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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 ${\text{Q}}_{10}$ . 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.

Elemental and gaseous oxygen presents a conundrum in that it is simultaneously essential for and potentially destructive to human life. Traditionally the ability to consume large volumes of oxygen has been assumed to be totally beneficial to the organism. In the past 10 years it has become clear that oxygen radicals are generated even during normal resting metabolism Nevertheless, such radicals are usually of no appreciable threat since a wide array of protective biochemical systems exist. However, under certain circumstances aerobic exercise may increase free radical production to a level that overwhelms those defenses. A broad array of nutrients such as vitamin C, vitamin E, p-carotene, and so forth are known to suppress such radical events. This paper reviews the status of our knowledge relative to the potential benefits of nutritional modification in augmenting the organism's normal defense against harmful radical chemistry.

The purpose of this investigation was to determine the effects of antioxidant supplementation on DNA damage following exercise. Fourteen subjects were randomly assigned to one of two groups and required to ingest either antioxidants (400 mg α-lipoic acid, 200 mg co-enzyme Q10, 12 mg manganese, 600 mg vitamin C, 800 mg N-acetyl cysteine, 400 μg selenium, and 400 IU α-tocopherol per day) or placebos for 7 d. Exercise increased DNA damage, PS, FRAP, and LDH (P < 0.05), but not selectively between groups. LDH and PS concentration decreased 1 h post-exercise (P < 0.05), while LH concentration decreased 1 h post-exercise in the antioxidant group only (P < 0.05). The antioxidant group had a higher concentration of LH (P < 0.05), perhaps due to a selective difference between groups post-exercise (P < 0.05). The main findings of this investigation demonstrate that exhaustive aerobic exercise induces DNA damage, while anti-oxidant supplementation does not protect against damage.

We investigated whether 6 wk of antioxidant supplementation (AS) would enhance 30 km time trial (TT) cycling performance. Eleven elite male cyclists completed a randomized, double-blind, cross-over study to test the effects of twice daily AS containing essential vitamins plus quercetin (FRS), and AS minus quercetin (FRS-Q) versus a baseline TT (B). MANOVA analysis showed that time to complete the 30 km TT was improved by 3.1% on FRS compared to B (P ≤ 0.01), and by 2% over the last 5 km (P ≤ 0.05). Absolute and relative (%HR_max) heart rates and percent VO_2max were not different between trials, but average and relative power (% peak power) was higher on FRS (P ≤ 0.01). Rates of carbohydrate and fat oxidation were not different between trials. Thus, FRS supplementation significantly improved high-intensity cycling TT performance through enhancement of power output. Further study is needed to determine the potential mechanism(s) of the antioxidant efficacy.

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.

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, VO_2max = 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% W_max, 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.

High-kilocalorie feedings induce oxidative stress. Acute exercise has the potential to attenuate postprandial oxidative stress. No study has determined whether there are racial differences in postprandial oxidative stress with and without a preceding bout of acute exercise.