Journal
EUROPEAN JOURNAL OF HEART FAILURE
Volume 12, Issue 4, Pages 323-330Publisher
WILEY
DOI: 10.1093/eurjhf/hfq028
Keywords
Exercise training; Myocardial infarction; Autophagic function; Fatty acid utilization; Oxidative status
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Funding
- NSC [98-2314-B-002-111]
- National Center of Excellence for General Clinical Trial and Research at the National Taiwan University Hospital
- [DOH97-TD-B-111-001]
- [NTUH.97-S808]
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Aims To explore whether exercise can improve cardiac function in a post-myocardial infarction (MI) rabbit model and to determine contributing factors in the left ventricle (LV). Methods and results Adult male New Zealand White rabbits (2.5-3 kg) underwent MI by ligation of the left anterior descending coronary artery. For 8 weeks after surgery, sham-operated, and post-MI rabbits were housed under sedentary conditions or assigned to a 4-week treadmill exercise protocol at a speed of 1.0 km/h for 30 min 5 days per week, then sacrificed. The non-infarcted region of the LV was harvested for further analysis. MI decreased left ventricular ejection fraction (LVEF) and increased thiobarbituric acid reactive substances (TBARS) generation in the LV. Exercise improved the cardiac function of MI rabbits. Left ventricular LC3II/LC3I (microtubule-associated protein light chain 3) in the MI group was 2.1-fold higher than that of the sham group, exercise significantly decreased LC3II/LC3I in the MI group. MI down-regulated the expression of heart-type fatty acid binding protein (h-FABP), and exercise up-regulated h-FABP. In addition, LVEF had a significantly positive correlation with h-FABP and a negative correlation with LC3II/LC3I. Conclusion Exercise induced change in autophagic function and fatty acid utilization may contribute to the improvement in ventricular function in the infarcted heart.
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