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Inhibition of exercise-induced oxida...

Mastaloudis, Angela.

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Inhibition of exercise-induced oxidative stress, inflammation and muscle damage by prior supplementation with the antioxidant vitamins E and C.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Inhibition of exercise-induced oxidative stress, inflammation and muscle damage by prior supplementation with the antioxidant vitamins E and C./
作者:	Mastaloudis, Angela.
面頁冊數:	158 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-05, Section: B, page: 2350.
Contained By:	Dissertation Abstracts International65-05B.
標題:	Health Sciences, Nutrition. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3133396
ISBN:	9780496806362

Inhibition of exercise-induced oxidative stress, inflammation and muscle damage by prior supplementation with the antioxidant vitamins E and C.
Mastaloudis, Angela.

Inhibition of exercise-induced oxidative stress, inflammation and muscle damage by prior supplementation with the antioxidant vitamins E and C. - 158 p.

Source: Dissertation Abstracts International, Volume: 65-05, Section: B, page: 2350.

Thesis (Ph.D.)--Oregon State University, 2004.

To determine if 6 weeks prior supplementation with vitamins E and C could alleviate exercise-induced DNA damage, prevent lipid peroxidation and inflammation, slow the rate of vitamin E utilization and/or attenuate muscle damage, 22 subjects (11 females: 11 males) were studied during a 50 km (32 mile) ultramarathon. Subjects were randomly assigned to treatment groups: placebos (PL) or antioxidants (AO, vitamin E (300 mg RRR-alpha-tocopheryl acetate) and 1000 mg vitamin C (500 mg twice per day)). Subjects consumed deuterium-labeled vitamin E (75 mg d6-RRR-alpha-tocopheryl acetate) 48 h prior to race start. Multiple blood samples were obtained for measurements of DNA damage, unlabeled and labeled alpha-tocopherols and their metabolites, ascorbic acid, markers of lipid peroxidation (plasma F2-isoprostanes (F2-IsoPs)), inflammation and muscle damage. Maximal voluntary contraction (MVC) of the knee flexors/extensors was assessed. Plasma alpha-tocopheryl and ascorbic acid increased in the AO but not the PL group following 6 weeks of supplementation. All subjects completed the race; average run time 7.1 +/- 0.1 h. The run induced non-persistent DNA damage; % DNA damage increased at mid-race (p < 0.02), but returned to baseline by 2 h post-race. One day post-race, AO women had 62% less DNA damage than PL women (p < 0.0008). Although F2-ISOP levels were similar between groups at baseline, F2-IsoPs increased during the run only in the PL group (from 28 +/- 2 to 41 +/- 3 pg/ml). Markers of inflammation increased in response to the run regardless of treatment. alpha-Tocopherol disappeared faster during exercise compared with rest, in women compared with men and in AO supplemented compared with PL subjects. Substantial MVC force deficits and increases in muscle damage markers post-race were similar between treatment groups. The ultramarathon run elicited oxidative stress, muscle damage and inflammation.

ISBN: 9780496806362Subjects--Topical Terms:

1017801
Health Sciences, Nutrition.

Inhibition of exercise-induced oxidative stress, inflammation and muscle damage by prior supplementation with the antioxidant vitamins E and C.
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520 $a To determine if 6 weeks prior supplementation with vitamins E and C could alleviate exercise-induced DNA damage, prevent lipid peroxidation and inflammation, slow the rate of vitamin E utilization and/or attenuate muscle damage, 22 subjects (11 females: 11 males) were studied during a 50 km (32 mile) ultramarathon. Subjects were randomly assigned to treatment groups: placebos (PL) or antioxidants (AO, vitamin E (300 mg RRR-alpha-tocopheryl acetate) and 1000 mg vitamin C (500 mg twice per day)). Subjects consumed deuterium-labeled vitamin E (75 mg d6-RRR-alpha-tocopheryl acetate) 48 h prior to race start. Multiple blood samples were obtained for measurements of DNA damage, unlabeled and labeled alpha-tocopherols and their metabolites, ascorbic acid, markers of lipid peroxidation (plasma F2-isoprostanes (F2-IsoPs)), inflammation and muscle damage. Maximal voluntary contraction (MVC) of the knee flexors/extensors was assessed. Plasma alpha-tocopheryl and ascorbic acid increased in the AO but not the PL group following 6 weeks of supplementation. All subjects completed the race; average run time 7.1 +/- 0.1 h. The run induced non-persistent DNA damage; % DNA damage increased at mid-race (p < 0.02), but returned to baseline by 2 h post-race. One day post-race, AO women had 62% less DNA damage than PL women (p < 0.0008). Although F2-ISOP levels were similar between groups at baseline, F2-IsoPs increased during the run only in the PL group (from 28 +/- 2 to 41 +/- 3 pg/ml). Markers of inflammation increased in response to the run regardless of treatment. alpha-Tocopherol disappeared faster during exercise compared with rest, in women compared with men and in AO supplemented compared with PL subjects. Substantial MVC force deficits and increases in muscle damage markers post-race were similar between treatment groups. The ultramarathon run elicited oxidative stress, muscle damage and inflammation.
520 $a Supplementation with vitamins E and C completely inhibited exercise-induced lipid peroxidation and appeared to benefit women with respect to DNA damage during recovery, but had no effect on exercise-induced inflammation, or muscle damage markers. Thus, vitamin E and C supplements are beneficial in preventing lipid peroxidation, but not the other adverse consequences of extreme exercise.
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