Moderate- and high-intensity endurance training alleviate diabetes-induced adverse cardiac remodeling and dysfunction

Introduction: A sedentary lifestyle and unhealthy diet contribute to the global epidemic of type 2 diabetes (T2DM), which is associated with an increased risk for adverse cardiac remodeling and cardiac dysfunction. Although endurance exercise training has been proposed as a promising strategy to treat diabetic heart diseases, the impact of exercise intensity is unknown. Therefore, we aim to investigate whether moderate-intensity training (MIT) and high-intensity interval training (HIIT) alleviate the progression of T2DM with adverse cardiac remodeling and dysfunction in rats.

Methods: Male rats received control (n=10) or Western diet (WD, n=22) for 18 weeks to induce T2DM with adverse cardiac remodeling and dysfunction. Hereafter, WD rats were randomly subjected to a sedentary lifestyle (n=8), MIT (n=7) or HIIT (n=7) on a treadmill for 12 additional weeks (5 days/week). Insulin resistance was defined as homeostatic model assessment (HOMA-IR) value. Glucose tolerance was assessed with 1h oral glucose tolerance tests. Plasma lipid profile and advanced glycation end product (AGE) levels were evaluated. Echocardiographic and hemodynamic measurements were performed to evaluate cardiac remodeling and function. Cardiac tissue was stained for interstitial fibrosis. Cardiac citrate synthase activity was determined by colorimetry.
Results: MIT and HIIT significantly inhibited weight gain and T2DM progression, demonstrated by lower HOMA-IR values and blood glucose levels compared to sedentary WD rats. Both exercise interventions improved plasma triglyceride levels while only HIIT normalized free fatty acids. MIT decreased plasma levels of harmful glycated compounds or AGE. In the heart, MIT and HIIT normalized the increased end-diastolic pressure, wall thickness and interstitial collagen deposition seen in sedentary WD rats. Cardiac citrate synthase activity, a marker for mitochondrial aerobic capacity, raised after MIT and HIIT. Lastly, MIT but not HIIT restored the decreased ejection fraction.
Conclusions: We show that MIT and HIIT are equally effective to inhibit the progression of T2DM. Both exercise interventions alleviate diastolic dysfunction and pathological cardiac remodeling, by reducing fibrosis and increasing mitochondrial capacity, while only MIT rescues systolic function in T2DM. Given their cardioprotective effects, moderate- and high-intensity endurance training should be cornerstones in the treatment of T2DM individuals with cardiac dysfunction.


Sarah D'Haese(1,2), Maxim Verboven(1), Lize Evens(1), Dorien Deluyker(1), BO Eijnde(1,3,4), Dominique Hansen(5,6), Virginie Bito(1)


Faculty of Medicine and Life Sciences, BIOMED Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium(1), Department of Internal Medicine, CARIM School for Cardiovascular Diseases, Maastricht University Medical Centre, Maastricht, the Netherlands(2), SMRC Sports Medical Research Center, Hasselt University, Diepenbeek, Belgium(3), Faculty of Medicine & Health Sciences, Division of Sport Science, Stellenbosch University, Stellenbosch, South Africa(4), Faculty of Rehabilitation Sciences, REVAL Rehabilitation Research Centre, Hasselt University, Diepenbeek, Belgium(5), Department of Cardiology, Heart Centre Hasselt, Jessa Hospital, Hasselt, Belgium(6)

Presenting author

Sarah D'Haese, Phd Student , Faculty of Medicine and Life Sciences, BIOMED Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium
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