Antioxidant Status of Interval-Trained Athletes in Various Sports

Dekany, M.; Nemeskéri, V.; Györe, István; Harbula, I.; Malomsoki, J.; Pucsok, József Márton

doi:10.1055/s-2005-865634

Cited by 43 publications

(21 citation statements)

References 14 publications

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“…These findings are supported by previous literature, in particular with regards to higher oxidative stress in men compared to women [47] and in obese compared to overweight and/or normal weight subjects [48,49]. With regards to the antioxidant capacity in exercise-trained compared to untrained subjects, mixed results are available; some supporting our finding of lower antioxidant capacity in trained individuals [50] and some refuting this [51,52]. Those findings in support of our data may be linked to the acute increase in ROS experienced by exercise-trained individuals, which may partially deplete endogenous antioxidants over time [50].…”

Section: Discussionsupporting

confidence: 90%

A 21 day Daniel Fast improves selected biomarkers of antioxidant status and oxidative stress in men and women

et al. 2011

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BackgroundDietary modification via both caloric and nutrient restriction is associated with multiple health benefits, some of which are related to an improvement in antioxidant status and a decrease in the production of reactive oxygen species. The Daniel Fast is based on the Biblical book of Daniel, is commonly partaken for 21 days, and involves food intake in accordance with a stringent vegan diet. The purpose of the present study was to determine the effect of a 21 day Daniel Fast on biomarkers of antioxidant status and oxidative stress.Methods43 subjects (13 men; 30 women; 35 ± 1 yrs; range: 20-62 yrs) completed a 21 day Daniel Fast following the guidelines provided by investigators. Subjects reported to the lab in a 12 hour post-absorptive state both pre fast (day 1) and post fast (day 22). At each visit, blood was collected for determination of malondialdehyde (MDA), hydrogen peroxide (H2O2), nitrate/nitrite (NOx), Trolox Equivalent Antioxidant Capacity (TEAC), and Oxygen Radical Absorbance Capacity (ORAC). Subjects recorded dietary intake during the 7 day period immediately prior to the fast and during the final 7 days of the fast.ResultsA decrease was noted in MDA (0.66 ± 0.0.03 vs. 0.56 ± 0.02 μmol L-1; p = 0.004), while H2O2 demonstrated a trend for lowering (4.42 ± 0.32 vs. 3.78 ± 0.21 μmol L-1; p = 0.074). Both NOx (18.79 ± 1.92 vs. 26.97 ± 2.40 μmol L-1; p = 0.003) and TEAC (0.47 ± 0.01 vs. 0.51 ± 0.01 mmol L-1; p = 0.001) increased from pre to post fast, while ORAC was unchanged (5243 ± 103 vs. 5249 ± 183 μmol L-1 TE; p = 0.974). As expected, multiple differences in dietary intake were noted (p < 0.05), including a reduction in total calorie intake (2185 ± 94 vs. 1722 ± 85).ConclusionModification of dietary intake in accordance with the Daniel Fast is associated with an improvement in selected biomarkers of antioxidant status and oxidative stress, including metabolites of nitric oxide (i.e., NOx).

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Section: Discussionsupporting

confidence: 90%

A 21 day Daniel Fast improves selected biomarkers of antioxidant status and oxidative stress in men and women

et al. 2011

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“…This result is in contrast to literature reports on the effect of exhaustive effort in trained and untrained subjects: depending on the type of activity, both increased and decreased antioxidant enzyme activities and increased levels of DNA damage have been observed after strenuous effort, but this response was always less pronounced in well-trained athletes than in nonfit subjects (9,29,38).…”

Section: Discussioncontrasting

confidence: 56%

DNA damage after long-term repetitive hyperbaric oxygen exposure

Gröger¹,

Öter²,

Šimková³

et al. 2009

Journal of Applied Physiology

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Gröger M, Ö ter S, Simkova V, Bolten M, Koch A, Warninghoff V, Georgieff M, Muth CM, Speit G, Radermacher P. DNA damage after long-term repetitive hyperbaric oxygen exposure. J Appl Physiol 106: 311-315, 2009. First published November 20, 2008 doi:10.1152/japplphysiol.90737.2008.-A single exposure to hyperbaric oxygen (HBO), i.e., pure oxygen breathing at supra-atmospheric pressures, causes oxidative DNA damage in humans in vivo as well as in isolated lymphocytes of human volunteers. These DNA lesions, however, are rapidly repaired, and an adaptive protection is triggered against further oxidative stress caused by HBO exposure. Therefore, we tested the hypothesis that long-term repetitive exposure to HBO would modify the degree of DNA damage. Combat swimmers and underwater demolition team divers were investigated because their diving practice comprises repetitive long-term exposure to HBO over years. Nondiving volunteers with and without endurance training served as controls. In addition to the measurement of DNA damage in peripheral blood (comet assay), blood antioxidant enzyme activities, and the ratio of oxidized and reduced glutathione content, we assessed the DNA damage and superoxide anion radical (O2•Ϫ ) production induced by a single ex vivo HBO exposure of isolated lymphocytes. All parameters of oxidative stress and antioxidative capacity in vivo were comparable in the four different groups. Exposure to HBO increased both the level of DNA damage and O2•Ϫ production in lymphocytes, and this response was significantly more pronounced in the cells obtained from the combat swimmers than in all the other groups. However, in all groups, DNA damage was completely removed within 1 h. We conclude that, at least in healthy volunteers with endurance training, long-term repetitive exposure to HBO does not modify the basal blood antioxidant capacity or the basal level of DNA strand breaks. The increased ex vivo HBO-related DNA damage in isolated lymphocytes from these subjects, however, may reflect enhanced susceptibility to oxidative DNA damage. combat swimmers; underwater demolition team divers; endurance training; comet assay; superoxide radical; superoxide dismutase; catalase; glutathione peroxidase EXPOSURE TO HYPERBARIC OXYGEN (HBO), i.e., pure oxygen breathing at supra-atmospheric pressures, increases the formation of oxygen radical species (21, 27), which in turn results in consumption of antioxidants (2, 23) and reduces antioxidant enzyme activity (4), ultimately causing lipid peroxidation (3, 4, 26, 31), organ injury (5), and DNA damage (10, 11, 17, 20, 26, 32-37, 39 -42). On the other hand, HBO was reported to promote protective preconditioning against ischemia-reperfusion-induced oxidative organ injury in the brain, spinal cord, heart, and liver (16,28,45,46). Furthermore, in healthy volunteers, the HBO-induced DNA damage not only rapidly disappeared after the end of the HBO exposure, but a subsequent exposure did not cause oxidative DNA damage any more (10), indicating the induction of antioxidant de...

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“…Several studies showed a lower oxidative response in athletes than in controls both at rest and soon after M A N U S C R I P T A C C E P T E D ACCEPTED MANUSCRIPT 6 exercise, as malondialdehyde (MDA), protein carbonyls and 8-hydroxydeoxyguanosine resulted lower in trained compared with untrained subjects, while superoxide-dismutase (SOD) activity was higher in athletes compared to sedentary individuals [13,14]. Conversely, levels of antioxidant enzymes, such as catalase and glutathione-peroxidase, were higher than in sedentary subjects although these changes resulted sport-specific and related to the physical status and training level of athletes [15].…”

Section: Effects Of Exercise On Oxidative Stress and Healthmentioning

confidence: 84%