RESISTANCE EXERCISE PROTOCOL DOES NOT CAUSE ACUTE GENOTOXIC EFFECTS IN TRAINED INDIVIDUALS

Abstract

ABSTRACT Introduction: Resistance exercise, particularly strength training, has been progressively gaining more and more followers worldwide. Despite a considerable increase in the amount of research and literature available on this topic, resistance training is undergoing important developments. Anaerobic metabolism, which characterizes resistance training, enhances the ischemic process and blood reperfusion, thereby generating reactive oxygen species (ROS). The imbalance between the production of free radicals and antioxidant defenses may induce oxidative stress with subsequent protein oxidation, lipid peroxidation, DNA damage in several cells, and other effects. This process may be intensified at rest because the O2 deficit is counteracted by a process known as excess post-exercise oxygen consumption. Objective: To analyze the effects of ROS in strength training on the DNA of human lymphocyte, biomarkers of lipid damage (TBARS) and metabolism (triglycerides, protein, glycose, albumin and urea). Methods: Comet assay involving a count of 100 cells, which were divided into five classes of damage (no damage = 0, maximum damage = 4), thereby constituting an indication of DNA damage, and the micronucleus test, where the cell samples were centrifuged at 1000-1500 RPM for ten minutes at room temperature for the micronuclei analysis. Results: An elevation in triglyceride concentrations was observed 5h post-exercise (p=0.018), probably due to nutrition. There were no significant differences in the other biochemical parameters. In terms of the DNA damage measured by the Comet assay and micronucleus test, no statistical differences were observed until 5h post-exercise. Conclusion: The proposed training session did not cause oxidative or genotoxic damage in trained individuals under the proposed conditions. Level of Evidence II; Prognostic studies-Investigation of the effect of patient characteristics on the disease outcome.