High and moderate intensity training normalizes ventricular function and mechanoenergetics in diet-induced obese mice
- Anne D Hafstad, PhD1,
- Jim Lund, MS1,
- Elin Hadler-Olsen, PhD2,
- Anje C Höper, MD1,
- Terje S Larsen, PhD1 and
- Ellen Aasum, PhD1
- 1Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, Norway
- 2Tumor Biology Research Group, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, Norway
- Corresponding author: Anne D Hafstad,
Although exercise reduces several cardiovascular risk factors associated with obesity/diabetes, the metabolic effects of exercise on the heart are not well known. This study was designed to investigate whether high intensity interval training (HIT) is superior to moderate intensity training (MIT) in counteracting obesity-induced impairment of left ventricular (LV) mechanoenergetics and function. Diet-induced obese C57BL/6J (DIO) mice, displaying a cardiac phenotype with altered substrate utilization and impaired mechanoenergetics, were subjected to a sedentary lifestyle or 8-10 weeks of isocaloric HIT or MIT. Although both modes of exercise equally improved aerobic capacity and reduced obesity, only HIT improved glucose tolerance. Hearts from sedentary DIO mice developed concentric LV remodelling with diastolic and systolic dysfunction, which was prevented by both HIT and MIT. Both modes of exercise also normalized LV mechanical efficiency and mechanoenergetics. These changes were associated with altered myocardial substrate utilization, improved mitochondrial capacity and efficiency, as well as reduced oxidative stress, fibrosis and intracellular matrixmetalloproteinase 2 content. As both modes of exercise equally ameliorated the development of diabetic cardiomyopathy by preventing LV remodelling and mechanoenergetic impairment, this study advocates the therapeutic potential of physical activity in obesity-related cardiac disorders.
- Received November 16, 2012.
- Accepted March 8, 2013.
- © 2013 by the American Diabetes Association.
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