Abstract
Abstract Aim: The present study aimed to verify the cardiac oxidative stress biomarker responses to high-intensity interval training (HIIT) in rats. Methods: Sixteen male Wistar rats weighing 250 to 300 g were equally divided into two groups (8 animals/group): sedentary control (SC) and trained group (HIIT). The exercise protocol consisted of high-intensity swimming (14% of body weight, 20 s of activity with 10 s of pause performed 14 times) which was performed for 12 consecutive days. Results: The cardiac tissue concentrations of malondialdehyde and carbonylated proteins showed no significant changes; on the other hand, hydroperoxide levels were higher in the HIIT group than in the SC group. The activities of superoxide dismutase, catalase, and glutathione peroxidase enzymes and the levels of reduced glutathione and sulfhydryl remained unchanged. Conclusion: It is possible to conclude that short-term high-intensity interval training induces changes in the cardiac oxidative stress biomarker but with no effect on the antioxidant enzymes.
Highlights
High-intensity interval training (HIIT) is characterized by brief and repeated episodes of vigorous activity followed by short periods of passive or active rest with exercises[1,2,3]
The production and exacerbated release of ROS generated by physical exercise can disrupt intracellular redox homeostasis[11], which can lead to protein oxidation, lipid peroxidation, and DNA damage[12] as well as lesions in cardiac cells[10]
Regarding the cardiac oxidative stress biomarkers (Table 1), there was a significant increase for the HIIT group in the HPx levels when compared to the CS group
Summary
High-intensity interval training (HIIT) is characterized by brief and repeated episodes of vigorous activity (approximately 85%-100% of the maximal oxygen uptake [VO2max]) followed by short periods of passive or active rest with exercises[1,2,3]. There is already evidence that HIIT can induce less membrane peroxidation, and greater competence in the antioxidant system, reduction in central mediators of necroptosis induced by myocardial infarction, in addition to cardioprotection against ischemia-reperfusion injury[21] and the expression of cardioprotective proteins in a similar way to continuous exercise[22]. In this sense, the control of the training load is fundamental for the achievement of your specific objectives, among them, the improvement of performance. The hypothesis is that HIIT can prevent the occurrence of exacerbated oxidative stress in the cardiac tissue
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