MiPsummer Programme pdf - Mitochondrial Physiology Society

56
Exercise prevent obesity-induced myocardial oxygen waste and development of left
ventricular dysfunction - also when the heart is challenged with a high fat load
Abstract # 27
Jim Lund, Anne D Hafstad, Martin Hagve, Terje S Larsen, Ellen Aasum
Cardiovascular Research Group, Faculty of Health Sciences, University of Tromsø, Norway
Background Mechanical inefficiency and increased myocardial oxygen consumption are hallmarks
of diabetes-induced cardiomyopathy. We have recently shown that exercise training counteract
obesity-induced impairment of left ventricular (LV) function and mechanoenergetics, by decreasing
work-independent myocardial oxygen consumption (MVO 2 ).
Objectives As acute elevations in the supply of fatty acids (FA) are also known to induce
myocardial oxygen waste, we have investigated whether exercise-induced reduction in MVO 2 is
maintained in the presence of elevated FA.
Methods and Results Diet-induced insulin resistant obese C57BL/6J (DIO) mice, subjected to 8-10
weeks of high intensity training (interval running, 10x4 min at 85-95% of VO 2max ), showed
increased aerobic capacity, improved glucose tolerance and reduced obesity. LV function and workindependent
MVO 2 were measured in isolated perfused hearts in the presence of high fatty acid
levels (2.4 mM) and mitochondrial respiration was measured using high resolution respirometry in
isolated cardiac mitochondria using malate and glutamate as substrates. Sedentary DIO mice exhibit
LV diastolic and systolic dysfunction, accompanied with a 20% (p