## 4 Discussion  
Physical exercise such as walking or resistance exercise improves cardiovascular and muscular endurance [42] and anxiety [43] and reduces the risk of metabolic diseases [44]. Figure 4: Percentage of SOD changes at 50%, 60%, and 70% \(\dot{\mathrm{V}}\)O\({}_{2}\)pk during exercise. * significantly different from 70% \(\dot{\mathrm{V}}\)O\({}_{2}\)pk (\(p<0.05\)). Figure 5: Percentage of AE changes at 50%, 60%, and 70% \(\dot{\mathrm{V}}\)O\({}_{2}\)pk during exercise. * significantly different from 70% \(\dot{\mathrm{V}}\)O\({}_{2}\)pk (\(p<0.05\)). These adaptations are optimally seen following moderate-intensity training [45]. In addition, training at any intensity above 60% of VO2 max, including high intensity, is likely to improve maximal oxygen uptake in healthy adults [46]. Hence, high-intensity exercise also can reduce the risk of developing cardiovascular diseases and all-cause mortality by increasing the VO2 max [47]. However, exercise at high-intensity loads may adversely affect tissues and contribute to overuse injuries [48]. [PERSON] et al. [48] also found that high-intensity endurance exercise increases oxidative stress levels in the blood in untrained subjects. The amount of oxidant production was not only contributed by intensity and duration of exercise but also by exercise mode [49]. Cycling, as one of the non-weight-bearing exercise modes, is becoming increasingly popular, especially in weight loss programs. Exercise results in a 1- to 3-fold increase in superoxide during muscle contraction [50]. Previous studies have reported increased oxidative stress for healthy and diseased subjects following single bouts of exercise [51; 52]. A study by [PERSON] et al. [27] revealed that the increase in oxidative stress among trained subjects occurred following short duration, 30 and 60 min of moderate intensity exercise. This is consistent with the present study, which showed increased oxidative stress, as measured by MDA, immediately following each exercise bout of moderate-to-high intensity and short-to-moderate duration. According to [PERSON] et al., the magnitude of oxidative damage due to exercise depends on oxygen consumption, ROS production rate, and the balance between antioxidants and ROS [10]. In contrast, [PERSON] et al. [8] found that the MDA was not increased after cycling for 30 min at an intensity of 70% VO2 max among 10 trained male athletes. This might be stipulated by active participants or trained athletes possessing greater protection against ROS oxidation than sedentary participants [10]. A high level of protection against ROS reduces lipid peroxidation (MDA). [PERSON] et al. [53] also suggested that the oxidative stress produced from exercise depends on the capacity and the adaptability of the antioxidant defense in the body. This study also discovered that even low intensity, as in 50% VO2 pk, increased the MDA level in sedentary healthy young adults. Thus, we can conclude that the exercise threshold for stimulating oxidative stress during cycling is between 10 to 30 min of 50% to 70% VO2 pk in sedentary young adults. However, 30 min duration at 70% VO2 pk has caused a marked increase in MDA. The intensity of exercise exaggerates the respiration rate [54], leading to the amplification of oxygen consumption and electron transport chain reaction [10]. It is estimated that the whole body's oxygen consumption may increase by 10-20 fold [55], while a staggering figure of up to 100-200 fold is seen in the exercising muscles [10]. An increase in MDA following exercise is accompanied by increased antioxidant responses [56; 57] that were also discovered in the present study, particularly AE, SOD, and CAT. Antioxidant enzyme activities increased following exercise to counteract the rise in ROS production [6; 19; 52; 58]. The present study discovered that SOD activities increased immediately after cycling at all intensities and duration, resulting in the overproduction of H2O2 (hydrogen peroxide) and subsequently overwhelming the GPx and CAT enzymes.