An interesting finding of our study was that, in the heart, SOD activity was reduced in the sedentary group that was supplemented with creatine, in comparison to both the control group and the RT creatine supplemented group. This was in accordance with Siu and colleagues [38], where low intensity exercise (walking) for 8 and 20 weeks was not able to increase SOD activity in the heart of rats. Resistance exercise is characterized by a pressure overload in the

heart during its execution, causing an increase in cardiac muscle mass [39]. This suggests that, in part, the RT-Cr group increased SOD activity as an adaptive response to a higher formation of anion superoxide in this tissue under physical training conditions, and that the increased production of this ROS occurs through the xanthine oxidase

pathway [40, 41]. Creatine supplementation may have exerted a synergistic effect with RT Mizoribine clinical trial in relation to SOD activity modulation in the heart. In chronic-progressive stress conditions, and in RT, supplementation appears to exert a synergistic effect with regard to adaptation to RT with creatine supplementation, involving the cellular signaling enzymatic adaptation of SOD in cardiac tissue. This mechanism occurs via activation of the NAD(P)H oxidase system that, through vasoactive (angiotensin II) and inflammatory mediators (IL-6, TNF-α), modulates the selleck chemical expression of antioxidant enzymes in a short period [42, 43]. CAT activity in cardiac

tissue seems to be modulated by the interaction of creatine supplementation with RT, as observed by McClung and colleagues [44], who evaluated the effect of the association of creatine with high intensity Bay 11-7085 exercise on cardiac function in rats and found that this interaction was able to up-regulate the cardiac functional capacity. These results indicate a possible direct or indirect enzymatic modulation of creatine in synergism with training. As creatine is not synthesized exclusively in the kidney and in the pancreas, but at higher proportions in the liver, and is then mainly transported to the skeletal muscle, we investigated the liver with the aim of developing a hypothesis about the redox state of this organ in the presence of supplementation, either associated or not with resistance training. Our results are different to those found by Radak and colleagues [45], who reported an attenuation of lipoperoxidation levels in the animals submitted to treadmill running training which was adapted for rats. The difference in training protocols, age and animal species may have directly influenced the difference between the results obtained and those of our study. Studies that have evaluated the effect of creatine supplementation on oxidative stress in different structures are very limited.