Oxygen radical generation of neutrophils: a reason for oxidative stress during marathon running?

Hessel, Elke; Haberland, Annekathrin; Müller, Maria; Lerche, D.; Schimke, Ingolf

doi:10.1016/s0009-8981(00)00295-3

Cited by 68 publications

(38 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The maintenance of high CK activities after recovery could be an indicator of muscle repair with neutrophil participation [14]. The APIR induced by the half marathon is not influenced by the antioxidant diet supplementation in accordance with other authors [39,40] Plasma is susceptible to suffering from oxidative damage after exhaustive exercise, increasing lipid peroxidation [41,42]. Several studies have evidenced that vitamin C and, especially, vitamin E supplementation reduces the increased rate of lipid peroxidation induced by exercise [13,14].…”

Section: Discussionsupporting

confidence: 70%

Antioxidant supplementation influences the neutrophil tocopherol associated protein expression, but not the inflammatory response to exercise

et al. 2007

View full text Add to dashboard Cite

Abstract:Intense exercise induces inflammatory-like changes and oxidative stress in immune cells. Our aim was to study the effects of antioxidant diet supplementation on the neutrophil inflammatory response and on the tocopherol associated protein (TAP) expression after exhaustive exercise. Fourteen male-trained amateur runners were randomly divided in two placebo and supplemented groups. Vitamins C (152 mg/d) and E (50 mg/d) supplementation were administrated to the athletes for a month, using an almond based isotonic and energetic beverage. Non-enriched beverage was given to the placebo group. After one month, the subjects participated in a half-marathon race (21 km-run). Neutrophil TAP mRNA expression and markers of the inflammatory response were determined before, immediately after, and 3 h after finishing the half-marathon race. TAP expression increased after exercise mainly in the neutrophils of the placebo group. Exercise induced an inflammatory response in both placebo and supplemented groups, manifested with neutrophilia, increased creatine kinase and lactate dehydrogenase serum activities, neutrophil luminol chemiluminescence and myeloperoxidase release. Plasma malondialdehyde only increased in the placebo group after exercise. Diet supplementation with moderate levels of antioxidant vitamins avoids plasma damage in response to exhaustive exercise without the effects on the inflammatory process. Neutrophil degranulation and increased tocopherol associated protein could contribute to the neutrophil protection from the oxidative stress.

show abstract

Section: Discussionsupporting

confidence: 70%

Antioxidant supplementation influences the neutrophil tocopherol associated protein expression, but not the inflammatory response to exercise

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Whether this is a characteristic change over the time course of this enzymatic activity post-exercise or a measure of oxidant response requires further investigation. The significantly increased blood GSH in humans following exercise is considered to be part of a self-protecting mechanism against exercise-induced oxidative stress (Hessel et al 2000;Ji et al 1993). GSH acts as a substrate for glutathione peroxidase in peroxidase ROS inhibition, and directly detoxifies ROS, thereby enhancing the functional antioxidant capacity of vitamins C and E (Finaud et al 2006).…”

Section: Early Recovery Periodmentioning

confidence: 99%

Serum oxidant and antioxidant status during early and late recovery periods following an all-out 21-km run in trained adolescent runners

et al. 2010

View full text Add to dashboard Cite

It is well documented that intense exercise precipitates oxidative stress in adults. However, there is lack of related studies concerning oxidant and antioxidant status during early and late recovery periods in adolescent athletes, following endurance exercise in particular. This study investigated aspects of the serum oxidant and antioxidant status of 12 male adolescent (16.2 ± 0.6 years) trained runners during early and late recovery periods after an all-out 21-km run. Venous blood samples were taken immediately before, 2 and 4 h following (early recovery period), and 24 h following (late recovery period) the 21-km run. Samples were analyzed for serum concentrations of thiobarbituric acid-reactive substances (TBARS), uric acid (UA), reduced glutathione (GSH), and enzymatic activity of xanthine oxidase (XO), superoxide dismutase (SOD), and catalase (CAT). During the early recovery period, there were increases in the 4-h GSH (194.8 ± 10.4 vs. 211.8 ± 11.4 mg l(-1), P < 0.05), 2- and 4-h UA (307.8 ± 68.6 vs. 327.4 ± 63.8; 330.2 ± 65.1 μmol l(-1), P < 0.05), and 2-h CAT (2.05 ± 0.44 vs. 3.07 ± 0.51 U ml(-1), P < 0.05), and decreases in the 2-h XO (11.1 ± 1.5 vs. 10.3 ± 1.2 U l(-1), P < 0.05) compared to the corresponding pre-exercise level, respectively. No change was observed in SOD (P > 0.05). At the late recovery period, there was an increase in CAT (2.80 ± 0.49 U ml(-1), P < 0.05) and TBARS (2.99 ± 0.83 vs. 4.40 ± 1.38 nmol ml(-1), P < 0.05). These data indicate that although the antioxidant capacity of adolescent runners is augmented during the early recovery period following the 21-km run, they were not completely protected from oxidative stress during the later recovery period.

show abstract

“…During running training, ROS production has been attributed to high oxygen consumption, which may reach 10-20 times the systemic levels (Astrand et al 1986) and as much as 100-200 times the skeletal muscle levels (Halliwell and Gutteridge 2007), resulting in substantially increased mitochondrial electron Xux. Research in humans suggests that intense exercise is associated with accelerated oxygen radical generation that results in acute Sureda et al 2005) and chronic (Hessel et al 2000;Tsai et al 2001) blood oxidation.…”

Section: Introductionmentioning

confidence: 99%

Physical exercise increases mitochondrial function and reduces oxidative damage in skeletal muscle

et al. 2009

View full text Add to dashboard Cite

The present study investigated mitochondrial adaptations and oxidative damage after 4 and 8 weeks of running training in skeletal muscle of mice. Twenty-one male mice (CF1, 30-35 g) were distributed into the following groups (n = 7): untrained (UT); trained-4 weeks (T4); trained-8 weeks (T8). Forty-eight hours after the last training session the animals were killed by decapitation and quadriceps (red portion) were removed and stored at -70 degrees C. Succinate dehydrogenase (SDH), complexes I, II, II-III and IV, lipoperoxidation (TBARS), protein carbonyls (PC) and total thiol content were measured. Results show that endurance training (8-wk) increases the SDH activity and complexes (I, II, III, IV), decreases oxidative damage (TBARS, CP) and increases total thiol content in skeletal muscle when compared to untrained animals. In conclusion, eight weeks of running training are necessary for increases in mitochondrial respiratory chain enzyme activities to occur, in association with decreased oxidative damage.

show abstract

Oxygen radical generation of neutrophils: a reason for oxidative stress during marathon running?

Cited by 68 publications

References 24 publications

Antioxidant supplementation influences the neutrophil tocopherol associated protein expression, but not the inflammatory response to exercise

Antioxidant supplementation influences the neutrophil tocopherol associated protein expression, but not the inflammatory response to exercise

Serum oxidant and antioxidant status during early and late recovery periods following an all-out 21-km run in trained adolescent runners

Physical exercise increases mitochondrial function and reduces oxidative damage in skeletal muscle

Contact Info

Product

Resources

About