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      Effect of Different Volumes of Interval Training and Continuous Exercise on Interleukin-22 in Adults with Metabolic Syndrome: A Randomized Trial

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          Abstract

          Introduction

          IL-22 may have a role in the alleviation of the metabolic syndrome (MetS) via protection of pancreatic beta and endothelial cells from oxidative and lipid-induced damage. We aimed to investigate the effects of moderate-intensity continuous training (MICT) and different volumes of high-intensity interval training (HIIT) on changes in circulating IL-22.

          Methods

          This was a sub-study of the “Exercise in the prevention of Metabolic Syndrome” (EX-MET) a multi-center, randomized trial. This study used data collected at the Brisbane site. Thirty-nine individuals with MetS were randomized to one of three 16-wk interventions: 1) MICT (n=10, 30min at 60–70% HR peak, 5x/wk); 2) 4HIIT (n=13, 4x4min at 85–95% HR peak, interspersed with 3min of active recovery at 50–70% HR peak, 3x/wk); or 3) 1HIIT (n=16, 1x4min at 85–95% HR peak, 3x/wk). Serum IL-22 concentration was measured following a 12-hr fast via an enzyme linked immunosorbent assay, before and after the intervention. MetS severity, insulin resistance (IR), visceral adipose tissue (VAT), and cardiorespiratory fitness (CRF) were also measured via MetS z-score, HOMA-IR, dual-energy X-ray absorptiometry, and indirect calorimetry (maximal exercise test), respectively.

          Results

          The median (IQR) IL-22% changes from pre- to post-intervention in the MICT, 4HIIT, and 1HIIT groups were −17% (−43.0% to 31.3%), +16.5% (−18.9% to 154.9%), and +15.9% (−28.7% to 46.1%), respectively. Although there were no significant between-group differences in IL-22 concentration change, there was a medium-to-large group × time interaction effect [F(2,35)=2.08, p=0.14, η 2=0.14].

          Conclusion

          Although there was no statistically significant between-group difference in IL-22 change, the study suggests that different exercise intensities may have opposing effects on IL-22 concentration in individuals with MetS.

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          Most cited references 29

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          High-intensity interval training in patients with lifestyle-induced cardiometabolic disease: a systematic review and meta-analysis.

          Cardiorespiratory fitness (CRF) is a strong determinant of morbidity and mortality. In athletes and the general population, it is established that high-intensity interval training (HIIT) is superior to moderate-intensity continuous training (MICT) in improving CRF. This is a systematic review and meta-analysis to quantify the efficacy and safety of HIIT compared to MICT in individuals with chronic cardiometabolic lifestyle diseases. The included studies were required to have a population sample of chronic disease, where poor lifestyle is considered as a main contributor to the disease. The procedural quality of the studies was assessed by use of a modified Physiotherapy Evidence Base Database (PEDro) scale. A meta-analysis compared the mean difference (MD) of preintervention versus postintervention CRF (VO2peak) between HIIT and MICT. 10 studies with 273 patients were included in the meta-analysis. Participants had coronary artery disease, heart failure, hypertension, metabolic syndrome and obesity. There was a significantly higher increase in the VO2peak after HIIT compared to MICT (MD 3.03 mL/kg/min, 95% CI 2.00 to 4.07), equivalent to 9.1%. HIIT significantly increases CRF by almost double that of MICT in patients with lifestyle-induced chronic diseases. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
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            Influences of cardiorespiratory fitness and other precursors on cardiovascular disease and all-cause mortality in men and women.

            To quantify the relation of cardiorespiratory fitness to cardiovascular disease (CVD) mortality and to all-cause mortality within strata of other personal characteristics that predispose to early mortality. DESIGN--Observational cohort study. We calculated CVD and all-cause death rates for low (least fit 20%), moderate (next 40%), and high (most fit 40%) fitness categories by strata of smoking habit, cholesterol level, blood pressure, and health status. Preventive medicine clinic. Participants were 25341 men and 7080 women who completed preventive medical examinations, including a maximal exercise test. Cardiovascular disease and all-cause mortality. There were 601 deaths during 211996 man-years of follow-up, and 89 deaths during 52982 woman-years of follow-up. Independent predictors of mortality among men, with adjusted relative risks (RRs) and 95% confidence intervals (CIs), were low fitness (RR, 1.52;95% CI, 1.28-1.82), smoking (RR, 1.65; 95% CI, 1.39-1.97), abnormal electrocardiogram (RR, 1.64;95% CI, 1.34-2.01), chronic illness (RR, 1.63;95% CI, 1.37-1.95), increased cholesterol level (RR, 1.34; 95% CI, 1.13-1.59), and elevated systolic blood pressure (RR, 1.34; 95% CI, 1.13-1.59). The only statistically significant independent predictors of mortality in women were low fitness (RR, 2.10; 95% Cl, 1.36-3.21) and smoking (RR, 1.99; 95% Cl, 1.25-3.17). Inverse gradients were seen for mortality across fitness categories within strata of other mortality predictors for both sexes. Fit persons with any combination of smoking, elevated blood pressure, or elevated cholesterol level had lower adjusted death rates than low-fit persons with none of these characteristics. Low fitness is an important precursor of mortality. The protective effect of fitness held for smokers and nonsmokers, those with and without elevated cholesterol levels or elevated blood pressure, and unhealthy and healthy persons. Moderate fitness seems to protect against the influence of these other predictors on mortality. Physicians should encourage sedentary patients to become physically active and thereby reduce the risk of premature mortality.
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              Reduced Adipose Tissue Oxygenation in Human Obesity

              OBJECTIVE— Based on rodent studies, we examined the hypothesis that increased adipose tissue (AT) mass in obesity without an adequate support of vascularization might lead to hypoxia, macrophage infiltration, and inflammation. RESEARCH DESIGN AND METHODS— Oxygen partial pressure (AT pO2) and AT temperature in abdominal AT (9 lean and 12 overweight/obese men and women) was measured by direct insertion of a polarographic Clark electrode. Body composition was measured by dual-energy X-ray absorptiometry, and insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp. Abdominal subcutaneous tissue was used for staining, quantitative RT-PCR, and chemokine secretion assay. RESULTS— AT pO2 was lower in overweight/obese subjects than lean subjects (47 ± 10.6 vs. 55 ± 9.1 mmHg); however, this level of pO2 did not activate the classic hypoxia targets (pyruvate dehydrogenase kinase and vascular endothelial growth factor [VEGF]). AT pO2 was negatively correlated with percent body fat (R = −0.50, P < 0.05). Compared with lean subjects, overweight/obese subjects had 44% lower capillary density and 58% lower VEGF, suggesting AT rarefaction (capillary drop out). This might be due to lower peroxisome proliferator–activated receptor γ1 and higher collagen VI mRNA expression, which correlated with AT pO2 (P < 0.05). Of clinical importance, AT pO2 negatively correlated with CD68 mRNA and macrophage inflammatory protein 1α secretion (R = −0.58, R = −0.79, P < 0.05), suggesting that lower AT pO2 could drive AT inflammation in obesity. CONCLUSIONS— Adipose tissue rarefaction might lie upstream of both low AT pO2 and inflammation in obesity. These results suggest novel approaches to treat the dysfunctional AT found in obesity.
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                Author and article information

                Journal
                Diabetes Metab Syndr Obes
                Diabetes Metab Syndr Obes
                DMSO
                dmso
                Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
                Dove
                1178-7007
                09 July 2020
                2020
                : 13
                : 2443-2453
                Affiliations
                [1 ]Centre for Research on Exercise, Physical Activity and Health, School of Human Movement and Nutrition Sciences, The University of Queensland , Brisbane, Queensland, Australia
                [2 ]Caring Futures Institute and SHAPE Research Centre, Exercise Science and Clinical Exercise Physiology, College of Nursing and Health Sciences, Flinders University , Adelaide, South Australia, Australia
                [3 ]Recreation, Exercise, and Sport Science Department, Western State Colorado University , Gunnison, Colorado, USA
                [4 ]Immunopathology Group, Mater Research Institute - The University of Queensland, Translational Research Institute , Brisbane, Queensland, Australia
                [5 ]Australian Infectious Disease Research Centre, University of Queensland , Brisbane, Queensland, Australia
                [6 ]Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne , Melbourne, Victoria, Australia
                [7 ]K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology , Trondheim, Sor Trondelag, Norway
                Author notes
                Correspondence: Joyce S Ramos Email joyce.ramos@flinders.edu.au
                Article
                251567
                10.2147/DMSO.S251567
                7368330
                © 2020 Ramos et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 2, Tables: 2, References: 41, Pages: 11
                Categories
                Original Research

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