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Oxidative Medicine and Cellular Longevity
Volume 2014, Article ID 457429, 14 pages
http://dx.doi.org/10.1155/2014/457429
Research Article

Exercise Training Preserves Ischemic Preconditioning in Aged Rat Hearts by Restoring the Myocardial Polyamine Pool

1Department of Pathophysiology, Harbin Medical University, No. 157 Baojian Road, Nangang District, Harbin 150086, China
2Department of Pathology, Heilongjiang Electric Power Hospital, Harbin 150090, China
3Department of Pathophysiology, Qiqihar Medical University, Qiqihar 161006, China
4Department of Cardiology, The First Clinical Hospital of Harbin Medical University, Harbin 150001, China

Received 2 July 2014; Revised 6 September 2014; Accepted 21 September 2014; Published 23 October 2014

Academic Editor: Vittorio Calabrese

Copyright © 2014 Weiwei Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Ischemic preconditioning (IPC) strongly protects against myocardial ischemia reperfusion (IR) injury. However, IPC protection is ineffective in aged hearts. Exercise training reduces the incidence of age-related cardiovascular disease and upregulates the ornithine decarboxylase (ODC)/polyamine pathway. The aim of this study was to investigate whether exercise can reestablish IPC protection in aged hearts and whether IPC protection is linked to restoration of the cardiac polyamine pool. Methods. Rats aging 3 or 18 months perform treadmill exercises with or without gradient respectively for 6 weeks. Isolated hearts and isolated cardiomyocytes were exposed to an IR and IPC protocol. Results. IPC induced an increase in myocardial polyamines by regulating ODC and spermidine/spermine acetyltransferase (SSAT) in young rat hearts, but IPC did not affect polyamine metabolism in aged hearts. Exercise training inhibited the loss of preconditioning protection and restored the polyamine pool by activating ODC and inhibiting SSAT in aged hearts. An ODC inhibitor, α-difluoromethylornithine, abolished the recovery of preconditioning protection mediated by exercise. Moreover, polyamines improved age-associated mitochondrial dysfunction in vitro. Conclusion. Exercise appears to restore preconditioning protection in aged rat hearts, possibly due to an increase in intracellular polyamines and an improvement in mitochondrial function in response to a preconditioning stimulus.