Anaerobic Exercise and Oxidative Stress: A Review

2004 ◽  
Vol 29 (3) ◽  
pp. 245-263 ◽  
Author(s):  
Richard J. Bloomer ◽  
Allan H. Goldfarb
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Exercise Bout ◽  
Oxidative Modification ◽  
Anaerobic Exercise ◽  
Antioxidant Defenses ◽  
Protein Carbonyls ◽  
Anaerobic Work ◽  
Exercise Induced ◽  
And Oxidative Stress

Oxidative stress and subsequent damage to cellular proteins, lipids, and nucleic acids, as well as changes to the glutathione system, are well documented in response to aerobic exercise. However, far less information is available on anaerobic exercise-induced oxidative modifications. Recent evidence indicates that high intensity anaerobic work does result in oxidative modification to the above-mentioned macromolecules in both skeletal muscle and blood. Also, it appears that chronic anaerobic exercise training can induce adaptations that act to attenuate the exercise-induced oxidative stress. These may be specific to increased antioxidant defenses and/or may act to reduce the generation of pro-oxidants during and after exercise. However, a wide variety of exercise protocols and assay procedures have been used to study oxidative stress pertaining to anaerobic work. Therefore, precise conclusions about the exact extent and location of oxidative macromolecule damage, in addition to the adaptations resulting from chronic anaerobic exercise training, are difficult to indicate. This manuscript provides a review of anaerobic exercise and oxidative stress, presenting both the acute effects of a single exercise bout and the potential for adaptations resulting from chronic anaerobic training. Key words: antioxidants, free radicals, training, lipid peroxidation, protein carbonyls

Oxidants and antioxidants in exercise

1995 ◽  
Vol 79 (3) ◽  
pp. 675-686 ◽  
Author(s):  
C. K. Sen
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Exercise Training ◽  
Animal Studies ◽  
Dietary Habits ◽  
Antioxidant Defenses ◽  
Current State ◽  
Strenuous Physical Exercise ◽  
Long Duration ◽  
Exercise Induced

There is consistent evidence from human and animal studies that strenuous physical exercise may induce a state wherein the antioxidant defenses of several tissues are overwhelmed by excess reactive oxygen. A wide variety of physiological and dietary antioxidants act in concert to evade such a stress. Submaximal long-duration exercise training may augment the physiological antioxidant defenses in several tissues; however, this enhanced protection may not be sufficient to completely protect highly fit individuals from exhaustive exercise-induced oxidative stress. Regular physical activity in association with dietary habits that ensure adequate supply of a combination of appropriate antioxidants may be expected to yield desirable results. The significance of this area of research, current state of information, and possibilities of further investigation are briefly reviewed.

scholarly journals Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 485 ◽  
Author(s):  
Pereira-Maróstica ◽  
Castro ◽  
Gonçalves ◽  
Silva ◽  
Bracht ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Methyl Jasmonate ◽  
Lipid Peroxides ◽  
Mitochondrial Respiratory Chain ◽  
Antioxidant Defenses ◽  
Protein Carbonyls ◽  
Partial Recovery ◽  
Negative Effects ◽  
The Brain ◽  
And Oxidative Stress

Methyl jasmonate (MeJA), common in the plant kingdom, is capable of reducing articular and hepatic inflammation and oxidative stress in adjuvant-induced arthritic rats. This study investigated the actions of orally administered MeJA (75–300 mg/kg) on inflammation, oxidative stress and selected enzyme activities in the brain of Holtzman rats with adjuvant-induced arthritis. MeJA prevented the arthritis-induced increased levels of nitrites, nitrates, lipid peroxides, protein carbonyls and reactive oxygen species (ROS). It also prevented the enhanced activities of myeloperoxidase and xanthine oxidase. Conversely, the diminished catalase and superoxide dismutase activities and glutathione (GSH) levels caused by arthritis were totally or partially prevented. Furthermore, MeJA increased the activity of the mitochondrial isocitrate dehydrogenase, which helps to supply NADPH for the mitochondrial glutathione cycle, possibly contributing to the partial recovery of the GSH/oxidized glutathione (GSSG) ratio. These positive actions on the antioxidant defenses may counterbalance the effects of MeJA as enhancer of ROS production in the mitochondrial respiratory chain. A negative effect of MeJA is the detachment of hexokinase from the mitochondria, which can potentially impair glucose phosphorylation and metabolism. In overall terms, however, it can be concluded that MeJA attenuates to a considerable extent the negative effects caused by arthritis in terms of inflammation and oxidative stress.

Little change in markers of protein breakdown and oxidative stress in humans in immobilization-induced skeletal muscle atrophy

2010 ◽  
Vol 35 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Elisa I. Glover ◽  
Nobuo Yasuda ◽  
Mark A. Tarnopolsky ◽  
Arkan Abadi ◽  
Stuart M. Phillips
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Oxidative Modification ◽  
Skeletal Muscle Atrophy ◽  
Protein Carbonyls ◽  
Disuse Atrophy ◽  
Protein Breakdown ◽  
Protein Conjugates ◽  
Protein Ubiquitination ◽  
And Oxidative Stress

A number of studies in rodents suggest that disuse atrophy results from a large increase in proteolysis affected by, or accompanying, increased oxidative stress. Little information is available, however, about the effects of immobilization on markers of muscle protein breakdown and oxidative stress in humans. Therefore, the purpose of this investigation was to measure markers of breakdown or oxidative stress in subjects who underwent 14 days of knee-brace-mediated immobilization. Vastus lateralis samples taken from 21 young subjects before, and 2 days and 14 days after, single leg immobilization were measured for ubiquitin-protein conjugates, caspase 3/7 activity, the 14-kDa caspase-3 cleaved actin fragment, 4-hydroxy-2-nonenal (4-HNE) adducts, and protein carbonyls. Quadriceps cross-sectional area decreased by 5.7% ± 1.1% (p < 0.0001) following immobilization. Ubiquitin-protein conjugates were elevated at 2 days of immobilization (12%, p < 0.05) but were not different from baseline at 14 days. Levels of the 14-kDa actin fragment and caspase 3/7 activity did not change over the immobilization period. The oxidative stress markers, 4-HNE adducts and protein carbonyls, did not change at any time point. These static measures of breakdown and oxidative modification suggest that a small increase in protein ubiquitination occurs early (2 days), but elevations in ubiquitinated or oxidatively modified proteins are not sustained during the later phase (14 days) of uncomplicated disuse atrophy in humans, suggesting that these pathways are not playing a major role in simple disuse-induced atrophic loss of protein mass.

scholarly journals Cytokines and Oxidative Stress Status Following a Handball Game in Elite Male Players

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Douglas Popp Marin ◽  
Rita de Cassia Macedo dos Santos ◽  
Anaysa Paola Bolin ◽  
Beatriz Alves Guerra ◽  
Elaine Hatanaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant System ◽  
Stress Responses ◽  
Oxidative Modification ◽  
Protein Carbonyls ◽  
Antioxidant Enzyme Activities ◽  
Oxidative Stress Biomarkers ◽  
Damage Indices ◽  
Plasma Antioxidant Capacity ◽  
And Oxidative Stress

Background. Handball is considered an intermittent sport that places an important stress on a player's aerobic and anaerobic metabolism. However, the oxidative stress responses following a handball game remain unknown. We investigated the responses of plasma and erythrocyte antioxidant system and oxidative stress biomarkers following a single handball game.Methods. Fourteen male elite Brazilian handball athletes were recruited in the present study. Blood samples were taken before, immediately, and 24 hours after the game.Results. After the game and during 24 hours of recovery, the concentration of all oxidative stress indices changed significantly in a way indicating increased oxidative stress in the blood (thiol groups and reduced glutathione decreased, whereas TBARS and plasma antioxidant capacity was increased) as well as in erythrocyte (increased levels of TBARS and protein carbonyls). Erythrocyte antioxidant enzyme activities were also significantly changed by handball. Muscle damage indices (creatine kinase and lactate dehydrogenase) increased significantly after exercise. In addition, IL-6 increased after the game, whereas TNF-αdecreased during recovery.Conclusion. This study demonstrates that a single handball game in elite athletes induces a marked state of oxidative stress evidenced by the oxidative modification in plasma and erythrocyte macromolecules, as well as by changes in the enzymatic and nonenzymatic antioxidant system.

scholarly journals Oxidative Stress and Antioxidant Defense Mechanisms Linked to Exercise During Cardiopulmonary and Metabolic Disorders

2009 ◽  
Vol 2 (1) ◽  
pp. 43-51 ◽  
Author(s):  
Kelsey Fisher-Wellman ◽  
Heather K. Bell ◽  
Richard J. Bloomer
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Acute Exercise ◽  
Oxidant Stress ◽  
Anaerobic Exercise ◽  
Antioxidant Defenses ◽  
Subsequent Exposure ◽  
Disease Experience ◽  
Exercise Induced ◽  
Aerobic And Anaerobic

Oxidative stress has been implicated in the pathophysiology of multiple human diseases, in addition to the aging process. Although various stimuli exist, acute exercise is known to induce a transient increase in reactive oxygen and nitrogen species (RONS), evident by several reports of increased oxidative damage following acute bouts of aerobic and anaerobic exercise. Although the results are somewhat mixed and appear disease dependent, individuals with chronic disease experience an exacerbation in oxidative stress following acute exercise when compared to healthy individuals. However, this increased oxidant stress may serve as a necessary “signal” for the upregulation in antioxidant defenses, thereby providing protection against subsequent exposure to prooxidant environments within susceptible individuals. Here we present studies related to both acute exercise-induced oxidative stress in those with disease, in addition to studies focused on adaptations resulting from increased RONS exposure associated with chronic exercise training in persons with disease.

Effects of Antioxidant Supplementation and Exercise Training on Erythrocyte Antioxidant Enzymes

2006 ◽  
Vol 76 (5) ◽  
pp. 324-331 ◽  
Author(s):  
Marsh ◽  
Laursen ◽  
Coombes
Keyword(s):  
Antioxidant Enzymes ◽  
Exercise Training ◽  
Endurance Training ◽  
Young Male ◽  
Antioxidant Defenses ◽  
Antioxidant Enzyme Activities ◽  
Antioxidant Supplementation ◽  
Male Wistar Rats ◽  
Exercise Induced ◽  
Antioxidant Supplements

Erythrocytes transport oxygen to tissues and exercise-induced oxidative stress increases erythrocyte damage and turnover. Increased use of antioxidant supplements may alter protective erythrocyte antioxidant mechanisms during training. Aim of study: To examine the effects of antioxidant supplementation (α-lipoic acid and α-tocopherol) and/or endurance training on the antioxidant defenses of erythrocytes. Methods: Young male Wistar rats were assigned to (1) sedentary; (2) sedentary and antioxidant-supplemented; (3) endurance-trained; or (4) endurance-trained and antioxidant-supplemented groups for 14 weeks. Erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activities, and plasma malondialdehyde (MDA) were then measured. Results: Antioxidant supplementation had no significant effect (p > 0.05) on activities of antioxidant enzymes in sedentary animals. Similarly, endurance training alone also had no effect (p > 0.05). GPX (125.9 ± 2.8 vs. 121.5 ± 3.0 U.gHb–1, p < 0.05) and CAT (6.1 ± 0.2 vs. 5.6 ± 0.2 U.mgHb–1, p < 0.05) activities were increased in supplemented trained animals compared to non-supplemented sedentary animals whereas SOD (61.8 ± 4.3 vs. 52.0 ± 5.2 U.mgHb–1, p < 0.05) activity was decreased. Plasma MDA was not different among groups (p > 0.05). Conclusions: In a rat model, the combination of exercise training and antioxidant supplementation increased antioxidant enzyme activities (GPX, CAT) compared with each individual intervention.

Abstract 305: Nebivolol Confers Mitochondria-Targeted Cardioprotection in Isoproterenol-Induced Acute Stressor State

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Sumeet S Vaikunth ◽  
Karl T Weber ◽  
Syamal K Bhattacharya
Keyword(s):  
Oxidative Stress ◽  
Cardiac Tissue ◽  
Mitochondrial Permeability Transition ◽  
Therapeutic Potential ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Antioxidant Defenses ◽  
Sprague Dawley ◽  
Acute Stressor ◽  
And Oxidative Stress

Introduction: Isoproterenol-induced acute stressor state simulates injury from burns or trauma, and results in Ca 2+ overloading and oxidative stress in diverse tissues, including cardiac myocytes and their subsarcolemmal mitochondria (SSM), overwhelming endogenous Zn 2+ -based antioxidant defenses. We hypothesized that pretreatment with nebivolol (Nebi), having dual beta-1 antagonistic and novel beta-3 receptor agonistic properties, would prevent Ca 2+ overloading and oxidative stress and upregulate Zn 2+ -based antioxidant defenses, thus enhancing its overall cardioprotective potential in acute stressor state. Methods: Eight-week-old male Sprague-Dawley rats received a single subcutaneous dose of isoproterenol (1 mg/kg) and compared to those treated with Nebi (10 mg/kg by gavage) for 10 days prior to isoproterenol. SSM were harvested from cardiac tissue at sacrifice. Total Ca 2+ , Zn 2+ and 8-isoprostane levels in tissue, and mitochondrial permeability transition pore (mPTP) opening, free [Ca 2+ ] m and H 2 O 2 production in SSM were monitored. Untreated, age-/sex-matched rats served as controls; each group had six rats and data shown as mean±SEM. Results: Compared to controls, isoproterenol rats revealed: (1) Significantly (*p<0.05) increased cardiac tissue Ca 2+ (8.2±0.8 vs. 13.7±1.0*, nEq/mg fat-free dry tissue (FFDT)), which was abrogated ( # p<0.05) by Nebi (8.9±0.4 # ); (2) Reduced cardiac Zn 2+ (82.8±2.4 vs. 78.5±1.0*, ng/mg FFDT), but restored by Nebi (82.4±0.6 # ); (3) Two-fold rise in cardiac 8-isoprostane (111.4±13.7 vs. 232.1±17.2*, pmoles/mg protein), and negated by Nebi (122.3+14.5 # ); (4) Greater opening propensity for mPTP that diminished by Nebi; (5) Elevated [Ca 2+ ] m (88.8±2.5 vs. 161.5±1.0*, nM), but normalized by Nebi (93.3±2.7 # ); and (6) Increased H 2 O 2 production by SSM (97.4±5.3 vs. 142.8±7.0*, pmoles/mg protein/min), and nullified by Nebi (106.8±9.0 # ). Conclusions : Cardioprotection conferred by Nebi, a unique beta-blocker, prevented Ca 2+ overloading and oxidative stress in cardiac tissue and SSM, while simultaneously augmenting antioxidant capacity and promoting mPTP stability. Therapeutic potential of Nebi in patients with acute stressor states remains a provocative possibility that deserves to be explored.

Skeletal muscle adaptations to exercise are not influenced by metformin treatment in humans: secondary analyses of two randomised, clinical trials.

2021 ◽  
Author(s):  
Nanna Skytt Pilmark ◽  
Laura Oberholzer ◽  
Jens Frey Halling ◽  
Jonas M. Kristensen ◽  
Christina Pedersen Bønding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Metformin Treatment ◽  
Ampk Activation ◽  
Double Blind ◽  
Parallel Group ◽  
Exercise Induced

Metformin and exercise both improve glycemic control, but in vitro studies have indicated that an interaction between metformin and exercise occurs in skeletal muscle, suggesting a blunting effect of metformin on exercise training adaptations. Two studies (a double-blind, parallel-group, randomized clinical trial conducted in 29 glucose-intolerant individuals and a double-blind, cross-over trial conducted in 15 healthy lean males) were included in this paper. In both studies, the effect of acute exercise +/- metformin treatment on different skeletal muscle variables, previously suggested to be involved in a pharmaco-physiological interaction between metformin and exercise, was assessed. Furthermore, in the parallel-group trial, the effect of 12 weeks of exercise training was assessed. Skeletal muscle biopsies were obtained before and after acute exercise and 12 weeks of exercise training, and mitochondrial respiration, oxidative stress and AMPK activation was determined. Metformin did not significantly affect the effects of acute exercise or exercise training on mitochondrial respiration, oxidative stress or AMPK activation, indicating that the response to acute exercise and exercise training adaptations in skeletal muscle is not affected by metformin treatment. Further studies are needed to investigate whether an interaction between metformin and exercise is present in other tissues, e.g. the gut. Trial registration: ClinicalTrials.gov (NCT03316690 and NCT02951260). Novelty bullets • Metformin does not affect exercise-induced alterations in mitochondrial respiratory capacity in human skeletal muscle • Metformin does not affect exercise-induced alterations in systemic levels of oxidative stress nor emission of reactive oxygen species from human skeletal muscle • Metformin does not affect exercise-induced AMPK activation in human skeletal muscle

246 Effects of Feeding Thermally Processed Spray-dried Egg Whites on Growth Performance, Apparent Digestibility, and Oxidative Stress in Nursery Pigs

2021 ◽  
Vol 99 (Supplement_1) ◽  
pp. 91-92
Author(s):  
Victoria C Wilson ◽  
Brian J Kerr
Keyword(s):  
Oxidative Stress ◽  
Growth Performance ◽  
Liver Tissue ◽  
Protein Carbonyls ◽  
Nursery Pigs ◽  
Thermally Processed ◽  
Markers Of Oxidative Stress ◽  
Dietary Treatments ◽  
And Oxidative Stress ◽  
Spray Dried

Abstract The objectives of this study were to determine if feeding thermally processed (TP, heated at 100°C for 120 h) spray-dried egg whites (SDEW) to nursery pigs would impact growth performance, apparent total tract digestibility (ATTD) of GE, N, and S, and oxidative stress. Thirty-two barrows, (initial BW 7.1 kg) were randomly assigned to dietary treatments with 1 pig per pen. In a preliminary study, thermally processing SDEW at 100°C for 120 h increased protein carbonyls (PC) from 6 µmol/g to 19.4 µmol/g (P ≤ 0.01). Diets included either 12% SDEW, 6% TP-SDEW plus 6% SDEW, or 12% TP-SDEW. The experiment lasted 24 d for collection of growth performance data, while plasma was collected on d 21 and liver tissue harvested on d 24 to analyze for markers of oxidative stress. Feces were collected on d 22 for measures of ATTD. Daily gain, daily feed intake, feed efficiency, and ATTD of GE were not found to be different among dietary treatments (P ≥ 0.57). In contrast, ATTD of N (P = 0.11) and S (P = 0.03) were found to increase with increasing protein oxidation in the diet. There was no change in the plasma or liver F2-isoprostanes and 8-hydroxy-2’-deoxyguanosine among dietary treatments (P ≥ 0.28). An increase in plasma PC (P = 0.02) was observed in pigs fed 12% TP-SDEW compared to pigs fed 12% SDEW and pigs fed 6% TP-SDEW. In contrast, a decrease in liver tissue PC (P = 0.04) was observed in pigs fed 6% TP-SDEW compared to pigs fed 12% SDEW and 12% TP-SDEW. These results indicate that feeding TP-SDEW does not affect growth performance, ATTD of GE, and oxidative stress as indicated by F2-isoprostanes or 8-hydroxy-2’-deoxyguanosine; but appeared to have variable effects on oxidative stress as measured by PC.

scholarly journals Exercise Training Attenuates Sympathetic Activation and Oxidative Stress in Diet-Induced Obesity

2015 ◽  
pp. 355-367 ◽  
Author(s):  
G. LI ◽  
J.-Y. LIU ◽  
H.-X. ZHANG ◽  
Q. LI ◽  
S.-W. ZHANG
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Sympathetic Activity ◽  
The Body ◽  
Plasma Norepinephrine ◽  
Sympathetic Activation ◽  
Sprague Dawley ◽  
Tissue Mass ◽  
Diet Induced Obesity ◽  
And Oxidative Stress

It is known that excessive sympathetic activity and oxidative stress are enhanced in obesity. This study aimed to clarify whether exercise training (ET) attenuates sympathetic activation and oxidative stress in obesity. The obesity was induced by high-fat diet (HFD) for 12 weeks. Male Sprague-Dawley rats were assigned to four groups: regular diet (RD) plus sedentary (RD-S), RD plus ET (RD-ET), HFD plus sedentary (HFD-S), and HFD plus ET (HFD-ET). The rats in RD-ET and HFD-ET groups were trained on a motorized treadmill for 60 min/day, five days/week for 8 weeks. The sympathetic activity was evaluated by the plasma norepinephrine (NE) level. The superoxide anion, malondialdehyde and F2-isoprostanes levels in serum and muscles were measured to evaluate oxidative stress. The ET prevented the increases in the body weight, arterial pressure and white adipose tissue mass in HFD rats. The NE level in plasma and oxidative stress related parameters got lower in HFD-ET group compared with HFD-S group. We have found decreased mRNA and protein levels of toll-like receptor (TLR)-2 and TLR-4 by ET in HFD rats. These findings suggest that ET may be effective for attenuating sympathetic activation and oxidative stress in diet-induced obesity.

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