title: Exercise training promotes cardioprotection through oxygen-sparing action in high fat-fed mice.
abstract: Although exercise training has been demonstrated to have beneficial cardiovascular effects in diabetes, the effect of exercise training on hearts from obese/diabetic models is unclear. In the present study, mice were fed a high-fat diet, which led to obesity, reduced aerobic capacity, development of mild diastolic dysfunction, and impaired glucose tolerance. Following 8 wk on high-fat diet, mice were assigned to 5 weekly high-intensity interval training (HIT) sessions (10 × 4 min at 85-90% of maximum oxygen uptake) or remained sedentary for the next 10 constitutive weeks. HIT increased maximum oxygen uptake by 13%, reduced body weight by 16%, and improved systemic glucose homeostasis. Exercise training was found to normalize diastolic function, attenuate diet-induced changes in myocardial substrate utilization, and dampen cardiac reactive oxygen species content and fibrosis. These changes were accompanied by normalization of obesity-related impairment of mechanical efficiency due to a decrease in work-independent myocardial oxygen consumption. Finally, we found HIT to reduce infarct size by 47% in ex vivo hearts subjected to ischemia-reperfusion. This study therefore demonstrated for the first time that exercise training mediates cardioprotection following ischemia in diet-induced obese mice and that this was associated with oxygen-sparing effects. These findings highlight the importance of optimal myocardial energetics during ischemic stress.
authors: Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway; jim.lund@uit.no.
authors: J
authors: J
authors: Lund
authors: Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway;
authors: A D
authors: AD
authors: Hafstad
authors: Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway;
authors: N T
authors: NT
authors: Boardman
authors: Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway;
authors: L
authors: L
authors: Rossvoll
authors: K. G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology and Saint Olavs Hospital, Trondheim University Hospital, Trondheim, Norway; and.
authors: N P
authors: NP
authors: Rolim
authors: Institute for Surgical Research, Department of Cardiology, Center for Heart Failure Research, Oslo University Hospital-Rikshospitalet, University of Oslo, Oslo, Norway.
authors: M S
authors: MS
authors: Ahmed
authors: Institute for Surgical Research, Department of Cardiology, Center for Heart Failure Research, Oslo University Hospital-Rikshospitalet, University of Oslo, Oslo, Norway.
authors: G
authors: G
authors: Florholmen
authors: Institute for Surgical Research, Department of Cardiology, Center for Heart Failure Research, Oslo University Hospital-Rikshospitalet, University of Oslo, Oslo, Norway.
authors: H
authors: H
authors: Attramadal
authors: K. G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology and Saint Olavs Hospital, Trondheim University Hospital, Trondheim, Norway; and.
authors: U
authors: U
authors: Wisløff
authors: Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway;
authors: T S
authors: TS
authors: Larsen
authors: Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway;
authors: E
authors: E
authors: Aasum
mesh_terms: D000818:Animals; D059305:Diet, High-Fat / Q000009:adverse effects*; D005355:Fibrosis / Q000517:prevention & control; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000150:complications / Q000209:etiology; D010101:Oxygen Consumption; D005082:Physical Exertion; D017382:Reactive Oxygen Species / Q000378:metabolism; D018754:Ventricular Dysfunction / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*
chemical_list: D017382:Reactive Oxygen Species
keywords: cardiac efficiency; diet-induced obesity; high-intensity exercise; mechanoenergetics; myocardial oxygen consumption