11 cm) were examined at baseline (fasting) and 4 hours after consuming a McDonald's breakfast (900 calories, 50 grams of fat). Using the EndoPat 2000, arterial stiffness was measured by fingertip tonometry derived augmentation index (AI); endothelial function was measured by fingertip plethysmography that reflects the forearm blood flow dilation response to brachial artery occlusion and release, which yields a reactive hyperemia index (RHI). Subjects also underwent fitness testing on a treadmill to determine maximal oxygen capacity (VO2max) and general and central obesity was determined by dual energy x-ray absorptiometry. RESULTS: Fasting BP was 124 ± 14 / 74 ± 10 mm Hg; HR: 66 ± 10 bpm; RHI: 2.3 ± 0.5 %; and AI, 17.2 ± 15.2 %. RHI and HR were unchanged, whereas AI fell to 10.3 ± 14.5 % (p< 0.01) in response to the meal. In a bivariate analysis, a lower postprandial AI was associated with younger age (r=0.50, p<0.01), higher VO2max (r=-0.34, p<0.05) and lower total percent body fat (r=0.25, p=0.05). No association was found between postprandial AI with RHI, or markers of central obesity. Using a multivariate regression model that included sex, baseline AI emerged as the only independent predictor of postprandial AI. CONCLUSIONS: A high fat meal did not worsen resistance vessel endothelial function, whereas arterial stiffness was markedly reduced. These data suggest that a high-fat meal results in acute changes in vascular tone, which is influenced by baseline arterial stiffness but is independent of age, fitness, and fatness.

The Effect of a High-Fat Meal on Postprandial Arterial Stiffness in Men with Obesity and Type 2 Diabetes

Postprandial dysmetabolism is emerging as an important cardiovascular risk factor. Augmentation index (AIx) is a measure of systemic arterial stiffness and independently predicts cardiovascular outcome. The objective of this study was to assess the effect of a standardized high-fat meal on metabolic parameters and AIx in 1) lean, 2) obese nondiabetic, and 3) subjects with type 2 diabetes mellitus (T2DM). Male subjects (lean, n = 8; obese, n = 10; and T2DM, n = 10) were studied for 6 h after a high-fat meal and water control. Glucose, insulin, triglycerides, and AIx (radial applanation tonometry) were measured serially to determine the incremental area under the curve (iAUC). AIx decreased in all three groups after a high-fat meal. A greater overall postprandial reduction in AIx was seen in lean and T2DM compared with obese subjects (iAUC, 2251 +/- 1204, 2764 +/- 1102, and 1187 +/- 429% . min, respectively; P < 0.05). The time to return to baseline AIx was significantly delayed in subjects with T2DM (297 +/- 68 min) compared with lean subjects (161 +/- 88 min; P < 0.05). There was a significant correlation between iAUC AIx and iAUC triglycerides (r = 0.50; P < 0.05). Obesity is associated with an attenuated overall postprandial decrease in AIx. Subjects with T2DM have a preserved, but significantly prolonged, reduction in AIx after a high-fat meal. The correlation between AIx and triglycerides suggests that postprandial dysmetabolism may impact on vascular dynamics. The markedly different response observed in the obese subjects compared with those with T2DM was unexpected and warrants additional evaluation.

Long chain n − 3 PUFA-rich meal reduced postprandial measures of arterial stiffness

The consumption of long chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) is known to be cardio-protective. Data on the influence of LC n-3 PUFA on arterial stiffness in the postprandial state is limited. The aim of this study was to investigate the acute effects of a LC n-3 PUFA-rich meal on measures of arterial stiffness. Twenty-five healthy subjects (12 men, 13 women) received a control and a LC n-3 PUFA-rich meal on two occasions in a random order. Arterial stiffness was measured at baseline, 30, 60, 90, 120, 180 and 240 min after meal consumption by pulse wave analysis and digital volume pulse to derive an augmentation index and a stiffness index respectively. Blood samples were taken for measurement of lipids, glucose and insulin. Consumption of the LC n-3 PUFA-rich meal had an attenuating effect on augmentation index (P=0.02) and stiffness index (P=0.03) compared with the control meal. A significant treatment effect (P=0.036) was seen for plasma non-esterified fatty acids concentrations. These data indicate that acute LC n-3 PUFA-rich meal consumption can improve postprandial arterial stiffness. This has important implications for the beneficial properties of LC n-3 PUFA and cardiovascular risk reduction.

A High-Fat Meal Enriched with Eicosapentaenoic Acid Reduces Postprandial Arterial Stiffness Measured by Digital Volume Pulse Analysis in Healthy Men ,

Diets rich in eicosapentaenoic acid [EPA; 20:5(n-3)] are associated with decreased arterial stiffness, but postprandial effects on vascular function are unknown. We investigated whether an EPA-enriched high-fat meal could improve postprandial vascular function. Seventeen healthy men ingested 2 test meals (51 g fat), 1 wk apart, in random order: 5 g EPA plus high-oleic sunflower oil (HOS) vs. HOS only. A second high-fat meal (44 g fat), the same on both study days, was provided 4 h later. Blood pressure and arterial function were measured using digital volume pulse (DVP) to derive a stiffness index (DVP-SI) and reflection index in fasting subjects at 3 and 6 h following the test meal. Blood samples were taken following the test meal for plasma 8-isoprostane F2α, nitric oxide (NO) metabolites (NOx), glucose, insulin, triacylglycerol, and fatty acid analysis. The plasma EPA concentration (mean ± SD) reached a peak of 2.10 ± 0.99 mmol/L following the EPA meal (5 h) and did not rise above 0.27 ± 0.16 mmol/L 1 h following the placebo meal. ∆DVP-SI did not differ between the 2 test meals at 3 h but was greater at 6 h following EPA (6 h −0.65 ± 0.65 m/s) compared with placebo (6 h −0.33 ± 1.26 m/s). Plasma 8-isoprostane F2α concentrations increased by 48% at 6 h compared with baseline following the EPA meal and plasma NOx decreased following both meals, with no differences between the meals in the changes. Changes in other variables measured also did not differ after subjects consumed the 2 meals. In conclusion, adding EPA to a high-fat meal results in acute changes in vascular tone, independent of changes in oxidative stress.