Exercise has been shown to increase the production of reactive oxygen species to a point that can exceed antioxidant defenses to cause oxidative stress. Dietary intake of antioxidants, physical activity levels, various antioxidants and oxidative stress markers were examined in 20 exercise-trained “athletes” and 20 age- and sex-matched sedentary “controls.” Plasma F2-isoprostanes, antioxidant enzyme activities, and uric acid levels were similar in athletes and sedentary controls. Plasma α-tocopherol and β-carotene were higher in athletes compared with sedentary controls. Total antioxidant capacity tended to be lower in athletes, with a significant difference between male athletes and male controls. Dietary intakes of antioxidants were also similar between groups and well above recommended dietary intakes for Australians. These findings suggest that athletes who consume a diet rich in antioxidants have elevated plasma α-tocopherol and β-carotene that were likely to be brought about by adaptive processes resulting from regular exercise.
Trent A. Watson, Lesley K. MacDonald-Wicks, and Manohar L. Garg
David C. Nieman, Courtney L. Goodman, Christopher R. Capps, Zack L. Shue, and Robert Arnot
( Kempf et al., 2010 ; Liang & Kitts, 2015 ; Lopez-Garcia et al., 2006 ; Tajik et al., 2017 ). In vitro indicate that CQAs have antioxidant and anti-inflammatory activity, alleviate oxidative stress and inflammation in various animal disease models, and reduce related biomarkers in human clinical
Mohamed A. Bouzid, Omar Hammouda, Régis Matran, Sophie Robin, and Claudine Fabre
This comparative study examined the effects of regular low intensity aerobic exercise on oxidative stress markers in older adults. The study was carried out on 15 sedentary subjects (age: 65.1 ± 3.5 years) versus 18 subjects performing fitness exercises (age: 65.8 ± 3.3 years). Before and after an incremental exercise test, oxidative stress markers were assessed. Superoxide dismutase was higher at rest and at the recovery for the physically active subjects compared with sedentary subjects (p < .05). At recovery, glutathione peroxidase and α -Tocopherol increased significantly above the resting values only in the active group (p < .05). Malondialdehyde had increased in both groups (p < .01), associated with a higher level in the sedentary group (p < .05) at the recovery. These data suggest that low intensity aerobic exercise may be useful to prevent the decline of antioxidants linked with aging.
Edith Filaire, Alain Massart, Hugues Portier, Matthieu Rouveix, Fatima Rosado, Anne S. Bage, Mylène Gobert, and Denys Durand
The aim of this investigation was to assess the effects of 6 wk of eicosapentanoic acid (EPA) and docosahexanoic acid (DHA) supplementation on resting and exercise-induced lipid peroxidation and antioxidant status in judoists. Subjects were randomly assigned to receive a placebo or a capsule of polyunsaturated fatty acids (PUFAs; 600 mg EPA and 400 mg DHA). Blood samples were collected in preexercise and postexercise conditions (judo-training session), both before and after the supplementation period. The following parameters were analyzed: α-tocopherol, retinol, lag phase, maximum rate of oxidation (Rmax) during the propagating chain reaction, maximum amount of conjugated dienes (CDmax) accumulated after the propagation phase, nitric oxide (NO) and malondyaldehide (MDA) concentrations, salivary glutathione peroxidase activity, and the lipid profile. Dietary data were collected using a 7-day dietary record. A significant interaction effect between supplementation and time (p < .01) on triglycerides was noted, with values significantly lower in the n-3 long-chain-PUFA (LCPUFA) group after supplementation than in the placebo group. Significant interaction effects between supplementation and time on resting MDA concentrations and Rmax were found (p = .03 and p = .04, respectively), with elevated values in the n-3 LCPUFA group after supplementation and no change in the placebo group’s levels. The authors observed a significantly greater NO and oxidative-stress increase with exercise (MDA, Rmax, CDmax, and NO) in the n-3 LCPUFA group than with placebo. No main or interaction effects were found for retinol and α-tocopherol. These results indicate that supplementation with n-3 LCPUFAs significantly increased oxidative stress at rest and after a judo-training session.
Allan H. Goldfarb, Stephen W. Patrick, Scott Bryer, and Tongjian You
Vitamin C supplementation (VC) (either 500 or 1000 mg/d for 2 wk) was compared to a placebo treatment (P) to ascertain if VC could influence oxidative stress. Twelve healthy males (25 ± 1.4 y) were randomly assigned in a counter-balanced design with a 2-wk period between treatments. Data were analyzed using repeated measures ANOVA. Exercise intensity measures (VO2, RER, RPE, HR, lactate) were similar across treatments. Resting blood oxidative-stress markers were unaffected by treatment. Exercise decreased total blood glutathione (TGSH) and reduced glutathione (GSH) and increased oxidized glutathione (GSSG) (P < 0.01) independent of treatment. Protein carbonyls (PC) increased 3.8 fold in the P (P < 0.01). VC attenuated the PC exercise response in a dose-dependent manner (P < 0.01). Thiobarbituric acid reactive substances (TBARS) was not influenced by exercise (P = 0.68) or VC. These data suggest that VC supplementation can attenuate exercise-induced protein oxidation in a dose-dependent manner with no effect on lipid peroxidation and glutathione status.
Sang-Ho Lee, Steven D. Scott, Elizabeth J. Pekas, Jeong-Gi Lee, and Song-Young Park
weight over a short period of time prior to competition. 4 This rapid weight change with high-intensity exercise training may result in the deterioration of the health and sports performance of these athletes, as it can lead to an abrupt disturbance of metabolism and increased oxidative stress, which
Nathan A. Lewis, Andrew J. Simpkin, Sarah Moseley, Gareth Turner, Mark Homer, Ann Redgrave, Charles R. Pedlar, and Richard Burden
-performance support team. Oxidative stress (OS), historically and simply defined as a disturbance in the prooxidant to antioxidant balance in favor of the former, 4 is evident in athletes diagnosed with overtraining syndrome 5 , 6 . Indeed, increases in biomarkers of OS correlate strongly with increases in training
Yijian Ding and Xi Xu
-cause mortality, chronic disease, and premature death ( McPhee et al., 2016 ; Mora & Valencia, 2018 ; World Health Organization, 2020 ). The beneficial effect of physical activity on aging may be related to its regulatory function on inflammation and oxidative stress, which are major causes of the progression
John Quindry, Lindsey Miller, Graham McGinnis, Megan Irwin, Charles Dumke, Meir Magal, N. Travis Triplett, Jeffrey McBride, and Zea Urbiztondo
Acute strength exercise elicits a transient oxidative stress, but the factors underlying the magnitude of this response remain unknown. The purpose of this investigation was to determine whether muscle-fiber type relates to the magnitude of blood oxidative stress after eccentric muscle activity. Eleven college-age men performed 3 sets of 50 eccentric knee-extensions. Blood samples taken pre-, post-, and 24, 48, 72, and 96 hr postexercise were assayed for comparison of muscle damage and oxidative-stress biomarkers including protein carbonyls (PCs). Vastus lateralis muscle biopsies were assayed for relative percentage of slow- and fast-twitch muscle fibers. There was a mixed fiber composition (Type I = 39.6% ± 4.5%, Type IIa = 35.7% ± 3.5%, Type IIx = 24.8% ± 3.8%; p = .366). PCs were elevated 24, 48, and 72 hr (p = .032) postexercise, with a peak response of 126% (p = .012) above baseline, whereas other oxidative-stress biomarkers were unchanged. There are correlations between Type II muscle-fiber type and postexercise PC. Further study is needed to understand the mechanisms responsible for the observed fast-twitch muscle-fiber oxidative-stress relationship.
John Quindry, Lindsey Miller, Graham McGinnis, Brian Kliszczewiscz, Dustin Slivka, Charles Dumke, John Cuddy, and Brent Ruby
Previous research findings indicate that environmental temperature can influence exercise-induced oxidative-stress responses, although the response to variable temperatures is unknown. The purpose of this study was to investigate the effect of warm, cold, and “neutral,” or room, environmental temperatures on the blood oxidative stress associated with exercise and recovery. Participants (N = 12, age 27 ± 5 yr, VO2max = 56.7 ± 5.8 ml · kg-1 · min-1, maximal cycle power output = 300 ± 39 W) completed 3 exercise sessions consisting of a 1-hr ride at 60% Wmax, at 40% relative humidity in warm (33 °C), cold (7 °C), and room-temperature environments (20 °C) in a randomized crossover fashion. Rectal core temperature was monitored continually as participants remained in the respective trial temperature throughout a 3-hr recovery. Blood was collected preexercise and immediately, 1 hr, and 3 hr postexercise and analyzed for oxidative-stress markers including ferric-reducing ability of plasma (FRAP), Trolox-equivalent antioxidant capacity (TEAC), lipid hydroperoxides, and protein carbonyls. Core temperature was significantly elevated by all exercise trials, but recovery core temperatures reflected the given environment. FRAP (p < .001), TEAC (p < .001), and lipid hydroperoxides (p < .001) were elevated after warm exercise while protein carbonyls were not altered (p > .05). These findings indicate that moderate-intensity exercise and associated recovery in a warm environment elicits a blood oxidative-stress response not observed at comparable exercise performed at lower temperatures.