DNA Damage After Exhaustive Treadmill Running in Trained and Untrained Men

Nieß, Andreas M.; Hartmann, Andreas; Grünert-Fuchs, M.; Poch, Bertram; Speit, Günter

doi:10.1055/s-2007-972868

Cited by 153 publications

(112 citation statements)

References 13 publications

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“…Endurance training can elevate antioxidant enzyme activities in erythrocytes (Miyazaki et al 2001). It also seems to be capable of reducing DNA damage in white blood cells after exhaustive exercise (Niess et al 1996), and strengthens GSH dependent tissue antioxidant defense by increasing cellular concentrations of GSH in skeletal muscles (Powers et al 1999;Sen 1999). However, we found no differences in GSH sea level values between our trained and sedentary subjects.…”

Section: Discussioncontrasting

confidence: 55%

Moderate altitude but not additional endurance training increases markers of oxidative stress in exhaled breath condensate

et al. 2009

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Oxidative stress occurs at altitude, and physical exertion might enhance this stress. In the present study, we investigated the combined effects of exercise and moderate altitude on redox balance in ten endurance exercising biathletes, and five sedentary volunteers during a 6 week stay at 2800 m. As a marker for oxidative stress, hydrogen peroxide (H 2 O 2 ) was analyzed by the biosensor measuring system Ecocheck TM , and 8-iso prostaglandin F2α (8-iso PGF2α) was determined by enzyme immunoassay in exhaled breath condensate (EBC). To determine the whole blood antioxidative capacity, we measured reduced glutathione (GSH) enzymatically using Ellman's reagent. Exercising athletes and sedentary volunteers showed increased levels of oxidative markers at moderate altitude, contrary to our expectations, there was no difference between both groups. Therefore, all subjects' data were pooled to examine the oxidative stress response exclusively due to altitude exposure. H 2 O 2 levels increased at altitude and remained elevated for 3 days after returning to sea level (p ≤ 0.05). On the other hand, 8-iso PGF2α levels showed a tendency to increase at altitude, but declined immediately after returning to sea level (p ≤ 0.001).Hypoxic exposure during the first day at altitude resulted in elevated GSH levels (p ≤ 0.05), that decreased during prolonged sojourn at altitude (p ≤ 0.001). In conclusion, a stay at moderate altitude for up to 6 weeks increases markers of oxidative stress in EBC independent of additional endurance training. Notably, this oxidative stress is still detectable 3 days upon return to sea level.

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Section: Discussioncontrasting

confidence: 55%

Moderate altitude but not additional endurance training increases markers of oxidative stress in exhaled breath condensate

et al. 2009

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“…Oxidative stress during exercise induces apoptosis of lymphocytes and the loss of cellularity of lymphoid tissues by generating ROS with consequent damage directly to DNA (33) or indirectly by rapid consumption of antioxidant defenses resulting in membrane lipid peroxidation (3). ROS production may also play a role in cell loss during exercise by affecting lymphocyte migration (39).…”

Section: Discussionmentioning

confidence: 99%

Adrenalectomy in mice does not prevent loss of intestinal lymphocytes after exercise

Hoffman‐Goetz

Quadrilatero

Boudreau

et al. 2004

Journal of Applied Physiology

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Exhaustive exercise is associated with an increase in circulating glucocorticoids (GCs), lymphocyte apoptosis, and a reduction in intestinal lymphocyte number. The present study examined the role of GCs on the numerical changes seen in intestinal lymphocytes after exercise. Female C57BL/6 mice were bilaterally adrenalectomized (ADX; n ϭ 18) or given sham surgery (Sham; n ϭ 18) and assigned to one of three exercise conditions: treadmill running (28 m/min, 90 min, 2°slope) and killed immediately or after 24 h recovery, or not exercised and killed immediately after 90-min exposure to the treadmill environment. Lymphocytes were isolated from the intestines with CD45 ϩ cells collected by positive selection using magnetic bead separation columns, and lymphocyte subpopulations were analyzed by flow cytometry for CD45 ϩ , CD3␣␤ ϩ , CD3␥␦ ϩ , CD8␤ ϩ , CD8␣ ϩ , CD4 ϩ , and NK ϩ phenotypic markers. ADX mice had significantly more intestinal CD45 ϩ leukocytes (P Ͻ 0.05) and CD3␣␤ ϩ (P Ͻ 0.05), CD3␥␦ ϩ (P Ͻ 0.01), CD8␣ ϩ (P Ͻ 0.001), and NK ϩ (P Ͻ 0.05) intestinal lymphocytes than Sham mice. There was a significant effect of exercise condition on total intestinal CD45 ϩ leukocytes (P Ͻ 0.01) and CD3␣␤ ϩ (P Ͻ 0.05), CD8␣ ϩ (P Ͻ 0.001), and CD4 ϩ (P Ͻ 0.05) intestinal lymphocytes, with fewer cells at 24 h postexercise compared with the other treatment conditions. There were no surgical ϫ exercise interaction effects on the CD3 and CD8 phenotype numbers. Plasma corticosterone was virtually nil in ADX mice regardless of exercise condition but was significantly elevated in Sham mice immediately postexercise (P Ͻ 0.001). The data indicate that ADX does not prevent the loss of lymphocytes from the intestinal mucosa 24 h after strenuous exercise and GCs are not directly causal in the leukopenia of exercise. treadmill running; adrenal glands; glucocorticoids NUMEROUS STUDIES HAVE SHOWN that acute exercise is associated with induction of apoptosis or programmed cell death and loss of lymphocytes from blood, thymus, and spleen in humans and laboratory animals (9,20,28,29). Lymphocyte loss and/or apoptosis have been observed in other situations characterized by extreme physiological stress, including burn injury (15), electrical shock (48), and chronic restraint stress (42), and may reflect release of stress hormones, in particular glucocorticoids (GCs). GCs trigger apoptosis in lymphocytes by acting on an intracellular pathway via the mitochondria (2), which results in the accumulation of mitochondrial derived cytochrome c within the cytosol, loss of mitochondrial membrane integrity, externalization of phosphatidylserine at cell membranes, and DNA fragmentation (27,45).The intestinal intraepithelial lymphocytes (IELs) are a unique population of T cells that function as a first line of defense against exogenous pathogens, many of which develop independently of the thymus gland [i.e., T cells with the ␥␦ form of the T cell receptor (TCR)] (35). IELs play an important role in protection from epithelial tumor cells through their function a...

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“…Similar findings were obtained during an 8 d long-distance-running training camp, but the levels in lymphocyte DNA were unchanged . Treadmill running to exhaustion produced more DNA damage, as measured by the comet assay, in untrained men compared with trained men (Niess et al 1996), and training after myocardial infarction abolished the pre-training increase in plasma H 2 O 2 concentration (Deskur et al 1998). The pattern from these observations appears to be quite consistent; immediately after exercise, irrespective of the intensity, there does not appear to be any signs of oxidative damage to DNA.…”

Section: Exercise Oxidative Dna Damage and Antioxidant Interventionmentioning

confidence: 77%

Methods to detect DNA damage by free radicals: relation to exercise

Poulsen

Weimann

Loft³

1999

Proc. Nutr. Soc.

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Abbreviations: EC, electrochemical detection; MS, mass spectrometry; 8-oxodG, 8-oxo-7,8-dihydro-2′-guanosine Epidemiological investigations repeatedly show decreased morbidity from regular exercise compared with sedentary life. A large number of investigations have demonstrated increased oxidation of important cellular macromolecules, whereas other investigators have found no effects or even signs of lowering of oxidation of macromolecules. In particular, extreme and longduration strenuous exercise appears to lead to deleterious oxidation of cellular macromolecules. The oxidation of DNA is important because the oxidative modifications of DNA bases, particularly the 8-hydroxylation of guanine, are mutagenic and have been implicated in a variety of diseases such as ageing and cancer. The methodologies for further investigation of the relationship between DNA oxidation and exercise are available. The preferred methods rely on HPLC or GC-mass spectrometry; whereas the theoretically-attractive liquid chromatographytandem mass spectrometry is being developed. Caution should be taken to avoid artifacts because of the six orders of magnitude of difference between oxidized and non-oxidized DNA bases in tissues. The methods can be used to estimate tissue levels, i.e. a local concentration of oxidized DNA, or to estimate the rate of body DNA oxidation by the urinary output of repair products, the latter being a method that is independent of repair. During exercise there appears to be a shifting of dietary-dependent antioxidant, e.g. vitamin C and vitamin E, from muscle to plasma, and an increased oxidation in plasma of these antioxidants. Supplementation trials with antioxidants have not been able to increase exercise performance; however, optimum nutrition with antioxidants and possibly supplementation, could be important in the prevention of diseases in the long term. The pattern from these observations appears to be quite consistent; immediately after exercise, regardless of how intense, there do not appear to be any signs of oxidative damage to DNA. Acute or prolonged moderate exercise does not produce signs of oxidative DNA damage and might even be associated with lowering of the levels of oxidation of tissue DNA; however, after long-duration and intense exercise an increase in oxidative DNA modifications is apparent. We suggest as a hypothesis that the relationship between exercise and health is U-shaped. This hypothesis needs to be tested in detail in order to establish the maximum beneficial exercise level with regard to oxidative DNA modification, and also the level that could be deleterious and might even increase the risk for cancer and other diseases.

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DNA Damage After Exhaustive Treadmill Running in Trained and Untrained Men

Cited by 153 publications

References 13 publications

Moderate altitude but not additional endurance training increases markers of oxidative stress in exhaled breath condensate

Moderate altitude but not additional endurance training increases markers of oxidative stress in exhaled breath condensate

Adrenalectomy in mice does not prevent loss of intestinal lymphocytes after exercise

Methods to detect DNA damage by free radicals: relation to exercise

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