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      Electrocardiographic changes with the onset of diabetes and the impact of aerobic exercise training in the Zucker Diabetic Fatty (ZDF) rat

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          Abstract

          Background

          Early markers of diabetic autonomic neuropathy (DAN) in an electrocardiogram (ECG) include elevated R wave amplitudes, widening of QT c intervals and decreased heart rate variability (HRV). The severity of DAN has a direct relationship with mortality risk. Aerobic exercise training is a common recommendation for the delay and possible reversal of cardiac dysfunction. Limited research exists on ECG measures for the evaluation of aerobic exercise training in Zucker Diabetic Fatty (ZDF) rat, a model of type 2 diabetes. The objective of this study was to assess whether aerobic exercise training may attenuate diabetes induced ECG changes.

          Methods

          Male ZDF (obese fa/fa) and control Zucker (lean fa/+) rats were assigned to 4 groups: sedentary control (SC), sedentary diabetic (SD), exercised control (EC) and exercised diabetic (ED). The exercised groups began 7 weeks of treadmill training after the development of diabetes in the ED group. Baseline (prior to the training) and termination measurements included body weight, heart weight, blood glucose and glycated hemoglobin levels and ECG parameters. One way repeated measures ANOVA (group) analyzed within and between subject differences and interactions. Pearson coefficients and descriptive statistics described variable relationships and animal characteristics.

          Results

          Diabetes caused crucial changes in R wave amplitudes (p < 0.001), heart rate variability (p < 0.01), QT intervals (p < 0.001) and QT c intervals (p < 0.001). R wave amplitude augmentation in SD rats from baseline to termination was ameliorated by exercise, resulting in R wave amplitude changes in ED animals similar to control rats. Aerobic exercise training neither attenuated QT or QT c interval prolongation nor restored decreases in HRV in diabetic rats.

          Conclusion

          This study revealed alterations in R wave amplitudes, HRV, QT and QT c intervals in ZDF rats. Of these changes, aerobic exercise training was able to correct R wave amplitude changes. In addition, exercise has beneficial effect in this diabetic rat model in regards to ECG correlates of left ventricular mass.

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          Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association.

          Abbas Kitabchi, Guillermo E. Umpierrez, Mary Beth Murphy … (2006)
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            Use of tibial length to quantify cardiac hypertrophy: application in the aging rat.

            John Spurgeon, L Lakatta, K Rakusan … (1982)
            Fluctuations in body weight as occur with aging make body weight an unreliable reference for normalizing heart weight. We compared heart weight normalized by tibial length, which remains constant after maturity, with that normalized by body weight in 5- to 28-mo-old male Wistar rats. When normalized by tibial length or body weight, relative to the 5-mo heart, the senescent left ventricle undergoes 17 vs. 38% hypertrophy, respectively, and the right ventricle undergoes 0 vs. 28% hypertrophy, respectively. Histological measurements in the 25- compared with the 5-mo-old left ventricles reveal 6% larger myocyte diameters and 12% larger cellular cross-sectional areas, indicating about 15% hypertrophy; this value agrees more closely with the estimates based on tibial length than with those based on body weight. To allow prediction of left ventricular weight in a living rat, a regression equation using body weight, age, and tibial length was derived. This enabled us to perform a longitudinal aging study that verified that the above results were not biased by selective survival. Thus, in conditions in which body weight changes, cardiac hypertrophy can be more accurately quantified by relating heart weight to tibial length than to body weight. This approach may have applicability for assessing relative sizes of other organs as well.
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              Exercise training in patients with advanced chronic heart failure (NYHA IIIb) promotes restoration of peripheral vasomotor function, induction of endogenous regeneration, and improvement of left ventricular function.

              Stephan Gielen, Sandra Erbs, Gerhard Schuler … (2010)
              Attenuated peripheral perfusion in patients with advanced chronic heart failure (CHF) is partially the result of endothelial dysfunction. This has been causally linked to an impaired endogenous regenerative capacity of circulating progenitor cells (CPC). The aim of this study was to elucidate whether exercise training (ET) affects exercise intolerance and left ventricular (LV) performance in patients with advanced CHF (New York Heart Association class IIIb) and whether this is associated with correction of peripheral vasomotion and induction of endogenous regeneration. Thirty-seven patients with CHF (LV ejection fraction 24+/-2%) were randomly assigned to 12 weeks of ET or sedentary lifestyle (control). At the beginning of the study and after 12 weeks, maximal oxygen consumption (Vo(2)max) and LV ejection fraction were determined; the number of CD34(+)/KDR(+) CPCs was quantified by flow cytometry and CPC functional capacity was determined by migration assay. Flow-mediated dilation was assessed by ultrasound. Capillary density was measured in skeletal muscle tissue samples. In advanced CHF, ET improved Vo(2)max by +2.7+/-2.2 versus -0.8+/-3.1 mL/min/kg in control (P=0.009) and LV ejection fraction by +9.4+/-6.1 versus -0.8+/-5.2% in control (P<0.001). Flow-mediated dilation improved by +7.43+/-2.28 versus +0.09+/-2.18% in control (P<0.001). ET increased the number of CPC by +83+/-60 versus -6+/-109 cells/mL in control (P=0.014) and their migratory capacity by +224+/-263 versus -12+/-159 CPC/1000 plated CPC in control (P=0.03). Skeletal muscle capillary density increased by +0.22+/-0.10 versus -0.02+/-0.16 capillaries per fiber in control (P<0.001). Twelve weeks of ET in patients with advanced CHF is associated with augmented regenerative capacity of CPCs, enhanced flow-mediated dilation suggestive of improvement in endothelial function, skeletal muscle neovascularization, and improved LV function. Clinical Trial Registration- http://www.clinicaltrials.gov. Unique Identifier: NCT00176384.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cardiovasc Diabetol
                Title: Cardiovascular Diabetology
                Publisher: BioMed Central
                ISSN (Electronic): 1475-2840
                Publication date Collection: 2010
                Publication date (Electronic): 22 September 2010
                Volume: 9
                Page: 56
                Affiliations
                [1 ]Department of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, MS 2002, 3901 Rainbow Blvd, Kansas City, KS 66160, USA
                [2 ]Mid America Cardiology, University of Kansas Hospital, MS 4023, 3901 Rainbow Blvd, Kansas City, KS 66160, USA
                [3 ]Department of Allied Medical Sciences, Faculty of Applied Medical Sciences, Jordan University of Science and Technology, Irbid 22110, Jordan
                Article
                Publisher ID: 1475-2840-9-56
                DOI: 10.1186/1475-2840-9-56
                PMC ID: 2954909
                PubMed ID: 20860788
                SO-VID: 00bbe543-5385-47d5-91b4-9ecb1a7d135b
                Copyright © Copyright ©2010 VanHoose et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 5 August 2010
                Date accepted : 22 September 2010
                Categories
                Subject: Original Investigation

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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