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      Effect of acute intradialytic strength physical exercise on oxidative stress and inflammatory responses in hemodialysis patients

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          Abstract

          Background

          Oxidative stress and inflammation are common findings in chronic kidney disease (CKD) patients, and they are directly related to the increased risk of developing cardiovascular disease, which is the major cause of death in these patients, particularly for those undergoing hemodialysis (HD). Strength physical exercise is a new therapeutic approach to reduce these complications in CKD patients. Following this, the purpose of this study was to assess the effect of acute intradialytic strength physical exercise on oxidative stress and inflammatory responses in HD patients.

          Methods

          Sixteen HD patients were studied (11 women; 44.4±14.6 years; body mass index 23.3±4.9 kg/m 2; 61.6±43.1 months of dialysis) and served as their own controls. Acute (single session) intradialytic physical exercise were performed at 60% of the one-repetition maximum test for three sets of 10 repetitions for four exercise categories in both lower limbs during 30 minutes. Blood samples were collected on two different days at exactly the same time (30 minutes and 60 minutes after initiating the dialysis—with and without exercise). Antioxidant enzymes activity [superoxide dismutase (SOD), catalase, and glutathione peroxidase], lipid peroxidation marker levels (malondialdehyde), and inflammatory marker levels (high-sensitivity C-reactive protein) were determined.

          Results

          SOD plasma levels were significantly reduced after acute physical exercise from 244.8±40.7 U/mL to 222.4±28.9 U/mL ( P=0.03) and, by contrast, increased on the day without exercise (218.2±26.5 U/mL to 239.4±38.6 U/mL, P=0.02). There was no alteration in plasma catalase, glutathione peroxidase, malondialdehyde, or high-sensitivity C-reactive protein levels in on either day (with or without exercise). Additionally, there was no association between these markers and clinical, anthropometric, or biochemical parameters.

          Conclusion

          These data suggest that acute intradialytic strength physical exercise was unable to reduce oxidative stress and inflammation, and in addition, it seems to reduce plasma SOD levels, which could exacerbate the oxidative stress in HD patients.

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          Most cited references30

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          Body fat assessed from total body density and its estimation from skinfold thickness: measurements on 481 men and women aged from 16 to 72 years.

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            Anthropometric measurement of muscle mass: revised equations for calculating bone-free arm muscle area.

            Arm muscle area (AMA, cm2) is currently calculated from triceps skinfold thickness (TSF, cm), and midarm circumference (MAC, cm). In assessing the accuracy of the current equation by comparison to AMA measured by computerized axial tomography, error in each of the four approximations made was found to result in a 20 to 25% overestimate of AMA. Two correctible error sources were: a 10 to 15% overestimation caused by assuming a circular midarm muscle compartment and a 5 to 10% overestimation due to inclusion of midarm cross-sectional bone area. Corrected AMA equations for men and women were respectively: [(MAC - pi x TSF)2/4 pi] - 10, and [MAC - pi x TSF)2/4 pip] - 6.5. With two additional study groups, the overall improved accuracy of the new equations was confirmed, although the average error for a given patient was 7 to 8%; the relationship between corrected AMA and total body muscle mass was established [muscle mass (kg) = (ht, cm2) (0.0264 + 0.0029 x corrected AMA)]; and the minimal range of corrected AMA values compatible with survival (9 to 11 cm2) was defined. Bedside estimates of undernutrition severity and prognosis can therefore be calculated from two simple measurements, TSF and MAC.
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              Oxidative Stress and Inflammation in Heart Disease: Do Antioxidants Have a Role in Treatment and/or Prevention?

              Inflammation triggered by oxidative stress is the cause of much, perhaps even most, chronic human disease including human aging. The oxidative stress originates mainly in mitochondria from reactive oxygen and reactive nitrogen species (ROS/RNS) and can be identified in most of the key steps in the pathophysiology of atherosclerosis and the consequential clinical manifestations of cardiovascular disease. In addition to the formation of atherosclerosis, it involves lipid metabolism, plaque rupture, thrombosis, myocardial injury, apoptosis, fibrosis and failure. The recognition of the critical importance of oxidative stress has led to the enthusiastic use of antioxidants in the treatment and prevention of heart disease, but the results of prospective, randomized clinical trials have been overall disappointing. Can this contradiction be explained and what are its implications for the discovery/development of future antioxidant therapeutics?
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                Author and article information

                Contributors
                Journal
                Kidney Res Clin Pract
                Kidney Res Clin Pract
                Kidney Research and Clinical Practice
                Elsevier
                2211-9132
                2211-9140
                19 February 2015
                March 2015
                19 February 2015
                : 34
                : 1
                : 35-40
                Affiliations
                [1 ]University of Medicine of Lisbon, Post-Graduation in Clinical Nutrition, Lisbon, Portugal
                [2 ]Fluminense Federal University, Post-Graduation in Cardiovascular Sciences, Niterói-RJ, Brazil
                [c ]Fluminense Federal University, Post-Graduation in Medical Sciences, Niterói-RJ, Brazil
                Author notes
                [* ]Corresponding author. Rua Agostinho Neto, Number 22, 5°G, 1750-006 Lisbon, Portugal. martaesgalhado@ 123456hotmail.com
                Article
                S2211-9132(15)00008-X
                10.1016/j.krcp.2015.02.004
                4570601
                c4209a78-514e-4e61-82fe-a2585dcd961c
                Copyright © 2015. The Korean Society of Nephrology. Published by Elsevier.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 21 September 2014
                : 8 February 2015
                : 11 February 2015
                Categories
                Original Article

                chronic kidney disease,hemodialysis,acute physical exercise,inflammatory and oxidative stress markers

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