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      Endothelial function following interval exercise plus low‐calorie diet treatment in obese females

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          Abstract

          We determined if interval exercise plus a low‐calorie diet (LCD + INT) increases endothelial function more than an energy‐matched LCD. Obese women (47.2 ± 2.6y, 37.5 ± 1.3kg/m 2) were randomized to 13 days of a LCD ( n = 12; mixed meals of ~ 1200kcal/d) or LCD + INT ( n = 13; 12 supervised 60‐min INT bouts of 3 min at 90% and 50% HR peak). LCD + INT subjects received 350kcal postexercise to equate energy availability with LCD. Fitness (VO 2peak) and body composition (BodPod) were determined and a 120 min, 75 g oral glucose tolerance test was performed to examine fasting and postprandial flow‐mediated dilation (FMD, endothelial function), respiratory exchange ratio (RER) via indirect calorimetry as well as glucose and insulin incremental area under the curve (iAUC 120min). LCD + INT increased VO 2peak ( P = 0.02) compared with LCD, and both treatments decreased fat mass ( P < 0.001) and insulin iAUC 120min ( P = 0.03). There was no overall treatment effect on fasting or iAUC 120min FMD. However, in participants who increased fasting endothelial function after each treatment (Δ > 50%; LCD n = 5, LCD + INT n = 7), LCD + INT increased fasted ( P = 0.005) and decreased iAUC 120min ( P = 0.003) FMD compared with LCD. Enhanced fitness correlated with increased fasting FMD ( r = 0.43, P = 0.03) and diminished FMD iAUC 120min ( r = −0.44, P = 0.03). Decreased FMD iAUC 120min correlated with reduced glucose iAUC 120min ( r = 0.64, P = 0.001) as well as increased 60‐min RER ( = −0.42, P = 0.04). Low baseline fasting and iAUC 120min FMD was also linked to enhanced fasting and iAUC 120min FMD post‐treatment ( r = −0.71, P < 0.001; = −0.89, P < 0.001, respectively). In conclusion, increasing fitness via INT may increase the effect of LCD on lowering cardiovascular disease risk in obese women.

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          Obesity/insulin resistance is associated with endothelial dysfunction. Implications for the syndrome of insulin resistance.

          To test the hypothesis that obesity/insulin resistance impairs both endothelium-dependent vasodilation and insulin-mediated augmentation of endothelium-dependent vasodilation, we studied leg blood flow (LBF) responses to graded intrafemoral artery infusions of methacholine chloride (MCh) or sodium nitroprusside (SNP) during saline infusion and euglycemic hyperinsulinemia in lean insulin-sensitive controls (C), in obese insulin-resistant subjects (OB), and in subjects with non-insulin-dependent diabetes mellitus (NIDDM). MCh induced increments in LBF were approximately 40% and 55% lower in OB and NIDDM, respectively, as compared with C (P < 0.05). Euglycemic hyperinsulinemia augmented the LBF response to MCh by - 50% in C (P < 0.05 vs saline) but not in OB and NIDDM. SNP caused comparable increments in LBF in all groups. Regression analysis revealed a significant inverse correlation between the maximal LBF change in response to MCh and body fat content. Thus, obesity/insulin resistance is associated with (a) blunted endothelium-dependent, but normal endothelium-independent vasodilation and (b) failure of euglycemic hyperinsulinemia to augment endothelium-dependent vasodilation. Therefore, obese/insulin-resistant subjects are characterized by endothelial dysfunction and endothelial resistance to insulin's effect on enhancement of endothelium-dependent vasodilation. This endothelial dysfunction could contribute to the increased risk of atherosclerosis in obese insulin-resistant subjects.
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            The Effects of Free-Living Interval-Walking Training on Glycemic Control, Body Composition, and Physical Fitness in Type 2 Diabetic Patients

            OBJECTIVE To evaluate the feasibility of free-living walking training in type 2 diabetic patients and to investigate the effects of interval-walking training versus continuous-walking training upon physical fitness, body composition, and glycemic control. RESEARCH DESIGN AND METHODS Subjects with type 2 diabetes were randomized to a control (n = 8), continuous-walking (n = 12), or interval-walking group (n = 12). Training groups were prescribed five sessions per week (60 min/session) and were controlled with an accelerometer and a heart-rate monitor. Continuous walkers performed all training at moderate intensity, whereas interval walkers alternated 3-min repetitions at low and high intensity. Before and after the 4-month intervention, the following variables were measured: VO2max, body composition, and glycemic control (fasting glucose, HbA1c, oral glucose tolerance test, and continuous glucose monitoring [CGM]). RESULTS Training adherence was high (89 ± 4%), and training energy expenditure and mean intensity were comparable. VO2max increased 16.1 ± 3.7% in the interval-walking group (P < 0.05), whereas no changes were observed in the continuous-walking or control group. Body mass and adiposity (fat mass and visceral fat) decreased in the interval-walking group only (P < 0.05). Glycemic control (elevated mean CGM glucose levels and increased fasting insulin) worsened in the control group (P < 0.05), whereas mean (P = 0.05) and maximum (P < 0.05) CGM glucose levels decreased in the interval-walking group. The continuous walkers showed no changes in glycemic control. CONCLUSIONS Free-living walking training is feasible in type 2 diabetic patients. Continuous walking offsets the deterioration in glycemia seen in the control group, and interval walking is superior to energy expenditure–matched continuous walking for improving physical fitness, body composition, and glycemic control.
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              Impaired microvascular function in obesity: implications for obesity-associated microangiopathy, hypertension, and insulin resistance.

              Obesity is associated with an increased risk of developing microangiopathy, hypertension, and insulin resistance. We hypothesized that obesity is a primary cause of microvascular dysfunction, which may contribute to the development of these obesity-related disorders. We examined microvascular function in 16 lean (body mass index 30 kg/m2) healthy women (mean age, 38.9+/-6.7 years) in the basal state and during physiological systemic hyperinsulinemia. We determined skin capillary recruitment after arterial occlusion with capillaroscopy and skin endothelium-(in)dependent vasodilation by iontophoresis of acetylcholine and sodium nitroprusside. Obese women, compared with lean women, had higher systolic blood pressure (P<0.05), impaired insulin sensitivity (P<0.01), impaired capillary recruitment in the basal state (P<0.05) and during hyperinsulinemia (P<0.05), and impaired acetylcholine-mediated vasodilation in the basal state (P<0.05) and during hyperinsulinemia (P<0.01). Sodium nitroprusside-mediated vasodilation was similar in lean and obese women. Capillary recruitment and acetylcholine-mediated vasodilation were positively correlated with insulin sensitivity (r=0.58, P<0.01 and r=0.55, P<0.01, respectively) and negatively with blood pressure (r=-0.64, P<0.001 and r=-0.42, P<0.05, respectively) in both lean and obese women. Obesity is characterized by impaired microvascular function in the basal state and during hyperinsulinemia and, in both lean and obese women, microvascular dysfunction is associated with increased blood pressure and decreased insulin sensitivity. These findings are consistent with a contribution of impaired microvascular function to the development of obesity-related microangiopathy, hypertension, and insulin resistance.
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                Author and article information

                Contributors
                skm6n@virginia.edu
                Journal
                Physiol Rep
                Physiol Rep
                10.1002/(ISSN)2051-817X
                PHY2
                physreports
                Physiological Reports
                John Wiley and Sons Inc. (Hoboken )
                2051-817X
                25 September 2019
                September 2019
                : 7
                : 18 ( doiID: 10.14814/phy2.v7.18 )
                : e14239
                Affiliations
                [ 1 ] Department of Kinesiology University of Virginia Charlottesville Virginia
                [ 2 ] Division of Endocrinology & Metabolism Department of Medicine University of Virginia Charlottesville Virginia
                [ 3 ] Robert M. Berne Cardiovascular Research Center University of Virginia Charlottesville Virginia
                Author notes
                [*] [* ] Correspondence

                Steven K. Malin, Department of Kinesiology, 210 Emmet St., 225A Memorial Gymnasium, University of Virginia, Charlottesville, VA.

                Tel: (434) 243 – 6624

                Fax: (434) 924‐1389

                E‐mail: skm6n@ 123456virginia.edu

                Author information
                https://orcid.org/0000-0002-7360-6711
                Article
                PHY214239
                10.14814/phy2.14239
                6759506
                31552710
                b0fb01f9-8613-48e1-909a-32c93e0aa93c
                © 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 July 2019
                : 30 August 2019
                Page count
                Figures: 2, Tables: 2, Pages: 12, Words: 19896
                Funding
                Funded by: University of Virginia
                Funded by: Diabetes Action Research and Education Foundation
                Funded by: United States National Institute of Health
                Award ID: RO1‐HL130296
                Categories
                Adipose Tissue and Obesity
                Cardiovascular Conditions, Disorders and Treatments
                Exercise Metabolism
                Original Research
                Original Research
                Custom metadata
                2.0
                phy214239
                September 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.9 mode:remove_FC converted:25.09.2019

                energy deficit,fitness,flow‐mediated dilation,insulin
                energy deficit, fitness, flow‐mediated dilation, insulin

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