Anti-inflammatory effect of physical training in heart failure: role of TNF-alpha and IL-10.
Over the past 50 years, the understanding of the deteriorative changes involved in the progression of heart failure (HF), initially described as resulting from changes in salt and fluid retention, or changes in hemodynamic parameters, have changed significantly. Recently, several studies conducted in HF patients showed altered plasma (or serum) levels of pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), interleukins 1, 6, and 18, and cardiotropin-1, among other inflammatory markers. These changes were independent of HF etiology, suggesting a common pathogenic pathway. In response to these new findings, interventions to prevent and/or reduce these inflammatory changes have been proposed. The aerobic training-induced cardiovascular benefits of physical exercises performed at intensities ranging from mild to moderate have been previously reported. Moreover, it has been shown that moderate aerobic physical training seems to be able to modulate, in the presence of an abnormal chronic inflammatory condition, the overexpression of pro-inflammatory cytokines, soluble adhesion molecules, chemoattractant factors and oxidative stress. Altogether, these data indicate a possible anti-inflammatory effect induced by physical training. Therefore, this review aims to assess the role of physical training as an alternative non-pharmacological adjuvant to be administered in some pathological conditions in which TNF-alpha chronic changes are predominant, as in HF. The 'anti-inflammatory effect' induced by physical training seems to be primarily mediated by IL-10.
Batista
Miguel Luiz
ML
Grupo de Biologia Molecular da Célula - Instituto de Ciências Biomédicas I e Departamento de Medicina Interna - Universidade Federal de São Paulo, SP, Brasil.
Batista Júnior
Miguel Luiz
ML
Lopes
Renato Delascio
RD
Seelaender
Marília Cerqueira Leite
MC
Lopes
Antonio Carlos
AC
D005081:Exercise Therapy / Q000379:methods*; D006333:Heart Failure / Q000378:metabolism* / Q000628:therapy; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D016753:Interleukin-10 / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10