## 4 Discussion
This finding implies that an increase in exercise duration would more highly activate oxidative muscle fibers--type I and type IIa muscle fibers leading to a more significant increase in the SOD activity [59]. Thus, excessive H2O2 produced from the dismutation reaction of superoxide inhibited SOD and CAT enzymes by changing the redox condition in the cell and changes in the antioxidant enzyme's catalytic center [60; 61]. SOD is also sensitive to the overproduction of superoxide and hydrogen peroxide [61], a fact reflected in this study, whereby the SOD significantly decreased after exercising at 70% VO2 pk for 30 min. According to [PERSON] et al. [41], AE changes the equilibrium between the formation of hydrogen peroxide from superoxide dismutation and its decomposition by other enzymes (GPx, CAT) in erythrocytes. The reduction of AE and the increase of MDA in this study showed that exercising at 70% VO2 pk for longer than 20 min induces oxidative stress. These findings suggest that these results may support the theory that the contribution of antioxidant enzyme disequilibrium from oxidative stress during exercise is secondary to limited CAT activity and most likely due to an insufficient increase in the GPx activity. In other terms, oxidative stress is initiated by an imbalance in the activities of antioxidant enzymes, SOD, against GPx and CAT. It can be postulated that exercising at a higher intensity and for a longer duration is associated with the overproduction of free radicals (Figure 6). Another possible factor that affects CAT activity is blood glucose. It is stipulated that the increase in blood glucose inhibits CAT [62]. The exponential rise of adrenalin and noradrenalin hormones with intensity was much faster than the increment seen with exercise duration. The latter only showed a linear relationship [63]. Both adrenalin and noradrenalin hormones stimulate \(\beta\)-adrenergic receptors in the pancreas and increase glucagon secretion [64]. Resultant high glucagon in plasma increases the blood glucose level through the mobilization of free fatty acid (FFA) from adipose tissue, mobilization of glucose from the liver, and an increase of gluconeogenesis [65]. It appears that the sensitivity of cells to free radicals depends on the equilibrium between the formation of hydrogen peroxide from superoxide in the dismutation reaction catalyzed by SOD and its degradation by GPx and CAT rather than on the activities of individual antioxidant enzymes [66]. In this study, the AE was observed to increase significantly only after exercise at 60% and 70% \(\dot{\mathrm{V}}\mathrm{O}_{2}\mathrm{pk}\) for 10-, 20-, and 30-min, except for 70% \(\dot{\mathrm{V}}\mathrm{O}_{2}\mathrm{pk}\) intensity in 30-min duration, where the ratio was reduced. These results are primarily in agreement with a previous study by [PERSON] et al. [67] that observed a significant elevation of plasma total antioxidant capacity among healthy individuals after 30 min at 50-60% of the heart rate reserve on a cycle ergometer. The increment in plasma MDA with intensity and duration found in this study suggests that the balance of oxygen metabolism is compromised during exercise. Similarly, this finding supports the hypothesis of exercise-induced oxidative stress among sedentary adults [8; 44; 59; 68]. The reduction in all antioxidant enzyme activities (SOD, CAT and GPx) leading to high oxidative damage showed an utmost increment in MDA. Inadequate protection by antioxidants causes cellular damage to increase due to increased lipid peroxidation and oxidative stress [53; 69]. In the present study, lipid peroxidation increased with the intensity and duration of cycling exercise. When the intensity and duration of exercise are increased, oxygen consumption [70], metabolic stress [71], metabolism rate [72], and mechanical stress [72; 73] will escalate, leading to a higher production of ROS.