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Hala Youssef, Carole Groussard, Sophie Lemoine-Morel, Christophe Jacob, Elie Moussa, Abdallah Fazah, Jean-Claude Pineau, Joel Pincemail, Josiane Cillard and Arlette Delamarche

This study aimed to determine whether aerobic training could reduce lipid peroxidation and inflammation at rest and after maximal exhaustive exercise in overweight/obese adolescent girls. Thirty-nine adolescent girls (14-19 years old) were classified as nonobese or overweight/obese and then randomly assigned to either the nontrained or trained group (12-week multivariate aerobic training program). Measurements at the beginning of the experiment and at 3 months consisted of body composition, aerobic fitness (VO2peak) and the following blood assays: pre- and postexercise lipid peroxidation (15F2a-isoprostanes [F2-Isop], lipid hydroperoxide [ROOH], oxidized LDL [ox-LDL]) and inflammation (myeloperoxidase [MPO]) markers. In the overweight/obese group, the training program significantly increased their fat-free mass (FFM) and decreased their percentage of fat mass (%FM) and hip circumference but did not modify their VO2peak. Conversely, in the nontrained overweight/obese group, weight and %FM increased, and VO2peak decreased, during the same period. Training also prevented exercise-induced lipid peroxidation and/or inflammation in overweight/obese girls (F2-Isop, ROOH, ox-LDL, MPO). In addition, in the trained overweight/obese group, exercise-induced changes in ROOH, ox-LDL and F2-Isop were correlated with improvements in anthropometric parameters (waist-to-hip ratio, %FM and FFM). In conclusion aerobic training increased tolerance to exercise-induced oxidative stress in overweight/obese adolescent girls partly as a result of improved body composition.

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Barry Braun, Priscilla M. Clarkson, Patty S. Freedson and Randall L. Kohl

The effects of dietary supplementation with Coenzyme Q10 (CoQlO), a reputed performance enhancer and antioxidant, on physiological and biochemical parameters were examined. Ten male bicycle racers performed graded cycle ergometry both before and after being given 100 mg per day CoQlO or placebo for 8 weeks. Analysis of variance showed a significant difference between groups for postsupplementation serum CoQ10. Although both groups demonstrated training related improvements in all physiological parameters over the course of the study, there were no significant differences between the two groups (p>.05). Both groups showed a 21 % increase in serum MDA (an index of lipid peroxidation) after the presupplementation exercise test. After 8 weeks this increase was only 5 % , and again was identical for both groups. Supplementation with CoQlO has no measurable effect on cycling performance, VO2max, submaximal physiological parameters, or lipid peroxidation. However, chronic intense training seems to result in marked attenuation of exercise-induced lipid peroxidation.

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Manfred Lamprecht, Peter Hofmann, Joachim F. Greilberger and Guenther Schwaberger

Purpose:

To assess the effects of an encapsulated antioxidant concentrate (EAC) and exercise on lipid peroxidation (LIPOX) and the plasma antioxidant enzyme glutathione peroxidase (Pl-GPx).

Methods:

Eight trained male cyclists (VO2max > 55 ml · kg−1 · min−1) participated in this randomized, placebo-controlled, double-blinded, crossover study and undertook 4 cycle-ergometer bouts: 2 moderate exercise bouts over 90 min at 45% of individual VO2max and 2 strenuous exercise bouts at 75% of individual VO2max for 30 min. The first 2 exercise tests—1 moderate and 1 strenuous—were conducted after 4 weeks wash-out and after 12 and 14 days of EAC (107 IU vitamin E, 450 mg vitamin C, 36 mg β-carotene, 100 μg selenium) or placebo treatment. After another 4 weeks wash-out, participants were given the opposite capsule treatment and repeated the 2 exercise tests. Physical exercise training was equal across the whole study period, and nutrition was standardized by a menu plan the week before the tests. Blood was collected before exercise, immediately postexercise, and 30 min and 60 min after each test. Plasma samples were analyzed for LIPOX marker malondialdehyde (MDA) and the antioxidant enzyme pl-GPx.

Results:

MDA concentrations were significantly increased after EAC supplementation at rest before exercise and after moderate exercise (p < .05). MDA concentrations showed no differences between treatments after strenuous exercise (p > .1). Pl-GPx concentrations decreased at all time points of measurement after EAC treatment (p < .05).

Conclusions:

The EAC induced an increase of LIPOX as indicated by MDA and decreased pl-GPx concentrations pre- and postexercise.

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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.

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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 Q10. The role (if any) that free radicals play in the development of exercise-induced tissue damage, or the protective role that antioxidants may play, remains to be elucidated. Current methods used to assess exercise-induced lipid peroxidation are not extremely specific or sensitive; research that utilizes more sophisticated methodologies should help to answer many questions regarding dietary antioxidants.

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Vitor Teixeira, Hugo Valente, Susana Casal, Franklim Marques and Pedro Moreira

Strenuous physical activity is known to generate reactive oxygen species to a point that can exceed the antioxidant defense system and lead to oxidative stress. Dietary intake of antioxidants, plasma enzymatic (superoxide dismutase, glutathione reductase [Gr], and glutathione peroxidase [GPx]) activities, nonenzymatic (total antioxidant status [TAS], uric acid, α-tocopherol, retinol, α-carotene, β-carotene, lycopene, and lutein + zeaxanthin) antioxidants, and markers of lipid peroxidation (thiobarbituricacid-reactive substances [TBARS]) and muscle damage (creatine kinase [CK]) were measured in 17 elite male kayakers and canoeists under resting conditions and in an equal number of age- and sex-matched sedentary individuals. Athletes showed increased plasma values of α-tocopherol (p = .037), α-carotene (p = .003), β-carotene (p = .007), and superoxide dismutase activity (p = .002) and a lower TAS level (p = .030). Antioxidant intake (α-tocopherol, vitamin C, and β-carotene) and plasmatic GPx, Gr, lycopene, lutein + zeaxanthin, retinol, and uric acid levels were similar in both groups. Nevertheless, TBARS (p < .001) and CK (p = .011) levels were found to be significantly higher in the kayakers and canoeists. This work suggests that despite the enhanced levels of antioxidants, athletes undergoing regular strenuous exercise exhibited more oxidative stress than sedentary controls.

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Hyun-Tae Kim

We investigated the effect of long-term treatment (6 wk) with selenium and vitamin E, in combination with aerobic exercise training, on malondialdehyde (MDA), oxidized low-density lipoprotein (ox-LDL), and glutathione peroxi-dase (GPx) in STZ-induced diabetic rats. The rats were assigned randomly to one of three treatment groups (n = 12 per group): 1) exercise group (EX), 2) selenium/vitamin E/exercise group (SVE), and 3) selenium/vitamin E group (SV). To estimate the acute effect of exercise, a 30-min endurance exercise was used. The MDA concentration was significantly lower in the SVE. The ox-LDL was significantly lower in the SVE and SV. The hepatic concentrations of selenium and vitamin E were significantly higher in the SVE. These results indicate that the increase in MDA is mildly attenuated in rats that were aerobically trained. Moreover, the joint administration of selenium and vitamin E with or without exercise training reduces the levels of ox-LDL.

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Andrew W. Subudhi, Scott L. Davis, Ronald W. Kipp and E. Wayne Askew

The goal of this field study was to assess antioxidant status and markers of oxidative damage in elite alpine ski racers during routine training. Subjects included 12 members of the U.S. Men’s Alpine Ski Team attending a 10-day summer training camp. Blood draws were collected at rest and after exercise: (a) prior to training, (b) following 2 days of dry land training, and (c) after 4 days of on-snow skiing. Seven measures of antioxidant status were determined using colorimetric and HPLC methods (Trolox “equivalent antioxidant capacity, uric acid, α-tocopherol, β-tocopherol, total glutathione, cytosolic glutathione peroxidase, and superoxide dismutase). Oxidative stress was assessed using 2 markers of lipid peroxidation (malondialdehyde and lipid hydroperoxides) and 2 markers of protein oxidation (carbonylated total proteins and carbonylated hemoglobin). The results of this study suggest that antioxidant status of elite alpine skiers may decline over a period of intense training. However, elevations in markers of oxidative stress were not evident.

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Kamal Azizbeigi, Mohammad Ali Azarbayjani, Maghsoud Peeri, Hamid Agha-alinejad and Stephen Stannard

This study was undertaken to investigate the effects of progressive resistance-training (PRT) on plasma oxidative stress and antioxidant enzyme activity in erythrocytes. Twenty male volunteers were randomly assigned to 2 groups: PRT and control. Blood samples were collected before and after 8 wk of PRT and analyzed for enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in erythrocytes, plasma total antioxidant capacity (TAC), and malondialdehyde concentration (MDA, an index of lipid per oxidation in plasma). Resistance training commenced with 8 exercises on nonconsecutive days for 8 wk at 50% of estimated 1-repetition maximum (E1RM) and reached 80% E1RM by Week 8. The results showed that PRT significantly increased erythrocyte SOD activity (1,323 ± 212.52 vs. 1,449.9 ± 173.8 U/g Hb, p = .014). Plasma concentration of MDA also decreased (5.39 ± 1.7 vs. 3.67.4 ± 0.7 nmol/ml, p = .030), although TAC (1.42 ± 0.21 vs. 1.61 ± 0.19 mmol/L, p = .1530) and GPx (39.87 ± 11.5 vs. 48.18 ± 14.48 U/g Hb, p = .883) activity did not undergo any considerable changes. Based on these data, the authors conclude that an 8-wk program of PRT strengthens the defensive system of erythrocytes against free-radical damage and therefore can be applied as a useful approach to alleviate oxidative stress.

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Kelsey H. Fisher-Wellman and Richard J. Bloomer

Background:

Carbohydrate powder in the form of maltodextrin is widely used by athletes for postexercise glycogen resynthesis. There is some concern that such a practice may be associated with a postprandial rise in reactive oxygen and nitrogen species production and subsequent oxidation of macromolecules. This is largely supported by findings of increased oxidative-stress biomarkers and associated endothelial dysfunction after intake of dextrose.

Purpose:

To compare the effects of isocaloric dextrose and maltodextrin meals on blood glucose, triglycerides (TAG), and oxidative-stress biomarkers in a sample of young healthy men.

Methods:

10 men consumed isocaloric dextrose and maltodextrin powder drinks (2.25 g/kg) in a random-order, crossover design. Blood samples were collected premeal (fasting) and at 1, 2, 4, and 6 hr postmeal and assayed for glucose, TAG, malondialdehyde, hydrogen peroxide, nitrate/nitrite, and Trolox-equivalent antioxidant capacity.

Results:

Significant meal effects were noted for glucose total area under the curve (p = .004), with values higher for the dextrose meal. No other statistically significant meal effects were noted (p > .05). With respect to the 2 (meal) × 5 (time) ANOVA, no significant interaction, time, or meal effects were noted for any variable (p > .05), with the exception of glucose, for which a main effect for both meal (p < .0001) and time (p = .0002) was noted.

Conclusions:

These data indicate that carbohydrate meals, consumed as either dextrose or maltodextrin, pose little postprandial oxidative insult to young, healthy men. As such, there should be minimal concern over such feedings, even at high dosages, assuming adequate glucose metabolism.