Acute bouts of aerobic exercise can induce a state of oxidative stress. Previous studies have reported increased oxidative stress for both healthy and diseased subjects following single bouts of exercise [44, 45]. This is consistent with the present study that found oxidative stress increased as measured by MDA immediately following each submaximal exercise bout. An increase in oxidative stress following exercise is accompanied by increased antioxidant responses [46, 47] that were also discovered in the present study–particularly CAT and SOD. Activities of SOD and CAT increased following exercise to counteract the rise in ROS production [6, 46, 48, 49, 50].
Even though aerobic exercise can cause oxidative stress, it appears that this stimulus is required to allow for an increased endogenous antioxidant defences and improved cardiorespiratory fitness. The degree of oxidation is proportional to the amount of oxidant production contributed by exercise mode, intensity, and duration [51]. Furthermore, the American College of Sports Medicine recommends that the appropriate exercise intensity for improving cardiorespiratory fitness in young adults be 4.8 to 7.1 METs, which is equivalent to 50–85 percent of VO2max and 60–90 percent of age-predicted HRmax [52]. As a result, the current study wants to determine whether oxidative stress levels and enzymatic antioxidant status are more affected by intensity or duration of exercise.
In this study, the effects of exercise intensity and duration on oxidative stress (measured through MDA and antioxidant enzymes activities) were analyzed systematically. This study employed nine exercise bouts with different intensities and duration prescribed explicitly for each healthy and sedentary young adult. The exercise was delivered using submaximal aerobic cycling in which the moderate intensity (50%, 60%, and 70% VO2pk) and duration (10, 20, and 30 mins) were manipulated.
The main findings of this study revealed that the percentage increment of MDA was dependent on the exercise intensity and duration. This is in agreement with Ammar et al. [47], Ribeiro-Samora et al. [53], El Abed et al. [54], and Boukhris et al. [55], which reported that the oxidative stress level is dependent on the intensity and duration of the exertion. Previous research showed that aerobic exercise performed at high intensity [8, 14, 29, 56, 57], particularly prolonged aerobic exercise [48], is associated with increased oxidative stress. A study by Johnson et al. [58], McAllister et al. [59], and McClean et al. [23] revealed that the increase in oxidative stress among trained subjects occurred following moderate intensity and short duration of exercise.
On the other hand, Bloomer et al. [9] found that the MDA was not increased after cycling for 30 minutes at an intensity of 70% VO2max among ten trained male athletes. This might be stipulated by active participants or trained athletes possessing greater protection against ROS oxidation than sedentary participants [12]. A high level of protection against ROS is shown to reduce lipid peroxidation (MDA). Leeuwenburgh and Heinecke [60] and Perrone et al. [61] also suggested that the oxidative stress produced from exercise depends on the capacity and the adaptability of the antioxidant defence in the body.
The magnitude of the oxidative damage due to exercise depends on oxygen consumption, ROS production rate, and the balance between antioxidants and ROS [11]. According to Sakellariou et al. [62], aerobic exercise results in a 1 to 3-folds increased of superoxide during muscle contraction. When the intensity and duration of exercise are increased, oxygen consumption [63], metabolic stress [64], mechanical stress [65, 66] and metabolism rate [67] will escalate, leading to higher production of ROS [68]. Inadequate protection by antioxidants causes cellular damage to increase due to increased lipid peroxidation and oxidative stress [61, 69].
This study has demonstrated a decrease in the percentage changes of CAT, SOD, and AE in response to exercise duration and intensity. The reduction in the SOD and CAT percentage instigated the rise in the MDA percentage. Furthermore, the percentage changes of AE, SOD, and CAT were dependent on the exercise intensity and duration. This is consistent with a study by He et al. [6] that proved the magnitude of SOD activities' magnitude depends on the intensity and duration.
The study design employed in this study permitted us to determine that intensity is the major determinant factor for MDA as indicated by through ANOVA analysis. This suggests that exercise intensity resulted in more significant responses of blood oxidative stress than the duration of exercise. This is in line with the previous studies which have observed that exercise intensity is the key determinant of oxidative stress following aerobic exercise [53, 58]. Earlier studies by He et al. [6] had discovered that for the same total energy expenditure, oxidative stress was also found to increase after exercise at a higher intensity but not after a longer duration. Intensity of exercise intensifies the respiration rate [70] leading to amplification of oxygen consumption and electron transport chain reaction [11]. It is estimated that the whole body oxygen consumption may increase up to 10–20 fold [72, 72] while staggering figure up to 100–200 fold is seen in the exercising muscles [73]. Despite such rise, only 0.15% of the utilised oxygen produce ROS.
Previous studies by Johnson et al. [58] and McAllister et al. [59] reported an increase in oxidative stress among trained subjects following 30 and 60 min of moderate aerobic exercise. Such finding is in concordance with the present study, where we have discovered moderate intensity and short duration of aerobic cycling exercise increased the oxidative stress in sedentary healthy young adults. Thus, we can conclude that the threshold intensity for stimulating an increased response of oxidative stress following aerobic exercise is between 50 and 70% VO2pk in sedentary young adults. Johnson et al. [58] have found that the duration required for aerobic exercise with threshold intensity of 50–70% VO2pk in trained subjects is between 20 and 60 minutes.
This study has discovered different determinant factors for each antioxidant enzyme. Here, exercise duration is the major determinant factor for SOD and AE. This finding implies that an increase in exercise duration would activate more highly oxidative muscle fibres – type I and type IIa muscle fibres leading to a more significant increase in the SOD activity [75]. 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 centre [76, 77]. Subsequently, an increase in exercise duration reduces AE.
On the other hand, exercise intensity is the main determinant factor for CAT. It is stipulated that the increase in blood glucose inhibits CAT [78]. The exponential rise of adrenalin and noradrenalin hormones with intensity was observed to be much faster than the increment seen with exercise duration. The latter only showed a linear relationship [79]. Both adrenalin and noradrenalin hormones stimulate β-adrenergic receptors on the pancreas and increase glucagon secretion [80]. 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 [81].
This study also revealed that the intensity of 70% VO2pk generated the highest stressor stimulus for pro-oxidative than the lower intensity exercises for all 10, 20 and 30 min exercise duration. Exercise at 70% VO2pk has affected the redox balance by producing more ROS and subsequently increased the SOD activity. An increase in glucose concentration in the blood could also inhibit the CAT enzyme [78]. Accumulation of H2O2 (hydrogen peroxide) produced following exercise at 70% for 30 minutes has also inhibited SOD and decreased its activity. Thus, this study discloses that exercise intensity above 60% VO2pk is more effective in controlling the response of antioxidant enzymes. This study also suggests that antioxidant enzymes appear to be selectively activated during exercise depending on the amount of ROS produced.
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 [82]. In this study, the AE was observed to increase significantly only after exercise at 60% and 70% VO2pk for 10-, 20-, and 30-minutes, except for 70% VO2pk intensity in 30-minutes duration where the ratio was reduced. These results are primarily in agreement with a previous study by Georgakouli et al. [83] 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. However, we did not observe any relationships or associations between the percentage changes in AE and the oxidative stress markers, MDA. Similarly, this finding supports the hypothesis of exercise-induced oxidative stress among sedentary adults [8, 47, 84, 85].
SOD is sensitive to the overproduction of superoxide and hydrogen peroxidase [86], and this fact is reflected in this study whereby the AE significantly decreased after exercising at 70% VO2pk for 30 minutes. According to Garaiová et al. [43], 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% VO2pk for longer than 20 minutes creates oxidative stress. These findings indicate the probability 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 (Fig. 6).
Moreover, these indicate that free radicals produced during exercise at 70% VO2pk for 30 minutes have exceeded the antioxidant enzymes' capacity. Although 70% VO2pk is classified as moderate intensity, exercising for more than 20 minutes can be conceived as a high exercise dose for sedentary young male adults, hence triggering ROS and subsequent oxidative stress. This finding supports the suggestion [87] for accumulating at least 30 minutes of exercise at moderate intensity each day to maintain cardiovascular fitness and reduce potential risks of non-communicable diseases. This finding is also incoherent with previous studies demonstrating increased oxidative stress after moderate-intensity exercise among young, healthy male subjects [23]. Moderate-intensity exercise is thought to confer beneficial effects, but prolonged exercise leads to elevated ROS production at higher exercise intensities [58, 88]. However, a significant elevation of plasma total antioxidant capacity was observed in a healthy untrained male adult after cycling for 30 minutes at 70% of maximum workload [89].
For any exercise to deliver the expected health benefit, there should be an optimal level of ROS produced during exercise that may induce favourable adaptations following repeated exposure [19], including increased expression of antioxidant enzymes over time such as superoxide dismutase and catalase [90]. However, the increase of oxidative stress above the optimal level may compromise health and performance. Too much ROS might impair antioxidant defence capacities leading to substantial cell damage [91, 92]. Prolonged and irreparable oxidative damage could predispose to diseases such as neurodegeneration and cardiovascular [88].
These findings further emphasize the need to achieve optimal exercise intensity and duration and provide physical trainers, exercise enthusiasts, and clinical practitioners with practical settings. Here, conducive and optimal exercise intensity and duration bring beneficial health outcomes. However, categorizing intensity is not straightforward because the functional capacities of each individual vary widely, especially for different age groups and fitness levels. Hence, future research should propose intensity categories based on age group, fitness level, and gender. Concurrently, works should evaluate the long-term effect of the optimal intensity and duration presented in this study. An investigation should be carried out to determine the chronic state of oxidative stress and antioxidant enzyme responses concerning exercise intensity and duration. Existing literature is yet to demonstrate the physiological mechanism that underpin the oxidative process during exercise, especially when intensity or duration are increased. Here, remains the opportunities for future research to evaluate the differences in production pathways of ROS and free radicals based on different exercise intensity and duration.