Exercise-Induced Oxidative Stress

Exercise-Induced Stress

Exercise-Induced Stress

Acute exercise-induced oxidative stress is well documented over the last decade. A single bout of physical Exercise induces the formation of ROS and RNS which promotes muscle damage and inflammation. Exercise has been shown to cause oxidative damage in untrained persons while in trained subjects, no such effects are observed due to increased resistance of such persons to oxidative stress. Therefore, ROS can have beneficial and detrimental effects depends on the ROS concentration, duration of ROS exposure and training status of the individual. ROS produced during exercise lead to increased expression of antioxidants and adaptation of muscle cells. Exercise generally causes a transient increase in circulating ascorbic acid in the hours following exercise, but a decline below pre-exercise levels occurs in the days after prolonged exercise. These changes could be associated with increased exercise-induced oxidative stress. Ascorbic acid is a powerful antioxidant scavenging free radicals such as the hydroxyl radical and singlet oxygen which cause tissue damage. It additionally protects vitamin E from destruction. Ascorbic acid is involved in a number of biochemical pathways that are important to exercise metabolism and the health of exercising individuals. However, there is growing evidence of the negative effects of the antioxidant supplement on exercise training. Therefore, the question remains whether sedentary females benefit from ascorbic acid supplementation during the moderate intensity of exercise. Our understanding of the processes involved in antioxidant systems and adaptation to exercise is still limited. In the present study, we investigated the effects of pre-workout vitamin C on circulating biomarkers of oxidative stress, inflammation and muscle damage following a single bout of moderate-intensity cycling exercise. We found that ingestion of ascorbic acid immediately before exercising acutely increased antioxidant power post-exercise, evidenced by the increased ferric reducing ability of plasma, decreased plasma lipid hydroperoxides and blunted superoxide dismutase enzyme activity in the red blood cell lysate. Nonetheless, plasma total creatine kinase activity increased in both groups while both lactate dehydrogenase and C-reactive protein remained unchanged post-exercise, indicating that 1) ascorbic acid did not markedly alter markers of muscle damage and 2) persistent inflammation did not develop in the subjects after completing about of moderate intensity exercise.

During moderate exercise, glucose uptake by the working muscle rises 7 to 20 times over the basal levels. This exercise-induced glucose utilization without an appropriate increase in endogenous glucose production coupled with delayed hepatic glucose production might explain significantly reduced levels of glucose in our exercising subjects. In addition, the metabolic fate of glucose was associated with ROS production. ROS are produced under conditions of either high or low glucose. High glucose stimulates ROS production through the activation of NADPH oxidase. Wang and colleagues reported that acute exposure to low glucose (40–70 mg/dL) rapidly induces endothelial dysfunction and mitochondrial oxidative stress. However, in subjects ingesting ascorbic acid, plasma glucose levels were not significantly changed after exercise and continued to elevate at 30 min post-exercise. In 1970, ascorbic acid and glucose were found to have a very similar chemical makeup and thus share transporters (GLUT1, GLUT3, and GLUT4). This study showed that in fasting state the ascorbic acid supplementation may interfere with glucose utilization or transportation and contribute to lower production of ROS.

Dehydration is higher during vigorous exercise compared with mild exercise or resting state. In the present study, a single bout of exercise was shown to contribute to increased levels of total protein and albumin immediately after exercise in plasma indicating dehydrated condition which was resolved after resting for 30 min. Ad libitum water consumption post-exercise was allowed and seemed to be effectively alleviated plasma volume in all subjects. Paik and colleagues showed that dehydration increased oxidative DNA damage during exercise but fluid replacement with water or sports drink alleviated it equally. The increase in plasma protein and albumin following a single bout exercise was not seen in ascorbic acid supplement subjects. There was a study in rats showed that after intracerebroventricular injection of ascorbic acid resulted in a significant decrease in urinary volume and a concomitant increase in the plasma levels of vasopressin. Ascorbic acid supplementation may promote adequate hydration status through antidiuretic hormone.

Plasma total CK and LDH activities were assessed as relevant blood markers of muscle damage after prolonged exercise. Plasma CK activity increased immediately after exercise in the placebo group whereas the increase was slightly delayed in the subjects ingesting ascorbic acid, with increased levels evident by 30 min after exercise. The current study concludes that acute supplementation with ascorbic acid does little to prevent exercise-induced muscle damage.

In this study, no change of hsCRP was observed within 30 min post-exercise indicating that cycling at moderate intensity for 30 min did not induce acute inflammatory responses. However, locally induced muscle damage causing inflammation may not be easily detected systemically and hsCRP was shown to elevate at 24 to 48 h post-eccentric exercise. Thus, additional later time points may be necessary to collect to capture the long term effect of ascorbic acid supplementation following acute exercise.

Numerous studies have reported an increase in TBARS following submaximal exercise in humans, with values typically returning to baseline within one-hour post-exercise. In opposition to these findings, a few studies have reported no increase in TBARS despite the use of submaximal protocols. Our previous report showed that outdoor running for 30 min at 65–75% of maximum heart rate resulted in increased lipid peroxidation [11]. However, different types of exercise may produce different amounts of lipid peroxidation. This study showed that cycling for 30 min resulted in increased SOD activity at 30 min post-exercise but supplementing with ascorbic acid attenuated this effect. Ascorbic acid supplementation also increased antioxidant ability as shown in FRAP assay, indicated more reducing power to protect cells from an oxidizing agent. Ascorbic acid is widely distributed throughout the body with the highest concentrations in the pituitary, adrenals, and leukocytes. Plasma and lymphocyte ascorbic acid levels increased in nine men who completed a 21-km race. However, this study showed that moderate-intensity exercise does not appear to alter blood levels of ascorbic acid. The observed increase level of ascorbic acid at 30 min post-exercise might be attributed to oral administration with ascorbic acid resulting in an increase in antioxidant capacity as shown in FRAP assay. The unaltered SOD activity after exercise in subjects receiving ascorbic acid may be explained by the increased level of ascorbic acid in the bloodstream which may be responsible for free radical scavenging.

There were some limitations associated with this study. First, the volunteers were healthy young adult women, therefore, the results cannot be generalized to unhealthy or older adults and the results might not be representative of the metabolic changes that occur in men as well as in the fed state. The volunteers in this study were in fasted state prior exercise. It is evidenced that pre-exercise feeding blunted signaling in skeletal muscle and adipose tissue implicated in regulating components of metabolism, including mitochondrial adaptation and substrate utilization. Thus, fasted exercise was conducted in this study. It was found that pre-exercise feeding enhanced prolonged (P = 0.012), but not shorter duration aerobic exercise performance (P = 0.687). Individuals with higher fitness levels might also react differently to the same exercise protocol. Second, the intensity of the exercise bout in this study was based on age-based prediction equation for maximal heart rate rather than from measurement obtained at maximal exercise. Multiple sample collections post-exercise is required in an attempt to provide valid ascorbic acid absorption kinetics and identification of time to peak absorption after ingestion. However, the collection time for oral intake of ascorbic acid in this study was 1 h which corresponded with the maximum concentration in plasma when orally administered at a dose of 1250 mg according to the previous report.

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