Interval training does not decrease oxidative stress in the heart of mice

Abstract

Physical exercise is characterized by an increase in O2 consumption by the whole body — particularly by heart tissues — linked with a rise in the production of ROS [ [1] Ascensão A. Ferreira R. Magalhães J. Exercise-induced cardioprotection biochemical, morphological and functional evidence in whole tissue and isolated mitochondria. Int J Cardiol. 2007; 117: 16-30 Abstract Full Text Full Text PDF PubMed Scopus (124) Google Scholar ], which in turn is associated with the mechanisms of cardiac dysfunction [ [2] Lefer D.J. Granger D.N. Oxidative stress and cardiac disease. Am J Med. 2000; 109: 315-323 Abstract Full Text Full Text PDF PubMed Scopus (400) Google Scholar ]. Studies on both involuntary treadmill exercise training [ [3] Silva L.A. Pinho C.A. Scarabelot K.S. et al. Physical exercise increases mitochondrial function and reduces oxidative damage in skeletal muscle. Eur J Appl Physiol. 2009; 105 (a): 861-867 Crossref PubMed Scopus (39) Google Scholar ] and voluntary wheel running [ [4] Allen D.L. Harrison B.C. Maass A. Bell M.L. Byrnes W.C. Leinwand L.A. Cardiac and skeletal muscle adaptations to voluntary wheel running in the mouse. J Appl Physiol. 2001; 90: 1900-1908 Crossref PubMed Scopus (268) Google Scholar ] in animals have consistently demonstrated that endurance with moderate intensity exercise is associated with increased aerobic capacity and improved oxidative stress parameters. Nevertheless, to date, no studies have compared the effect of interval training with continuous training on oxidative stress parameters in cardiac muscle.