Exercise training changes IL-10/TNF-alpha ratio in the skeletal muscle of post-MI rats.

Journal Article (Journal Article)

Heart failure (HF) is associated with changes in the skeletal muscle (SM) which might be a consequence of the unbalanced local expression of pro- (TNF-alpha) and anti- (IL-10) inflammatory cytokines, leading to inflammation-induced myopathy, and SM wasting. This local effect of HF on SM may, on the other hand, contribute to systemic inflammation, as this tissue actively secretes cytokines. Since increasing evidence points out to an anti-inflammatory effect of exercise training, the goal of the present study was to investigate its effect in rats with HF after post-myocardial infarction (MI), with special regard to the expression of TNF-alpha and IL-10 in the soleus and extensor digitorum longus (EDL), muscles with different fiber composition. Wistar rats underwent left thoracotomy with ligation of the left coronary artery, and were randomly assigned to either a sedentary (Sham-operated and MI sedentary) or trained (Sham-operated and MI trained) group. Animals in the trained groups ran on a treadmill (0% grade at 13-20 m/min) for 60 min/day, 5 days/week, for 8-10 weeks. The training protocol was able to reverse the changes induced by MI, decreasing TNF-alpha protein (26%, P<0.05) and mRNA (58%, P<0.05) levels in the soleus, when compared with the sedentary MI group. Training also increased soleus IL-10 expression (2.6-fold, P<0.001) in post-MI HF rats. As a consequence, the IL-10/TNF-alpha ratio was increased. This "anti-inflammatory effect" was more pronounced in the soleus than in the EDL, suggesting a fiber composition dependent response.

Full Text

Duke Authors

Cited Authors

  • Batista, ML; Rosa, JC; Lopes, RD; Lira, FS; Martins, E; Yamashita, AS; Brum, PC; Lancha, AH; Lopes, AC; Seelaender, M

Published Date

  • January 2010

Published In

Volume / Issue

  • 49 / 1

Start / End Page

  • 102 - 108

PubMed ID

  • 19948415

Electronic International Standard Serial Number (EISSN)

  • 1096-0023

Digital Object Identifier (DOI)

  • 10.1016/j.cyto.2009.10.007


  • eng

Conference Location

  • England