PURPOSE: Cardiovascular disease (CVD) is the leading cause of death in the Ireland and the EU and kills more people than all cancers combined. It accounts for 55% of all deaths in women across Europe and 43% of all deaths in men. The cost to the EU economy is 169 billion euro/year. Endothelial dysfunction induced by cardiovascular risk factors is considered to be one of the earliest stages in vascular damage and is associated independently with cardiovascular events. The balance between endothelial lesion and regeneration is critical for the maintenance of vessel integrity. Exposure to cardiovascular risk factors alters the homeostatic regulatory functions of the endothelium, subsequently progressing to pro-inflammatory activation, apoptosis, and undesirable vessel remodelling. The purpose of this study is to examine the effect of self-regulated exercise intensity on endothelial function in men with coronary artery disease. METHODS: Eight men with coronary artery disease (65.7 ± 4.5 yr, VO2max 18.6 ± 4.1 ml/kg/min, BMI 29.7±3.3 kg/m-2) underwent 20 min of treadmill walking at a self-regulated intensity. Endothelial dependent dilation of the brachial artery was assessed before and 1 h following the acute bout of exercise. Vessel diameter was determined using high resolution vascular ultrasonography (SonoSite, MicroMaxx) from flow mediated dilation (FMD) following 5 min of forearm occlusion. Endothelial independent vasodilation was measured at min 3, min 4 and min 5 following the administration of glyceryl trinitrate (0.4 mg). RESULTS: The subjects self-selected an average treadmill walking speed of 5.3 km/h and a grade of 0.7%. This intensity equated to 65.7% VO2max, and an RPE-O of 12.0. Compared to baseline, FMD was significantly increased (1 min (4.6 v 10.7%) and 3 min (6.2 v 11.0) post occlusion) at 60 min following the acute bout of self-regulated exercise. There was no change in endothelial independent dilation in response to the acute bout of exercise. CONCLUSION: These results indicate a beneficial effect of self regulated exercise on endothelial dependent vascular function in men with coronary artery disease. The study was supported with a grant from Science Foundation Ireland (PO7625 - SFI 07/CE/I1147).
Bone marrow-derived endothelial progenitor cells (EPC) are involved in vascular growth and repair. They increase in the circulation after a single bout of aerobic exercise, potentially related to muscle ischemia. Muscular endurance resistance exercise (MERE) bouts also have the potential to induce muscle ischemia if appropriately structured.The objective of this study is to determine the influence of a single bout of MERE on circulating EPC and related angiogenic factors.Thirteen trained men age 22.4 ± 0.5 yr (mean ± SEM) performed a bout of MERE consisting of three sets of six exercises at participants' 15-repetition maximum without resting between repetitions or exercises. The MERE bout duration was 12.1 ± 0.6 min. Blood lactate and HR were 11.9 ± 0.9 mmol·L and 142 ± 5 bpm, respectively, at the end of MERE. Blood was sampled preexercise and at 10 min, 2 h, and 24 h postexercise.Circulating EPC and serum concentrations of vascular endothelial growth factors (VEGF-A, VEGF-C, and VEGF-D), granulocyte colony stimulating factor, soluble Tie-2, soluble fms-like tyrosine kinase-1, and matrix metalloproteinases (MMP-1, MMP-2, MMP-3, MMP-9, and MMP-9) were higher (P < 0.05) in the postexercise period. Circulating EPC levels were unchanged at 10 min postexercise but higher at 2 h postexercise (P < 0.05). The concentration of most angiogenic factors and metalloproteinases were higher at 10 min postexercise (VEGF-A, +38%; VEGF-C, +40%; VEGF-D, +9%; soluble Tie-2, +15%; soluble fms-like tyrosine kinase-1, +24%; MMP-1, +62%; MMP-2, +3%; MMP-3, +54%; and MMP-9, +45%; all P < 0.05). Soluble E-selectin was lower (P < 0.05) at 2 and 24 h postexercise, with endothelial microparticles and thrombomodulin unchanged.Short intense bouts of MERE can trigger increases in circulating EPC and related angiogenic factors, potentially contributing to vascular adaptation and vasculoprotection.
PURPOSE: Physiologically based exercise prescriptions normally involve identifying an intensity range that elicits a predetermined VO2 or heart rate. In many instances prescribed exercise that exceeds an individual's preferred level of intensity may establish a negative attitude toward physical activity. Longitudinal studies report that participants tend to deviate from physiologically based prescribed levels of intensity in favour of their apparently preferred levels. Self-regulated exercise intensity may increase enjoyment and promote adherence by allowing individuals successfully complete an activity within their perceptual preference range and without undue physiological strain. This study examined the physiological and perceptual responses during self-regulated exercise in men with CAD. METHODS: Eight men with CAD (65.7 ± 4.5 yr, VO2max 18.6 ± 4.1 ml/kg/min, BMI 29.7±3.3 kg/m-2) exercised on a treadmill for 20 min at a self-regulated intensity. They were allowed to change the velocity and grade every 5 min. Respiratory metabolic and gas exchange variables were measured continuously using open circuit spirometry. Heart rate was continuously recorded using telemetry, and undifferentiated RPE (RPE-O) was recorded every 5 min using the Borg 15-category scale. RESULTS: Perceptual and physiological responses remained stable after the first 5 min of exercise. Subjects exercised at 65.7 ± 14.2 % VO2max and 94 ± 5.0 % HRpeak during the final 15 min of self regulated exercise. This equates to a treadmill velocity of 5.3 ± 0.9 km/h, and a grade of 0.7 ± 1.1. The RPE-O was 12.0 ± 2.0, and falls between the verbal descriptors of fairly light and somewhat hard. CONCLUSION: When allowed to self-regulate their exercise intensity, men with CAD select an intensity that is perceived to be fairly light to somewhat hard, and elicits a physiological response likely to improve cardiovascular health. The study was supported with a grant from Science Foundation Ireland (PO7625 - SFI 07/CE/I1147).
Low-carbohydrate diets (LCD) are increasing in popularity, but their effect on vascular health has been questioned. Endothelial microvesicles (EMV) are membrane-derived vesicles with the potential to act as a sensitive prognostic biomarker of vascular health and endothelial function. The aim of this study was to examine the influence of a LCD on EMV and other endothelial biomarkers of protein origin. Twenty-four overweight women (age, 48.4 ± 0.6 years; height, 1.60 ± 0.07 m; body mass, 76.5 ± 9.1 kg; body mass index, 28.1 ± 2.7 kg·m(-2); waist circumference, 84.1 ± 7.4 cm; mean ± standard deviation) were randomised to either 24 weeks on their normal diet (ND) or a LCD, after which they crossed over to 24 weeks on the alternative diet. Participants were assisted in reducing carbohydrate intake, but not below 40 g·day(-1). Body composition and endothelial biomarkers were assessed at the crossover point and at the end of the study. Daily carbohydrate intake (87 ± 7 versus 179 ± 11 g) and the percentage of energy derived from carbohydrate (29% versus 44%) were lower (p < 0.05) on the LCD compared to the ND, but absolute fat and saturated fat intake were unchanged. Body mass and waist circumference were 3.7 ± 0.8 kg and 3.5 ± 1.0 cm lower (p < 0.05), respectively, after the LCD compared with the ND phases. CD31(+)CD41(-)EMV, soluble (s) thrombomodulin, sE-selectin, sP-selectin, serum amyloid A and C-reactive protein were lower (p < 0.05) after the LCD compared to the ND, but serum lipids and apolipoproteins were not different. EMV along with a range of endothelial and inflammatory biomarkers are reduced by a LCD that involves modest weight loss.
PURPOSE: Microparticles (MP) are small membranous vesicles shed from formed elements such as circulating platelets and vascular endothelial cells. They express surface antigens characteristic of their cell-of-origin and contain DNA, RNA, miRNA and intracellular proteins. Depending on the dynamic morphological state of the parent cell, phenotypically varied MP may be released into the circulation. MP serve not only as markers, but also potential mediators of inflammation, coagulation and endothelial dysfunction. This study examined the relation between total MP, endothelial MP (EMP), platelet MP (PMP) and endothelial function (a validated surrogate measure of early atherosclerosis) in response to acute exercise in men with coronary artery disease (CAD). METHODS: Eight men with CAD (65.7 ± 4.5 yr, VO2max 18.6 ± 4.1 ml/kg/min, BMI 29.7±3.3 kg/m-2) underwent 20 min of treadmill walking at 66 % VO2max. Endothelial dependent dilation of the brachial artery was assessed before and 1 h following the acute bout of exercise. Vessel diameter was determined using high resolution vascular ultrasonography (SonoSite, MicroMaxx) from flow mediated dilation (FMD) following 5 min of forearm occlusion. Endothelial independent vasodilation (EID) was measured following the administration of glyceryl trinitrate (0.4 mg). MP counts were enumerated by flow cytometry from platelet poor plasma (PPP) stored at -80°C. MP were characterized based on size (0.5 - 1.0 μm sizing gate) and their ability to bind annexin V. MP had also to bind to CD62E or CD41 to be of endothelial or platelet origin respectively. RESULTS: Compared to baseline, FMD was significantly increased at 60 min following the acute bout of exercise. There was no change in EID. There was significant relation between the percent change in total MP (annexin V+ events) and the percent changes in flow mediated dilation 60 min after the exercise bout and between the percent change in EMP (annexin V+/CD62E+ events) and the percent changes in flow mediated dilation 60 min after the exercise bout. CONCLUSION: Changes in endothelial function in response to acute exercise may be mediated by alterations in circulating levels of MP. The study was supported with a grant from Science Foundation Ireland (PO7625 - SFI 07/CE/I1147).
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