Oxidative stress has been defined as an imbalance between oxidants and antioxidants in favor of the oxidants ( Sies, 2015 ). Elevations in reactive oxygen species (ROS) production are commonly thought of in a negative light for their role in producing deleterious effects or distress. However, ROS
Ahmed Ismaeel, Michael Holmes, Evlampia Papoutsi, Lynn Panton, and Panagiotis Koutakis
Ian H. Gillam, Ross B. Cunningham, and Richard D. Telford
While reactive-oxygen and nitrogen species produced during exercise in skeletal muscle play a critical role in the regulation of cell signaling and muscular function, 1 – 3 oxidative stress caused by intense or prolonged endurance exercise may overwhelm the cellular antioxidant defenses. This in
Kyle L. Timmerman, Kevin D. Ballard, Michael A. Deal, Lisa C. Tagariello, Jenna M. Karrow, Gabrielle A. Volk, Adam Meisler, Ian D. Connors, and Rachael E. Mott
, 2 – 4 whereas ROS accumulation results in cellular damage 5 and may contribute to the pathogenesis of numerous age-related diseases and conditions (eg, cardiovascular disease, type II diabetes, Alzheimer’s disease, and sarcopenia). 6 – 9 Endogenous antioxidant enzymes, including superoxide
Mitchell M. Kanter
Free radicals have been implicated in the development of diverse diseases such as cancer, diabetes, and cataracts, and recent epidemic-logical data suggest an inverse relationship between antioxidant intake and cardiovascular disease risk. Data also suggest that antioxidants may delay aging, Research has indicated that free radical production and subsequent lipid peroxidation are normal sequelae to the rise in oxygen consumption with exercise. Consequently, antioxidant supplementation may detoxify the peroxides produced during exercise and diminish muscle damage and soreness. Vitamin E, beta carotene, and vitamin C have shown promise as protective antioxidants. Other ingestible products with antioxidant properties include selenium and coenzyme
John C. Quindry, Steven R. McAnulty, Matthew B. Hudson, Peter Hosick, Charles Dumke, Lisa S. McAnulty, Dru Henson, Jason D. Morrow, and David Nieman
Previous research indicates that ultramarathon exercise can result in blood oxidative stress. The purpose of this investigation was to examine the efficacy of oral supplementation with quercetin, a naturally occurring compound with known antioxidant properties, as a potential countermeasure against blood oxidative stress during an ultramarathon competition. In double-blind fashion, 63 participants received either oral quercetin (250 mg, 4×/day; 1,000 mg/day total) or quercetin-free supplements 3 weeks before and during the 160-km Western States Endurance Run. Blood drawn before and immediately after (quercetin finishers n = 18, quercetin-free finishers n = 21) the event was analyzed for changes in blood redox status and oxidative damage. Results show that quercetin supplementation did not affect race performance. In response to the ultramarathon challenge, aqueous-phase antioxidant capacity (ferric-reducing ability of plasma) was similarly elevated in athletes in both quercetin and quercetin-free treatments and likely reflects significant increases in plasma urate levels. Alternatively, trolox-equivalent antioxidant capacity was not altered by exercise or quercetin. Accordingly, neither F2-isoprostances nor protein carbonyls were influenced by either exercise or quercetin supplementation. In the absence of postrace blood oxidative damage, these findings suggest that oral quercetin supplementation does not alter blood plasma lipid or aqueous-phase antioxidant capacity or oxidative damage during an ultramarathon challenge.
Zekine Lappalainen, Jani Lappalainen, David E. Laaksonen, Niku K.J Oksala, Savita Khanna, Chandan K. Sen, and Mustafa Atalay
Thioredoxin (TRX) is a protein disulfide reductase that plays an important role in many thiol-dependent cellular reductive processes, antioxidant protection, and signal transduction. Moreover, TRX reduces and maintains the function of many proteins during oxidative stress, which is increased in diabetes. The authors recently reported that diabetes impairs brain redox status and TRX response to exercise training. As a continuation of their studies, they hypothesized that alpha-lipoic acid, a natural thiol antioxidant, has a favorable effect on the brain TRX and glutathione (GSH) system in diabetes. Streptozotocin-induced diabetes was used as a chronic model and exhaustive exercise as an acute model for disrupted redox balance. Half the diabetic and nondiabetic animals were subjected to a bout of exhaustive exercise after 8 wk with or without lipoic acid and analyzed for key thiol antioxidants. Lipoic acid neither altered diabetes-induced oxidative stress as assessed by the increased ratio of oxidized to total GSH nor had any impact on the antioxidant protein response to exercise. However, lipoic acid increased mRNA of TRX-interacting protein, an inhibitor of TRX-1, and glutaredoxin-1 in diabetes. Exercise increased TRX-1 mRNA in both diabetic and nondiabetic animals but had no effect on TRX-1 protein. Cytosolic superoxide dismutase mRNA was only increased in diabetes, whereas exercise increased the protein levels in nondiabetic animals. The findings suggest that exhaustive exercise induces mRNA of TRX-1 in the brain and that lipoic acid cannot prevent diabetes-induced disturbances in GSH homeostasis. Because lipoic acid increased TRX-interacting protein transcription in diabetes, high doses may impair TRX-1 homeostasis.
Stephen Hill, Wesley Box, and Robert A. DiSilvestro
Lipid peroxides can be both a product and an initiator of oxidant stress. Conceivably, exercise can either increase concentrations of lipid peroxides (by causing oxidant stress), or decrease them (by accelerating peroxide breakdown). The net effect could depend on exercise intensity and nutritional intake of antioxidants. The present study examined the response of serum lipid peroxides to the combination of moderate intensity, weight resistance exercise plus intake of soy protein, a source of antioxidant phytochemicals. Recreationally trained, young adult men (N = 18) consumed soy protein or antioxidant-poor whey protein for 4 weeks (40 g protein/d) before a session of moderate intensity, weight resistance exercise. In the soy group, exercise decreased values for serum lipid peroxides at 5 min, 3 h, and 24 h post-exercise. The whey group showed the depression only at 24 h. In both the soy and whey groups, a small rise was seen for interleukin-8, which is consistent with the idea that the exercise session induced a moderate muscle stress. In summary, a moderate intensity, weight resistance exercise session, despite inducing mild inflammation, depressed plasma serum peroxide values, especially when combined with 4 weeks of soy consumption.
Andrea J. Braakhuis, Will G. Hopkins, and Timothy E. Lowe
The beneficial effects of exercise and a healthy diet are well documented in the general population but poorly understood in elite athletes. Previous research in subelite athletes suggests that regular training and an antioxidant-rich diet enhance antioxidant defenses but not performance.
To investigate whether habitual diet and/or exercise (training status or performance) affect antioxidant status in elite athletes.
Antioxidant blood biomarkers were assessed before and after a 30-min ergometer time trial in 28 male and 34 female rowers. The antioxidant blood biomarkers included ascorbic acid, uric acid, total antioxidant capacity (TAC), erythrocyte- superoxide dismutase, glutathione peroxidase (GPx), and catalase. Rowers completed a 7-d food diary and an antioxidant-intake questionnaire. Effects of diet, training, and performance on resting biomarkers were assessed with Pearson correlations, and their effect on exercise-induced changes in blood biomarkers was assessed by a method of standardization.
With the exception of GPx, there were small to moderate increases with exercise for all markers. Blood resting TAC had a small correlation with total antioxidant intake (correlation .29; 90% confidence limits, ±.27), and the exercise-induced change in TAC had a trivial to small association with dietary antioxidant intake from vitamin C (standardized effect .19; ±.22), vegetables (.20; ±.23), and vitamin A (.25; ±.27). Most other dietary intakes had trivial associations with antioxidant biomarkers. Years of training had a small inverse correlation with TAC (−.32; ±.19) and a small association with the exercise-induced change in TAC (.27; ±.24).
Training status correlates more strongly with antioxidant status than diet does.
Trent A. Watson, Lesley K. MacDonald-Wicks, and Manohar L. Garg
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.
Antoni Aguiló, Pere Tauler, Emilia Fuentespina, Gerardo Villa, Alfredo Córdova, Josep A. Tur, and Antoni Pons
The aim of this work was to check the effects of antioxidant supplementation (vitamins E and C, and β-carotene) on the basal iron status of athletes prior to and following their training and competition season (3 months).
Eighteen amateur trained male athletes were randomly distributed in 2 groups: placebo (lactose) and antioxidant supplemented (vitamin E, 500 mg/d; vitamin C, 1 g/d; and β-carotene, 30 mg/d). The study was double blind. Hematological parameters, dietary intake, physical activity intensity, antioxidant status (GSH/GSSG ratio), and basal iron status (serum iron, transferrin, ferritin, and iron saturation index) were determined before and after the intervention trials.
Exercise decreased antioxidant defenses in the placebo group but not in the antioxidant-supplemented group. No changes were found in the number of erythrocytes, hematocrit, or hemoglobin concentration, or in values of serum iron parameters, after taking the antioxidant cocktail for 3 months, in spite of the exercise completed. The placebo group showed a high oxidative stress index, and decreases in serum iron (24%) and iron saturation index (28%), which can neither be attributed to aspects of the athletes’ usual diet, nor to hemoconcentration.
Antioxidant supplementation prevents the decrease of serum iron and the iron saturation index, and a link between iron metabolism and oxidative stress may also be suggested.