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Experimental Diabetes Research
Volume 2012, Article ID 213986, 8 pages
http://dx.doi.org/10.1155/2012/213986
Research Article

Persistence of Inflammatory Response to Intense Exercise in Diabetic Rats

1Institute of Physical Activity and Sport Sciences, Cruzeiro do Sul University, Rua Galvão Bueno, 868, 13° andar, 01506-000 São Paulo, SP, Brazil
2Institute of Biomedical Sciences, University of São Paulo, 05508-900 São Paulo, Brazil
3School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Dublin, Ireland
4School of Biomedical Sciences, Curtin University, Perth, WA 6000, Australia

Received 2 April 2012; Accepted 25 June 2012

Academic Editor: Raffaele Marfella

Copyright © 2012 José Ricardo Bortolon 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

In this study we evaluated the onset and resolution of inflammation in control and streptozotocin-induced diabetic rats subjected to a single session of intense exercise. The following measurements were carried out prior to, immediately after, and 2 and 24 hours after exercise: plasma levels of proinflammatory cytokines (TNF- , IL- , IL-6, CINC- , MIP-3 , and IL-6), immunoglobulins (IgA and IgM), acute phase proteins (CRP and C3), and creatine kinase (CK) activity. We also examined the occurrence of macrophage death by measurements of macrophages necrosis (loss of membrane integrity) and DNA fragmentation. An increase was observed in the concentration of IL- (3.3-fold) and TNF- (2.0-fold) and in the proportion of necrotic macrophages (4.5-fold) in diabetic rats 24 hours after exercise, while the control group showed basal measurements. Twenty-four hours after the exercise, serum CK activity was elevated in diabetic rats but not in control animals. We concluded that lesion and inflammations resulting from intense exercise were greater and lasted longer in diabetic animals than in nondiabetic control rats.