Endurance training attenuates exercise-induced oxidative stress in erythrocytes in rat

The aim of this study was to investigate whether endurance training reduces exercise-induced oxidative stress in erythrocytes. Male rats (n=54) were divided into trained (n=28) and untrained (n=26) groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h·day^–1, 5 days a week for 8 weeks, reaching the speed of 2.1 km·h^–1 at the fourth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km·h^–1 at the 95th min, 10% uphill, and was continued until exhaustion. Acute exhaustive exercise increased the erythrocyte malondialdehyde level in sedentary but not in trained rats compared with the corresponding sedentary rest and trained rest groups, respectively. While acute exhaustive exercise decreased the erythrocyte superoxide dismutase activity in sedentary rats, it increased the activity of this enzyme in trained rats. On the other hand, acute exhaustive exercise increased the erythrocyte glutathione peroxidase activity in sedentary rats; however, it did not affect this enzyme activity in trained rats. Erythrocyte glutathione peroxidase activity was higher in trained groups compared with untrained sedentary group. Neither acute exhaustive exercise nor treadmill training affected the erythrocyte total glutathione level. Treadmill training increased the endurance time in trained rats compared with sedentary rats. The results of this study suggest that endurance training may be useful to prevent acute exhaustive exercise-induced oxidative stress in erythrocytes by up-regulating some of the antioxidant enzyme activities and may have implications in exercising humans.     

Preventive effects of Spirulina platensis on skeletal muscle damage under exercise-induced oxidative stress

The effects of spirulina supplementation on preventing skeletal muscle damage on untrained human beings were examined. Sixteen students volunteered to take Spirulina platensis in addition to their normal diet for 3-weeks. Blood samples were taken after finishing the Bruce incremental treadmill exercise before and after treatment. The results showed that plasma concentrations of malondialdehyde (MDA) were significantly decreased after supplementation with spirulina (P < 0.05). The activity of blood superoxide dismutase (SOD) was significantly raised after supplementation with spirulina or soy protein (P < 0.05). Both of the blood glutathione peroxidaes (GP _x ) and lactate dehydrogenase (LDH) levels were significantly different between spirulina and soy protein supplementation by an ANCOVA analysis (P < 0.05). In addition, the lactate (LA) concentration was higher and the time to exhaustion (TE) was significantly extended in the spirulina trail (P < 0.05). These results suggest that ingestion of S. platensis showed preventive effect of the skeletal muscle damage and that probably led to postponement of the time of exhaustion during the all-out exercise.     

Exercise training decreases DNA damage and increases DNA repair and resistance against oxidative stress of proteins in aged rat skeletal muscle

Regular physical exercise retards a number of age-associated disorders, in spite of the paradox that free radical generation is significantly enhanced with exercise. Eight weeks of treadmill running resulted in nearly a 40% increase in maximal oxygen uptake in both middle-aged (20-month-old) and aged (30-month-old) rats. The age-associated increase in 8-hydroxy-2'-deoxyguanosine (8-OHdG) content was significantly attenuated in gastrocnemius muscle by exercise. The 8-OHdG repair, as measured by the excision of 32P-labeled damaged oligonucleotide, increased in muscle of exercising animals. The reactive carbonyl derivatives (RCD) of proteins did not increase with aging. However, when the muscle homogenate was exposed to a mixture of 1 mM iron sulfate and 50 mM ascorbic acid, the muscle of old control animals accumulated more RCD than that of the trained or adult groups. The chymotrypsin-like activity of proteasome complex increased in muscle of old trained rats. We suggest that regular exercise-induced adaptation attenuates the age-associated increase in 8-OHdG levels, and increases the activity of DNA repair and resistance against oxidative stress in proteins.     

The relationship between exercise-induced oxidative stress and the menstrual cycle

The purpose of this study was to investigate the relationship between exercise-induced oxidative stress and the menstrual cycle in healthy sedentary woman. Eighteen women with regular menstrual cycles participated in this research. The subjects monitored their basal body temperature (BBT) and carried out a urinary ovulation test (twice) for 2 months prior to the study to determine their menstrual cycle. The subjects performed bicycle ergometer exercise (for 30 min at 60% O_2max) in each phase (menses, follicular and luteal phases) of the menstrual cycle. Serum estradiol and progesterone concentrations were determined from blood that was collected at rest. Serum thiobarbituric acid reactive substances (TBARS), total superoxide dismutase (T-SOD) and extracellular superoxide dismutase (EC-SOD) were determined as markers of oxidative stress in blood samples collected at rest and after exercise. TBARS was significantly lower after exercise [2.4 (0.5) nmol/ml] in the follicular phase, and T-SOD was significantly lower after exercise [3.2 (1.2) U/ml] in the luteal phase. EC-SOD did not show a significant change after exercise during each phase of the menstrual cycle. Furthermore, there was a negative correlation between estradiol and T-SOD (r=–0.46, P<0.05) and between estradiol and EC-SOD (r=–0.55, P<0.05) during the menses. All data are presented as the mean value and its standard deviation.The results of this study suggest that when the estradiol level is high in a menstrual cycle, free radicals produced as a consequence of exercise may be easily eliminated by sedentary women with normal menstrual cycles.     

Serum vaspin concentrations are decreased after exercise-induced oxidative stress

Elevated visceral adipose tissue-derived serpin (vaspin) serum concentrations are associated with impaired insulin sensitivity, but increase unexpectedly after long-term physical training. We therefore investigated the effect of an acute exercise bout and the effects of vitamin supplementation on chronic exercise effect and on serum vaspin concentrations. We measured serum vaspin and thiobarbituric acid-reactive substances (TBARS) concentrations in 80 individuals before and after a 1-hour acute exercise bout and independently in 40 healthy young men who were randomly assigned to either antioxidant (vitamin C (1,000 mg/day) and vitamin E (400 IU/day)) or to no supplementation after a standardized 4-week physical training program as a post hoc analysis. Serum vaspin concentrations significantly decreased after acute physical exercise as well as after 4 weeks of training in individuals without antioxidants. Changes in vaspin serum concentration correlate with increased TBARS serum concentrations both in response to a 1-hour exercise bout (r = -0.42, p < 0.01) and to the 4-week training (r = -0.31, p < 0.05). Interestingly, supplementation with antioxidants rather increased circulating vaspin levels in response to 4 weeks of exercise. In conclusion, vaspin serum concentrations are decreased by exercise-induced oxidative stress, but not by exercise-associated improvement in insulin sensitivity.     

Acute immune response in respect to exercise-induced oxidative stress

The relationship between exhaustive exercise, oxidative stress, the protective capacity of the antioxidant defense system and cellular immune response has been determined. Exhaustive exercise in well-trained young men (n=19)-induced leukocytosis, decreased proportion of activated-lymphocyte subsets (CD4+ and CD8+) expressing CD69, decreased lymphocyte mitogenic response to concanavalin A (ConA) and phytohemagglutinin (PHA), increased lipid peroxidation, increased total antioxidant status (TAS) and catalase activity, immediately after exercise. Suppressed blood concentration of T-lymphocyte subsets (CD3+, CD4+, CD8+, NK), increased TAS and blood total glutathione (TGSH) in early recovery period (30 min after exercise) were found. Strong positive correlation was observed between TGSH and lymphocyte mitogenic response to ConA and PHA (r=0.85 and 0.85, respectively) immediately after exercise. Moderate positive correlation was observed between TAS and lymphocyte mitogenic response to PHA (r=0.59) immediately after exercise as well as between TAS and lymphocyte mitogenic response to PHA and ConA (r=0.69 and 0.54, respectively). Moderate to weak correlation was observed between TAS and conjugated dienes with exercise (r=0.66) as well as in 30-min recovery (r=0.50). After a short-term bout of exhaustive exercise, immune system was characterized by acute phase response, which was accompanied with oxidative stress. Suppression of the cellular immunity 30 min after exercise shows that this period is not enough for recovery after exhaustive exercise. The results suggest the interactions between exercise-induced oxidative stress and immune response.     

Etiology of exercise-induced muscle damage.

Muscle damage is caused by strenuous and unaccustomed exercise, especially exercise involving eccentric muscle contractions, where muscles lengthen as they exert force. Damage can be observed both directly at the cellular level and indirectly from changes in various indices of muscle function. Several mechanisms have been offered to explain the etiology of the damage/repair process, including mechanical factors such as tension and strain, disturbances in calcium homeostasis, the inflammatory response, and the synthesis of stress proteins (heat shock proteins). Changes in muscle function following eccentric exercise have been observed at the cellular level as an impairment in the amount and action of transport proteins for glucose and lactate/H+, and at the systems level as an increase in muscle stiffness and a prolonged loss in the muscle's ability to generate force. This paper will briefly review factors involved in the damage/repair process and alterations in muscle function following eccentric exercise.     

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

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 2,800 m. As a marker for oxidative stress, hydrogen peroxide (H₂O₂) was analyzed by the biosensor measuring system Ecocheck™, 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. H₂O₂ 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.

---

The contribution of Max Gassmann and Katja Heinicke who are the senior authors was equivalent.     

Proanthocyanidin prevents methotrexate-induced intestinal damage and oxidative stress

Mucositis is an important dose-limiting side effect of methotrexate for which there is no definitive prophylaxis or treatment. This study was designed to investigate whether proanthocyanidin had a protective effect on methotrexate-induced small intestine damage. Twenty-eight albino rats were randomized into four groups. To the first group, methotrexate was applied as a single dose (20 mg/kg) intraperitoneally. To the second group, proanthocyanidin (100 mg/kg) was given orally every day by gavage in addition to methotrexate application until the rats were killed. To the third group, only proanthocyanidin was administered. The fourth group was the control. All animals were sacrificed 4 days after the intraperitoneal injection of methotrexate for histopathological examination and the assay for tissue malondialdehyde, superoxide dismutase and glutathione peroxidase levels. Methotrexate caused jejunal injury and increased malondialdehyde levels. Administration of proanthocyanidin decreased the jejunal damage and malondialdehyde level, which were caused by methotrexate treatment and increased superoxide dismutase and glutathione peroxidase levels. These results suggest that proanthocyanidin may protect the small intestine of rats from methotrexate-induced damage. The effects of proanthocyanidin could result from its antioxidant properties.     

Oxygen radical absorbance capacity (ORAC) and exercise-induced oxidative stress in trotters

Strenuous exercise is a potent inducer of oxidative stress, which has been suggested to be associated with disturbances in muscle homeostasis, fatigue and injury. There is no comprehensive or uniform view of the antioxidant status in horses. We have previously shown that moderate exercise induces protein oxidation in trotters. The aim of this study was to measure the antioxidative capacity of the horse in relation to different antioxidant components and oxidative stress markers after a single bout of moderate exercise to elucidate the mechanisms of antioxidant protection in horses. Eight clinically normal and regularly trained standard-bred trotters were treadmill-exercised for 53 min at moderate intensity. Blood samples were collected prior to and immediately after exercise and at 4 and 24 h of recovery. Muscle biopsies from the middle gluteal muscle were taken before exercise and after 4 h of recovery. Acute induction of oxygen radical absorbance capacity (ORAC) did not prevent exercise-induced oxidative stress, which was demonstrated by increased lipid hydroperoxides (LPO). Pre-exercise ORAC levels were, however, a determinant of total glutathione content of the blood after 4 and 24 h of recovery. Furthermore, baseline ORAC level correlated negatively with 4-h recovery LPO levels. Our results imply that horses are susceptible to oxidative stress, but a stronger antioxidant capacity may improve coping with exercise-induced oxidative stress.     

Reduction of exercise-induced asthma oxidative stress by lycopene, a natural antioxidant

BACKGROUND: Lycopene has previously been shown to have high antioxidative activity. In view of the controversy regarding the beneficial effect of antioxidants on asthma, the acute effects of lycopene (LYC-O-MATO) on airway hyperreactivity were assessed in patients with exercise-induced asthma (EIA). METHODS: Twenty patients with EIA participated in our study to verify the antioxidative effects. The test was based on the following sequence: measurement of baseline pulmonary function, 7-min exercise session on a motorized treadmill, 8-min rest and again measurement of pulmonary function, 1-week, oral, randomly administered, double-blind supplementation of placebo or 30 mg/day of lycopene (LYC-O-MATO), measurement of pulmonary function at rest, 7-min exercise session, and 8-min rest and again measurement of pulmonary function. A 4-week washout interval was allowed between each protocol. RESULTS: All patients given placebo showed significant postexercise reduction of more than 15% in their forced expiratory volume in 1 s (FEV1). After receiving a daily dose of 30 mg of lycopene for 1 week, 11 (55%) patients were significantly protected against EIA. Serum analyses of the patients by high-pressure liquid chromatography detected in the lycopene-supplemented patients an elevated level of lycopene compared to the placebo group, with no change in retinol, tocopherols, or in the other carotenoids. CONCLUSIONS: Our results indicate that a daily dose of lycopene exerts a protective effect against EIA in some patients, most probably through an in vivo antioxidative effect.     

Estrogen and gender effects on muscle damage, inflammation, and oxidative stress.

Information suggests that there may be gender-based differences in skeletal muscle responses to damaging exercise. Evidence demonstrates that estrogen has strong antioxidant properties and may be an important factor in maintaining postexercise membrane stability and limiting creatine kinase (CK) leakage from damaged muscle in female animals. Research demonstrates effects of estrogen and possible gender differences in other morphological and biochemical indices of postexercise muscle damage and leukocyte invasion. Nevertheless, there are conflicting findings suggesting that in some in vivo exercise models, estrogen administration has limited ability to affect exercise-induced oxidative stress and muscle damage and may cause loss of tissue vitamin C. Gender differences appear to exist in tissue levels of other important antioxidants such as vitamin E and glutathione. More research is needed to fully define the potential for estrogen to influence postexercise muscle damage and the inflammatory response and to determine the mechanisms by which it may operate.     

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

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°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.     

Intensive swimming exercise-induced oxidative stress and reproductive dysfunction in male wistar rats: protective role of alpha-tocopherol succinate.

In the present study, 30 male rats (age 3 mos, Wt 128.6 +/- 3.7 g) were randomly divided into Control group (CG), Experimental group (EG), and Supplemented group (SG), 10 per group. An exercise protocol (3 hrs swimming per day, 5 days a week for 4 weeks) was followed in EG and SG, with no exercise in CG. In SG, alpha-tocopherol succinate was injected sub-cutaneously at a dose of 50 mg x kg(- 1) per body weight per day. After 4 weeks of exercise, significant diminutions (p < 0.05) were noted in somatic indices of testes and accessory sex organs; seminiferous tubuler diameter (STD); testicular (delta (5), 3 beta-hydroxysteroid dehydrogenase delta(5), 3 beta-HSD), 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activities; plasma levels of testosterone (T), luteinizing hormone (LH); preleptotine spermatocytes (pLSc), mid-pachytene spermatocytes (mPSc), and Stage 7 spermatids (7 Sd); testicular alpha-tocopherol and glutathione (GSH) content; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione-s-transferase (GST) activities in EG when compared to CG. Moreover, a significant elevation (p < 0.05) in malondialdehyde (MDA) was found in testes of EG compared to CG. No significant alteration was noted in body weight among the groups. Co-administration of alpha-tocopherol succinate restored the above parameters. Intensive swimming exercise-induced oxidative stress causes dysfunction in the male reproductive system, which can be protected by alpha-tocopherol succinate.     

Massage and ultrasound as therapeutic modalities in exercise-induced muscle damage.

Although both massage and ultrasound treatment are used in clinical settings to enhance muscle functional recovery following exercise-induced muscle damage, there is a paucity of experimental evidence for their efficacy. Theoretically both massage and ultrasound could affect some physiological factors associated with enhancement of postexercise muscle recovery. However, the actual physiological mechanisms by which massage or ultrasound could influence postexercise muscle damage and repair are unknown. Most experimental evidence suggests that massage has little influence on muscle blood flow, clearance of "noxious" substances, recovery of postexercise muscle strength, or delayed soreness sensation. However, more data is needed before conclusions can be drawn as to the ability of massage to influence postexercise inflammatory response or various other physiological changes that characterize exercise-induced muscle damage and repair. There is even less information on the ability of ultrasound to influence physiological or functional factors associated with postexercise muscle damage. The few experiments that have been done tend to be contradictory and have yet to consider the range of ultrasound treatment parameters for therapeutic effectiveness in treating postexercise damage and influencing repair processes. Much more research is needed to determine whether either treatment modality can have any therapeutic effect on exercise-induced muscle damage and recovery of postexercise muscle function.     

TEGDMA induces mitochondrial damage and oxidative stress in human gingival fibroblasts

Free monomers including triethylene glycol dimethacrylate (TEGDMA) are released by resin composite. Recent studies in vitro have demonstrated that TEGDMA induced GSH depletion and production of radical oxygen species (ROS) in human gingival fibroblasts (HGF) but the exact mechanism of these events remains unclear. Our purpose is to investigate the origin of ROS production. TEGDMA induces a rapid (within 30 min) and drastic depletion of ATP concomitant with the GSH depletion. After 3h incubation, TEGDMA induced an increase of lipid peroxidation associated with LDH leakage. Our data also showed that TEGDMA produced damage at mitochondrial level. This is demonstrated by the collapse of mitochondrial membrane potential (MMP) in HGF treated with TEGDMA. The protective effect of carbonylcyanide m-chlorophenylhydrazone (CCCP), an uncoupler of oxidative phosphorylation on lipid peroxidation and LDH leakage suggests that mitochondria can be implicated in these events. Trolox, a soluble derivative of Tocopherol, weakly prevents ATP but not GSH depletion and totally protects the cells against lipid peroxidation, MMP collapse and cell death. Thus, the present results suggest that TEGDMA induces lipid peroxidation and mitochondrial damage, which contribute to cell death.     

Clothianidin induces DNA damage and oxidative stress in bronchial epithelial cells

Clothianidin (CHN) is a member of the neonicotinoid group of insecticides. Its oxidative and DNA damage potential for human lung cells are not known. Therefore, the present study was designed to examine the effects of CHN on DNA damage and oxidative stress in human bronchial epithelial cells (BEAS-2B) treated with CHN for 24, 72, and 120 hr. Our results indicate that CHN decreased cell viability in a concentration-dependent manner. CHN induced DNA single-strand breaks because alkaline comet parameters such as tail intensity, DNA in the tail, tail moment, and tail length increased. All CHN concentrations also significantly induced the formation of DNA double-strand breaks (DSBs) because it increased phosphorylated H2AX protein foci for all treatment times and p53-binding protein 1 foci for all treatments except for the lowest concentration (0.15 mM) of 120-hr treatment. DNA damage caused by DNA DSBs was not repaired in a 24-hr recovery period. CHN also induced oxidative stress by decreasing reduced glutathione and increasing lipid peroxidation. These results make it necessary to conduct studies about the detailed carcinogenic potential of CHN in humans because it can induce both oxidative and DNA damage.