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Am J Physiol Heart Circ Physiol. 2015 Apr 15;308(8):H823-9. doi: 10.1152/ajpheart.00734.2014. Epub 2015 Jan 30.

Exercise training promotes cardioprotection through oxygen-sparing action in high fat-fed mice.

Author information

1
Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway; jim.lund@uit.no.
2
Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway;
3
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.
4
Institute for Surgical Research, Department of Cardiology, Center for Heart Failure Research, Oslo University Hospital-Rikshospitalet, University of Oslo, Oslo, Norway.

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.

KEYWORDS:

cardiac efficiency; diet-induced obesity; high-intensity exercise; mechanoenergetics; myocardial oxygen consumption

PMID:
25637547
DOI:
10.1152/ajpheart.00734.2014
[Indexed for MEDLINE]
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