Influence of one bout of vigorous exercise on ascorbic acid in plasma and oxidative damage to DNA in blood cells and muscle in untrained rats

We investigated the influence of a single exhaustive bout of downhill running on oxidative damage to DNA and changes of antioxidant vitamin concentrations in rats. Plasma vitamin E levels were unchanged up to 48 hr postexercise. However, plasma ascorbic acid (AA) levels increased after the exercise, then decreased thereafter. This increase corresponded to a marked decrease in AA concentration in the adrenal glands. The activity of hepatic l-gulono-gamma-lactone oxidase, which catalyzes AA synthesis, was unaltered after the exercise. The weight of the adrenal glands was significantly increased 24 hr postexercise. These results indicate that the change in the plasma AA concentration after vigorous exercise was due mainly to the release of AA from the adrenal glands. The plasma creatine phosphokinase (CPK) activity and white blood cell (WBC) count increased 3 to 6 hr postexercise. Over this same period, a marker of oxidative DNA damage, 8-hydroxydeoxyguanosine in DNA, increased in the WBC, but not in the foreleg muscle. Lipid peroxide and vitamin E levels were also unchanged in the foreleg muscle. There was a positive correlation between CPK activity in the plasma and DNA damage in the WBC, suggesting that the DNA damage in the WBC was closely related with muscle damage due to exercise.     

Role of taurine supplementation to prevent exercise-induced oxidative stress in healthy young men

Summary. To evaluate the protective effects of taurine supplementation on exercise-induced oxidative stress and exercise performance, eleven men aged 18–20 years were selected to participate in two identical bicycle ergometer exercises until exhaustion. Single cell gel assay (SCG assay) was used to study DNA damage in white blood cells (WBC). Pre-supplementation of taurine, a significant negative correlation was found between plasma taurine concentration before exercise and plasma thiobaribituric-acid reactive substance (TBARS) 6hr after exercise (r=–0.642, p<0.05). WBC showed a significant increase in DNA strand breakage 6hr and 24hr after exercise. Seven-day taurine supplementation reduced serum TBARS before exercise (p<0.05) and resulted in a significantly reduced DNA migration 24hr after exercise (p<0.01). Significant increases were also found in VO₂max, exercise time to exhaustion and maximal workload in test with taurine supplementation (p<0.05). After supplementation, the change in taurine concentration showed positive correlations with the changes in exercise time to exhaustion and maximal workload. The results suggest that taurine may attenuate exercise-induced DNA damage and enhance the capacity of exercise due to its cellular protective properties.     

Effect of vitamin supplementation on cytokine response and on muscle damage after strenuous exercise

The present double-blinded, placebo-controlled study investigated whether antioxidant vitamin supplementation was able to modulate the cytokine and lymphocyte responses after strenuous eccentric exercise. Furthermore, muscle enzyme release was examined to see whether antioxidant treatment could reduce muscle damage. Twenty male recreational runners randomly received either antioxidants (500 mg of vitamin C and 400 mg of vitamin E) or placebo for 14 days before and 7 days after a 5% downhill 90-min treadmill run at 75% .VO(2 max). Although the supplemented group differed significantly with regard to plasma vitamin concentration before and after exercise when compared with the placebo group, the two groups showed identical exercise-induced changes in cytokine, muscle enzyme, and lymphocyte subpopulations. The plasma level of interleukin (IL)-6 and IL-1 receptor antagonist increased 20- and 3-fold after exercise. The plasma level of creatine kinase was increased sixfold the day after exercise. The concentrations of CD4+ memory T cells, CD8+ memory and na?ve T cells, and natural killer cells increased at the end of exercise. The total lymphocyte concentration was below prevalues in the postexercise period. In conclusion, the present study does not support the idea that exercise-induced inflammatory responses are induced by free oxygen radicals.     

Vitamin E inhibits protein oxidation in skeletal muscle of resting and exercised rats.

It is well known that exercise induces lipid peroxidation in skeletal muscle and that vitamin E prevents exercise-induced lipid damage. In this study we show for the first time, an increase in protein oxidation in skeletal muscle after a single bout of exercise, related to an exercise-induced decrease in lipophilic antioxidants, and substantial protection against both resting and exercise-induced protein oxidation by supplementation with various isomers (alpha-tocopherol, alpha-tocotrienol) of vitamin E.     

Exercise-induced lipid peroxidation and leakage of enzymes before and after vitamin E supplementation

1. The purpose of this study was to investigate the effects of vitamin E on serum levels of malondialdehyde following the acute exhaustive exercise in human, and to determine whether the magnitude of leakage of enzyme would be affected by vitamin E supplementation. 2. Increase of malondialdehyde after exercise before vitamin E supplementation was slight (but statistically significant), however after supplementation with vitamin E, malondialdehyde level after exercise was significantly decreased. 3. Leakage of enzyme was significantly increased after exercise before vitamin E supplementation, but it was lower following exercise after vitamin E supplementation. 4. Lipid peroxidation following a bout of acute heavy exercise can be inhibited by vitamin E supplementation.     

Role of vitamin C and E supplementation on IL-6 in response to training

Vitamin C and E supplementation has been shown to attenuate the acute exercise-induced increase in plasma interleukin-6 (IL-6) concentration. Here, we studied the effect of antioxidant vitamins on the regulation of IL-6 expression in muscle and the circulation in response to acute exercise before and after high-intensity endurance exercise training. Twenty-one young healthy men were allocated into either a vitamin (VT; vitamin C and E, n = 11) or a placebo (PL, n = 10) group. A 1-h acute bicycling exercise trial at 65% of maximal power output was performed before and after 12 wk of progressive endurance exercise training. In response to training, the acute exercise-induced IL-6 response was attenuated in PL (P < 0.02), but not in VT (P = 0.82). However, no clear difference between groups was observed (group × training: P = 0.13). Endurance exercise training also attenuated the acute exercise-induced increase in muscle-IL-6 mRNA in both groups. Oxidative stress, assessed by plasma protein carbonyls concentration, was overall higher in the VT compared with the PL group (group effect: P < 0.005). This was accompanied by a general increase in skeletal muscle mRNA expression of antioxidative enzymes, including catalase, copper-zinc superoxide dismutase, and glutathione peroxidase 1 mRNA expression in the VT group. However, skeletal muscle protein content of catalase, copper-zinc superoxide dismutase, or glutathione peroxidase 1 was not affected by training or supplementation. In conclusion, our results indicate that, although vitamin C and E supplementation may attenuate exercise-induced increases in plasma IL-6 there is no clear additive effect when combined with endurance training.     

Effect of antioxidant vitamin supplementation on muscle function after eccentric exercise

This study investigated the effects of antioxidant vitamin supplementation upon muscle contractile function following eccentric exercise and was performed double blind. Twenty-four physically active young subjects ingested either placebo (400 mg; n = 8), vitamin E (400 mg; n=8) or vitamin C (400 mg; n = 8) for 21 days prior to and for 7 days after performing 60 min of box-stepping exercise. Contractile function of the triceps surae was assessed by the measurement of maximal voluntary contraction (MVC) and the ratio of the force generated at 20 Hz and 50 Hz tetanic stimulation before and after eccentric exercise and for 7 days during recovery. Following eccentric exercise, MVC decreased to 75 (4) % [mean (SE); n = 24; P < 0.05] of the preexercise values and the 20/50 Hz ratio of tetanic tension from 0.76 (0.01) to 0.49 (0.03) [mean (SE); n = 24; P<0.05). Compared to the placebo group no significant changes in MVC were observed immediately post-exercise, though recovery of MVC in the first 24 h post-exercise was greater in the group supplemented with vitamin C. The decrease in 20/50 Hz ratio of tetanic tension was significantly less (P < 0.05) post-exercise and in the initial phase of recovery in subjects supplemented with vitamin C but not with vitamin E. These data suggest that prior vitamin C supplementation may exert a protective effect against eccentric exercise-induced muscle damage.     

Effect of vitamin E supplementation on post-exercise plasma lipid peroxidation and blood antioxidant status in smokers: with special reference to haemoconcentration effect

The oxidative effects were investigated of exhausting exercise in smokers, and the possible protective role of 400 mg day(-1) vitamin E (Vit E) supplementation over a period of 28 days. The subjects exercised to exhaustion including concentric-eccentric contractions following maximal cycling. The haematocrit and haemoglobin, leucocyte (WBC), plasma lactic acid (La) and malondialdehyde (MDA), erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx), serum Vit E and ceruloplasmin (CER) concentrations were measured pre and post exercise. Supplementation increased Vit E concentrations 28% and 31% in the controls and the smokers, respectively. Cigarette smoking and/or Vit E supplementation did not influence plasma lipid peroxidation or the antioxidant status at rest. Exercise caused significant haemoconcentration in all groups. When the post-exercise concentrations were adjusted for haemoconcentration, a significant elevation in La concentrations due to exercise was observed in all groups. Similarly, there were significant elevations in the adjusted WBC counts in all groups except the Vit E supplemented controls. The MDA concentrations on the other hand, when adjusted for haemoconcentration, did not exhibit any difference due to exercise. Exercise did not affect the GPx and CER activities either, while causing a SOD activity loss in all groups except the Vit E supplemented non-smokers. Serum Vit E concentrations diminished significantly in all groups after exercise. Post-exercise plasma MDA and blood antioxidant concentrations were not altered by smoking. The results would suggest that plasma volume changes should always be taken into account when assessing post-exercise plasma concentrations and that smoking and exercise do not have an additional collective effect on plasma lipid peroxidation and the dose of Vit E administered was insufficient to maintain the serum concentrations after exercise.     

Effect of vitamin E and eccentric exercise on selected biomarkers of oxidative stress in young and elderly men

Muscle damage resulting from eccentric exercise provides a useful model of oxyradical-induced injury and can be used to examine age-related responses to oxidative stress. Sixteen young (26.4 ± 3.3 years) and 16 older (71.1 ± 4.0 years) healthy men were randomly assigned to 1000 IU/d vitamin E or placebo for 12 weeks and ran downhill for 45 min at 75% VO₂max, once before and following supplementation. Blood samples were obtained before (baseline) and immediately postexercise (0 h), and at 6, 24, and 72 h postexercise to determine antioxidant status, muscle damage, lipid peroxidation, and DNA damage. Following exercise, young and older men experienced similar increases in serum creatine kinase (CK), F₂-isoprostanes (iPF₂; p < .001) and malondialdehyde (MDA; p < .01), although iPF₂ peaked at 72 h postexercise and MDA peaked at 0 h. Oxygen Radical Absorbance Capacity (ORAC) decreased at 72 h (p < .01) and correlated with the rise in iPF₂, MDA, and CK in the young men (p < .05). Leukocyte 8-hydroxy-2′-deoxyguanosine (8-OHdG) was unaffected by exercise. Vitamin E decreased peak CK in young men, while in older men it decreased resting levels of iPF₂ and suppressed the 24 h postexercise increases in iPF₂ (p < .05). Thus, vitamin E supplementation induced modest changes eccentric exercise-induced oxidative stress, although differentially between the young and older subjects, while age had no direct influence on these responses among this group of physically fit subjects.     

Ganoderma lucidum polysaccharides supplementation attenuates exercise-induced oxidative stress in skeletal muscle of mice

The present study was designed to determine the effects of Ganoderma lucidum polysaccharides (GL-PS) on exhaustive exercise-induced oxidative stress in skeletal muscle tissues of mice. The mice were divided into four groups (three GL-PS administered groups and the control group). The control group was administered with distilled water and GL-PS administered groups were administered with GL-PS (50, 100 and 200 mg/kg body weight per day). After 28 days, the mice performed an exhaustive swimming exercise, along with the determination of superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT) activities and malondialdehyde (MDA) levels in the skeletal muscle of mice. The results showed that GL-PS could increase antioxidant enzymes activities and decrease the MDA levels in the skeletal muscle of mice. This study provides strong evidence that GL-PS supplementation possessed protective effects against exhaustive exercise-induced oxidative stress.     

Effects of beta-hydroxy-beta-methylbutyrate on muscle damage after a prolonged run.

This study examined the effects of supplemental beta-hydroxy-beta-methylbutyrate (HMB) on muscle damage as a result of intense endurance exercise. Subjects (n = 13) were paired according to their 2-mile run times and past running experience. Each pair was randomly assigned a treatment of either HMB (3 g/day) or a placebo. After 6 wk of daily training and supplementation, all subjects participated in a prolonged run (20-km course). Creatine phosphokinase and lactate dehydrogenase (LDH) activities were measured before and after a prolonged run to assess muscle damage. The placebo-supplemented group exhibited a significantly greater (treatment main effect, P = 0.05) increase in creatine phosphokinase activity after a prolonged run than did the HMB-supplemented group. In addition, LDH activity was significantly lower (treatment main effect, P = 0.003) with HMB supplementation compared with the placebo-supplemented group. In conclusion, supplementation with 3.0 g of HMB results in a decreased creatine phosphokinase and LDH response after a prolonged run. These findings support the hypothesis that HMB supplementation helps prevent exercise-induced muscle damage.     

Effects of whole-body cryotherapy vs. far-infrared vs. passive modalities on recovery from exercise-induced muscle damage in highly-trained runners

Enhanced recovery following physical activity and exercise-induced muscle damage (EIMD) has become a priority for athletes. Consequently, a number of post-exercise recovery strategies are used, often without scientific evidence of their benefits. Within this framework, the purpose of this study was to test the efficacy of whole body cryotherapy (WBC), far infrared (FIR) or passive (PAS) modalities in hastening muscular recovery within the 48 hours after a simulated trail running race. In 3 non-adjoining weeks, 9 well-trained runners performed 3 repetitions of a simulated trail run on a motorized treadmill, designed to induce muscle damage. Immediately (post), post 24 h, and post 48 h after exercise, all participants tested three different recovery modalities (WBC, FIR, PAS) in a random order over the three separate weeks. Markers of muscle damage (maximal isometric muscle strength, plasma creatine kinase [CK] activity and perceived sensations [i.e. pain, tiredness, well-being]) were recorded before, immediately after (post), post 1 h, post 24 h, and post 48 h after exercise. In all testing sessions, the simulated 48 min trail run induced a similar, significant amount of muscle damage. Maximal muscle strength and perceived sensations were recovered after the first WBC session (post 1 h), while recovery took 24 h with FIR, and was not attained through the PAS recovery modality. No differences in plasma CK activity were recorded between conditions. Three WBC sessions performed within the 48 hours after a damaging running exercise accelerate recovery from EIMD to a greater extent than FIR or PAS modalities.     

Assessment of DNA strand breakage by the alkaline COMET assay in dialysis patients and the role of Vitamin E supplementation

Although the role of reactive oxygen species (ROS) in chronic renal failure (CRF) is not definitely demonstrated, a consistent number of observations has provided evidence for the presence of oxidative stress in uremic patients undergoing maintenance dialysis. In order to investigate this hypothesis further and to understand the role of antioxidant supplementation, peripheral blood lymphocytes were taken from 36 dialysis patients before and after Vitamin E supplementation in a dosage of 600 mg per day (2x300 mg) for 14 weeks and examined in the alkaline Comet assay for DNA strand breakage. The results were also compared with those of 36 controls with comparable age, sex, and smoking habits, and with no history of renal disease. The DNA breakage observed in the lymphocytes of patients before Vitamin E supplementation was significantly higher than in the controls (P<0.001) but a clear protective effect of Vitamin E supplementation were observed after 14 weeks of therapy.     

Effects of vitamin E supplementation on recovery from repeated bouts of resistance exercise

The purpose of this study was to examine the effects of vitamin E (VE) supplementation (1200 IU/day) on recovery responses to repeated bouts of resistance exercise. Non-resistance trained men were assigned to supplement with VE (n = 9) or placebo (PL; n = 9) for 3 weeks and then perform 3 resistance exercise sessions separated by 3 days of recovery (EX-1, EX-2, and EX-3). Performance was assessed at EX-1, EX-2, and EX-3. Fasting morning blood samples and perceived muscle soreness were obtained before EX-1 and for 10 consecutive days. Muscle soreness peaked after EX-1 and gradually returned to baseline values by day 6. Lower and upper body maximal strength and explosive power were significantly (p < or = 0.05) decreased at EX-2 and EX-3 (approximately 10%). Plasma malondialdehyde (MDA) was significantly elevated on days 7 and 8. There were no significant differences between VE and PL in muscle soreness, performance measures, or plasma MDA. Creatine kinase (CK) area under the curve from day 1 to day 10 was significantly greater for VE because of a nearly 2-fold greater increase in CK after EX-1 in VE, compared with PL (404 +/- 146 and 214 +/- 179 U/L, respectively). VE supplementation was not effective at attenuating putative markers of membrane damage, oxidative stress, and performance decrements after repeated bouts of whole-body concentric/eccentric resistance exercise.     

Dietary supplementation of Vitamin E protects heart tissue from exercise-induced oxidant stress

Exhaustive endurance exercise in adult female albino rats (C-Ex) increased the generation of free radicals (R ·) in the myocardium, probably through enhanced oxidative mechanisms. Free radical mediated lipid peroxidation measured in the form of tissue MDA content also increased in C-Ex animals, suggesting the exercise-induced oxidative stress in these animals. Dietary supplementation of Vit E, for a period of 60 days significantly increased Vit E incorporation into the serum and myocardium, more so in the myocardium. Vit E supplementation to exercising animals completely abolished the radical production. The protection of Vit E against oxidative stress appears to be not mediated through the improvement of antioxidant mechanisms by enzymes like SOD, catalase and Se-GSH Px. However the non Se-GSH Px, the enzyme involved in the reduction of endoperoxides increased significantly in control and Vit E fed animals in response to exercise. The protection of Vit E against exercise-induced oxidative stress was correlated with its multivarious activities like a) scavenger of free radicals; b) inhibition of lipoxygenases; and c) reduction of peroxides in association with lipoxygenases. These studies indicate that dietary supplementation of Vit E protects the animals from the possible oxidative damages of endurance exercise.     

Alpha-lipoic acid supplementation: tissue glutathione homeostasis at rest and after exercise.

Antioxidant nutrients have demonstrated potential in protecting against exercise-induced oxidative stress. alpha-Lipoic acid (LA) is a proglutathione dietary supplement that is known to strengthen the antioxidant network. We studied the effect of intragastric LA supplementation (150 mg/kg, 8 wk) on tissue LA levels, glutathione metabolism, and lipid peroxidation in rats at rest and after exhaustive treadmill exercise. LA supplementation increased the level of free LA in the red gastrocnemius muscle and increased total glutathione levels in the liver and blood. The exercise-induced decrease in heart glutathione S-transferase activity was prevented by LA supplementation. Exhaustive exercise significantly increased thiobarbituric acid-reactive substance levels in the liver and red gastrocnemius muscle. LA supplementation protected against oxidative lipid damage in the heart, liver, and red gastrocnemius muscle. This study reports that orally supplemented LA is able to favorably influence tissue antioxidant defenses and counteract lipid peroxidation at rest and in response to exercise.     

Increased lymphocyte antioxidant defences in response to exhaustive exercise do not prevent oxidative damage

It has been reported that exercise induces oxidative stress and causes adaptations in antioxidant defences. The aim of this study was to determine the adaptations of lymphocytes to the oxidative stress induced by an exhaustive exercise. Nine voluntary male subjects participated in the study. The exercise was a cycling mountain stage (171.8 km), and the cyclists took a mean of 283 min to complete it. Blood samples were taken the morning of the cycling stage day, after overnight fasting, and 3 h after finishing the stage. We determined the blood glutathione redox status (GSSG/GSH), lymphocyte antioxidant enzyme activities and superoxide dismutase (SOD) levels; the plasma and lymphocyte vitamin E levels; the serum lactate dehydrogenase (LDH) and creatine kinase (CK) activities and urate levels; the plasma carotene and malonaldehyde (MDA) levels; and the lymphocyte carbonyl index. The cycling stage induced significant increases in blood-oxidized (glutathione/GSSG), plasma MDA and serum urate levels. The exercise also produced increases in CK and LDH serum activities. The mountain cycling stage induced significant increases in lymphocyte vitamin E levels, glutathione peroxidase and glutathione reductase activities as well as increased SOD activity and protein levels. The protein carbonyl levels increased significantly in lymphocytes after the stage. In conclusion, in spite of increasing antioxidant defences in response to the oxidative stress induced by the exhaustive exercise, lymphocyte oxidative damage was produced after the stage as demonstrated by the increased carbonyl index even in very well trained athletes.     

Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes

Objectives: Physical exercise significantly impacts the biochemistry of the organism. Ubiquinone is a key component of the mitochondrial respiratory chain and ubiquinol, its reduced and active form, is an emerging molecule in sport nutrition. The aim of this study was to evaluate the effect of ubiquinol supplementation on biochemical and oxidative stress indexes after an intense bout of exercise.

Methods: 21 male young athletes (26?+?5 years of age) were randomized in two groups according to a double blind cross-over study, either supplemented with ubiquinol (200?mg/day) or placebo for 1 month. Blood was withdrawn before and after a single bout of intense exercise (40 min run at 85% maxHR). Physical performance, hematochemical parameters, ubiquinone/ubiquinol plasma content, intracellular reactive oxygen species (ROS) level, mitochondrial membrane depolarization, paraoxonase activity and oxidative DNA damage were analyzed.

Results: A single bout of intense exercise produced a significant increase in most hematochemical indexes, in particular CK and Mb while, on the contrary, normalized coenzyme Q₁₀ plasma content decreased significantly in all subjects. Ubiquinol supplementation prevented exercise-induced CoQ deprivation and decrease in paraoxonase activity. Moreover at a cellular level, in peripheral blood mononuclear cells, ubiquinol supplementation was associated with a significant decrease in cytosolic ROS while mitochondrial membrane potential and oxidative DNA damage remained unchanged.

Discussion: Data highlights a very rapid dynamic of CoQ depletion following intense exercise underlying an increased demand by the organism. Ubiquinol supplementation minimized exercise-induced depletion and enhanced plasma and cellular antioxidant levels but it was not able to improve physical performance indexes or markers of muscular damage.     

Assessment of DNA strand breakage by the alkaline COMET assay in dialysis patients and the role of Vitamin E supplementation

Although the role of reactive oxygen species (ROS) in chronic renal failure (CRF) is not definitely demonstrated, a consistent number of observations has provided evidence for the presence of oxidative stress in uremic patients undergoing maintenance dialysis. In order to investigate this hypothesis further and to understand the role of antioxidant supplementation, peripheral blood lymphocytes were taken from 36 dialysis patients before and after Vitamin E supplementation in a dosage of 600 mg per day (2×300 mg) for 14 weeks and examined in the alkaline Comet assay for DNA strand breakage. The results were also compared with those of 36 controls with comparable age, sex, and smoking habits, and with no history of renal disease. The DNA breakage observed in the lymphocytes of patients before Vitamin E supplementation was significantly higher than in the controls (P<0.001) but a clear protective effect of Vitamin E supplementation were observed after 14 weeks of therapy.     

NADPH氧化酶抑制剂apocynin对力竭运动大鼠运动性蛋白尿的影响

目的：研究NADPH氧化酶抑制剂apocynin对力竭运动大鼠运动性蛋白尿产生的影响及其机制。方法：32只SD雄性大鼠随机分为安静对照组（C组）、对照+药物组（CA组）、力竭运动组（E组）、力竭运动+药物组（EA组）。药物注射按10 mg/kg体重,每天一次,连续3 d,并在末次药物注射1 h后进行一次性跑台力竭运动。测定运动后尿UP、血液BUN水平、肾脏ROS浓度、NOS活性、NOS与3-NT蛋白含量。结果：结果显示,E组UP、肾脏ROS、iNOS含量及活性、3-NT明显升高,而EA组的这些指标与C组相比无显著性差异。结论：力竭运动可明显增加肾组织NADPH氧化酶活性,从而产生大量的ROS,后者可迅速地与由肾脏iNOS催化生成的NO反应,产生过量的ONOO^-,诱发运动性蛋白尿的生成。