# Moderate-Intensity Swimming Alleviates Oxidative Injury in Ischemic Heart
## 4 Discussion
Oxidative stress is most often defined as an imbalance between intracellular ROS production and the capacity to neutralize ROS, carried out by a system that includes, amongst others, CAT, SOD, GSH, and GPx. During an ischemic period, the efficiency of this system is drastically decreased, leading to cell death and cardiac dysfunction, and following reperfusion, the suddenly increased oxygen supply leads to the high levels of oxygen free radicals, causing lipid peroxidation, protein degradation, and DNA damage, further injuring the cardiac tissue [20]. In a study conducted on albino rats, [PERSON] and [PERSON] observed that ischemia-reperfusion-induced myocardial infarction is associated with significantly increased concentrations of cardiac injury and oxidative stress biomarkers (lactate dehydrogenase, creatine kinase, creatine kinase isoenzyme, lipid peroxidase) and reduced antioxidant capacity due to the reduced levels of CAT, SOD, and GSH [21]. The findings of [PERSON] et al. [22] present evidence that ISO-induced myocardial injury causes the elevated levels of malonaldehyde (MDA) and the decreased concentrations of SOD and GPx. The data regarding the effects of physical exercise and swimming in particular on maintaining cardiac antioxidant capacity after a myocardial infarction-induced ischemic injury are still fairly inconclusive. From one point of view, several studies focused on treadmill exercise found that this type of physical activity has a positive impact on maintaining the efficiency of the enzymatic antioxidant system through the improved levels of CAT, SOD, and GPx. On the other hand, some of these findings offer a positive but not significant correlation between exercise and antioxidant enzyme levels, and the significantly increased protein levels are usually restricted to mitochondria and cannot be found in the cytosol [23]. Endurance and resistance training have been shown to significantly increase GPx content and reduce myeloperoxidase and MDA activity, while having no significant impact on CAT concentration [24]. According to [PERSON] and [PERSON] [25], there is a significant increase in GPx activity in rats who went through a swimming training protocol, compared to sedentary animals; however, the study did not focus on cardiac injury, only on adaptive changes between trained and untrained animals. In contrast, [PERSON] et al. [26] studied the effects of preconditioning through swimming in mice with doxorubicin-induced cardiac oxidative damage but found no significant increase in CAT, SOD, or GPx levels that could be associated with the training. In this regard, to the best of our knowledge, our present study is the first one to demonstrate that moderate-intensity swimming training can be efficiently used to prevent myocardial infarction-induced ischemic injury, by inhibiting ROS production and strengthening intracellular antioxidant defense. Our results indicate that both cardiac injury biomarkers (ANP and BNP) and ROS levels were significantly lower in rats who partook in swimming training, compared to the sedentary animals. Moreover, the enzymatic components of the intracellular antioxidant system also showed increased resilience in trained animals after ISO-induced myocardial infarction. GPx, in particular, presented significantly increased concentrations in the swimming animals. Although SOD and CAT levels in this group were also slightly elevated, these changes were not considered statistically significant. Exercise triggers a complex adaptive response in the body, enhancing endogenous antioxidant defenses and improving the overall redox balance. This adaptive response involves the upregulation of enzymatic antioxidants such as SOD, CAT, and GPx, contributing to a more robust defense against oxidative stress [27].