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.

Antioxidant Supplementation and Adaptive Response to Training: A Systematic Review

2019 ◽  
Vol 25 (16) ◽  
pp. 1889-1912 ◽  
Author(s):  
Rosario Pastor ◽  
Josep A. Tur
Keyword(s):  
Antioxidant Enzymes ◽  
Cellular Response ◽  
Recovery Period ◽  
Chronic Administration ◽  
Antioxidant Response ◽  
Redox Status ◽  
Exercise Session ◽  
Acute Administration ◽  
Antioxidant Supplementation ◽  
Antioxidant Supplements

Background: Antioxidant supplementation has become a common practice among athletes to theoretically achieve a reduction in oxidative stress, promote recovery and improve performance. Objective: To assess the effect of antioxidant supplements on exercise. Methods: A systematic literature search was performed up to January 2019 in MEDLINE via EBSCO and Pubmed, and in Web of Sciences based on the following terms: “antioxidants” [Major] AND “exercise” AND “adaptation”; “antioxidant supplement” AND “(exercise or physical activity)” AND “(adaptation or adjustment)” [MesH]. Thirty-six articles were finally included. Results: Exhaustive exercise induces an antioxidant response in neutrophils through an increase in antioxidant enzymes, and antioxidant low-level supplementation does not block this adaptive cellular response. Supplementation with antioxidants appears to decrease oxidative damage blocking cell-signaling pathways associated with muscle hypertrophy. However, upregulation of endogenous antioxidant enzymes after resistance training is blocked by exogenous antioxidant supplementation. Supplementation with antioxidants does not affect the performance improvement induced by resistance exercise. The effects of antioxidant supplementation on physical performance and redox status may vary depending on baseline levels. Conclusion: The antioxidant response to exercise has two components: At the time of stress and adaptation through genetic modulation processes in front of persistent pro-oxidant situation. Acute administration of antioxidants immediately before or during an exercise session can have beneficial effects, such as a delay in the onset of fatigue and a reduction in the recovery period. Chronic administration of antioxidant supplements may impair exercise adaptations, and is only beneficial in subjects with low basal levels of antioxidants.

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 Analysis of cellular responses to free radicals: focus on exercise and skeletal muscle

1999 ◽  
Vol 58 (4) ◽  
pp. 1025-1033 ◽  
Author(s):  
Scott K. Powers ◽  
Shannon L. Lennon
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Endurance Training ◽  
Skeletal Muscles ◽  
Redox Status ◽  
Protective Mechanisms ◽  
Vitamins E And C ◽  
Exercise Induced ◽  
Enzymic Antioxidants ◽  
Β Carotene

Muscular exercise results in an increased production of radicals and other forms of reactive oxygen species (ROS). Recent evidence suggests that radicals and other ROS are an underlying aetiology in exercise-induced disturbances in muscle redox status. These exercise-induced redox disturbances in skeletal muscle are postulated to contribute to both muscle fatigue and/or exercise-induced muscle injury. To defend against ROS, muscle cells contain complex cellular defence mechanisms to reduce the risk of oxidative injury. Two major classes (enzymic and non-enzymic) of endogenous protective mechanisms work together to reduce the harmful effects of oxidants in the cell. Primary antioxidant enzymes include superoxide dismutase (EC 1.15.1.1; SOD), GSH peroxidase (EC 1.11.1.9; GPX), and catalase (EC 1.11.1.6); these enzymes are responsible for removing superoxide radicals, H2O2 and organic hydroperoxides, and H2O2 respectively. Important non-enzymic antioxidants include vitamins E and C, β-carotene, GSH and ubiquinones. Vitamin E, β-carotene and ubiquinone are located in lipid regions of the cell, whereas GSH and vitamin C are in aqueous compartments of the cell. Regular endurance training promotes an increase in both total SOD and GPX activity in actively-recruited skeletal muscles. High-intensity exercise training has been shown to be generally superior to low-intensity exercise in the upregulation of muscle SOD and GPX activities. Also, training-induced upregulation of antioxidant enzymes is limited to highly-oxidative skeletal muscles. The effects of endurance training on non-enzymic antioxidants remain a relatively uninvestigated area.

scholarly journals Effect of the Combination of Training and ERRα Inhibition on Liver Metabolism by Modulation of PDK4 and LXR-α Expression in STZ-Induced Diabetic and Healthy Rats

2020 ◽  
Vol 10 (6) ◽  
pp. 7011-7022 ◽  
Keyword(s):  
Exercise Training ◽  
Endurance Training ◽  
Dietary Habits ◽  
Metabolic Diseases ◽  
Life Quality ◽  
Public Health Problem ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Control Group ◽  
Male Wistar Rats

Diabetes is a public health problem that affects life quality. Exercise training (ET) and controlled dietary habits improve metabolic diseases such as diabetes. The mechanisms by which exercise training ameliorate metabolic diseases are not fully clear. We designed the current study to evaluate the combination of ERRα suppression and ET effects on the expression of LXR-α, PDK4, and PPARα in healthy and STZ-induced diabetic rats. Fifty-six male Wistar rats were divided into 8 groups (n = 7) as follows; control, diabetic control (a single dose of 45 mg/kg of STZ), ERRα inhibition group (received 0.48 mg/kg of XCT790), endurance training, diabetic rats which received XCT790, diabetic rats which performed endurance training, rats which received XCT790 and performed endurance training, and diabetic rats which received XCT790 and also performed endurance training. Expression of the target gene and protein was carried out on the liver tissue. Our results showed that ET significantly increased PDK4, PPARα, and ERRα expression. ERRα suppression significantly increased LXR-α and PDK4 expression in healthy rats compared to the healthy control group. In the diabetic group with ERRα suppression, LXR-α expression significantly upregulated. The combination of ET and ERRα suppression did not change LXR-α expression compared to healthy and diabetic groups (CTL/ERR), but the expression of PDK4, PPARα, and ERRα was significantly upregulated.

Training does not protect against exhaustive exercise-induced lactate transport capacity alterations

2000 ◽  
Vol 278 (6) ◽  
pp. E1045-E1052 ◽  
Author(s):  
Nicolas Eydoux ◽  
Guillaume Py ◽  
Karen Lambert ◽  
Hervé Dubouchaud ◽  
Christian Préfaut ◽  
...  
Keyword(s):  
Endurance Training ◽  
Exhaustive Exercise ◽  
Monocarboxylate Transporter ◽  
Transport Capacity ◽  
Lactate Transport ◽  
Monocarboxylate Transporter 1 ◽  
Saturation Properties ◽  
Apparent Loss ◽  
Male Wistar Rats ◽  
Exercise Induced

The effects of endurance training on lactate transport capacity remain controversial. This study examined whether endurance training 1) alters lactate transport capacity, 2) can protect against exhaustive exercise-induced lactate transport alteration, and 3) can modify heart and oxidative muscle monocarboxylate transporter 1 (MCT1) content. Forty male Wistar rats were divided into control (C), trained (T), exhaustively exercised (E), and trained and exercised (TE) groups. Rats in the T and TE groups ran on a treadmill (1 h/day, 5 days/wk at 25 m/min, 10% incline) for 5 wk; C and E were familiarized with the exercise task for 5 min/day. Before being killed, E and TE rats underwent exhaustive exercise (25 m/min, 10% grade), which lasted 80 and 204 min, respectively ( P < 0.05). Although lactate transport measurements (zero- trans) did not differ between groups C and T, both E and TE groups presented an apparent loss of protein saturation properties. In the trained groups, MCT1 content increased in soleus (+28% for T and +26% for TE; P < 0.05) and heart muscle (+36% for T and +33% for TE; P < 0.05). Moreover, despite the metabolic adaptations typically observed after endurance training, we also noted increased lipid peroxidation byproducts after exhaustive exercise. We concluded that 1) endurance training does not alter lactate transport capacity, 2) exhaustive exercise-induced lactate transport alteration is not prevented by training despite increased MCT1 content, and 3) exercise-induced oxidative stress may enhance the passive diffusion responsible for the apparent loss of saturation properties, possibly masking lactate transport regulation.

scholarly journals Short-term exercise training protects against doxorubicin-induced cardiac mitochondrial damage independent of HSP72

2010 ◽  
Vol 299 (5) ◽  
pp. H1515-H1524 ◽  
Author(s):  
Andreas N. Kavazis ◽  
Ashley J. Smuder ◽  
Kisuk Min ◽  
Nihal Tümer ◽  
Scott K. Powers
Keyword(s):  
Antioxidant Enzymes ◽  
Exercise Training ◽  
Cardiac Myocytes ◽  
Antitumor Agent ◽  
Mitochondrial Damage ◽  
Protein Abundance ◽  
Short Term ◽  
Cardiac Damage ◽  
Protease Activation ◽  
Exercise Induced

Doxorubicin (Dox) is an antitumor agent used in cancer treatment, but its clinical use is limited due to cardiotoxicity. Although exercise training can defend against Dox-mediated cardiac damage, the means for this cardioprotection remain unknown. To investigate the mechanism(s) responsible for exercise training-induced cardioprotection against Dox-mediated cardiotoxicity, we tested a two-pronged hypothesis: 1) exercise training protects against Dox-induced cardiotoxicity by preventing Dox-mediated mitochondrial damage/dysfunction and increased oxidative stress and 2) exercise training-induced cardiac expression of the inducible isoform of the 70-kDa heat shock protein 72 (HSP72) is essential to achieve exercise training-induced cardioprotection against Dox toxicity. Animals were randomly assigned to sedentary or exercise groups and paired with either placebo or Dox treatment (i.e., 20 mg/kg body wt ip Dox hydrochloride 24 h before euthanasia). Dox administration resulted in cardiac mitochondrial dysfunction, activation of proteases, and apoptosis. Exercise training increased cardiac antioxidant enzymes and HSP72 protein abundance and protected cardiac myocytes against Dox-induced mitochondrial damage, protease activation, and apoptosis. To determine whether exercise-induced expression of HSP72 in the heart is required for this cardioprotection, we utilized an innovative experimental strategy that successfully prevented exercise-induced increases in myocardial HSP72 levels. However, prevention of exercise-induced increases in myocardial HSP72 did not eliminate the exercise-induced cardioprotective phenotype that is resistant to Dox-mediated injury. Our results indicate that exercise training protects against the detrimental side effects of Dox in cardiac myocytes, in part, by protecting mitochondria against Dox-mediated damage. However, this exercise-induced cardioprotection is independent of myocardial HSP72 levels. Finally, our data are consistent with the concept that increases in cardiac mitochondrial antioxidant enzymes may contribute to exercise-induced cardioprotection.

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

Skeletal muscle oxidative capacity, antioxidant enzymes, and exercise training

1990 ◽  
Vol 68 (6) ◽  
pp. 2337-2343 ◽  
Author(s):  
M. H. Laughlin ◽  
T. Simpson ◽  
W. L. Sexton ◽  
O. R. Brown ◽  
J. K. Smith ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Exercise Training ◽  
Antioxidant Enzyme ◽  
Oxidative Capacity ◽  
Antioxidant Enzyme Activities ◽  
Sprague Dawley ◽  
Muscle Oxidative Capacity ◽  
Sprague Dawley Rats ◽  
The Relationship

The purposes of this study were to determine whether exercise training induces increases in skeletal muscle antioxidant enzymes and to further characterize the relationship between oxidative capacity and antioxidant enzyme levels in skeletal muscle. Male Sprague-Dawley rats were exercise trained (ET) on a treadmill 2 h/day at 32 m/min (8% incline) 5 days/wk or were cage confined (sedentary control, S) for 12 wk. In both S and ET rats, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) activities were directly correlated with the percentages of oxidative fibers in the six skeletal muscle samples studied. Muscles of ET rats had increased oxidative capacity and increased GPX activity compared with the same muscles of S rats. However, SOD activities were not different between ET and S rats, but CAT activities were lower in skeletal muscles of ET rats than in S rats. Exposure to 60 min of ischemia and 60 min of reperfusion (I/R) resulted in decreased GPX and increased CAT activities but had little or no effect on SOD activities in muscles from both S and ET rats. The I/R-induced increase in CAT activity was greater in muscles of ET than in muscles of S rats. Xanthine oxidase (XO), xanthine dehydrogenase (XD), and XO + XD activities after I/R were not related to muscle oxidative capacity and were similar in muscles of ET and S rats. It is concluded that although antioxidant enzyme activities are related to skeletal muscle oxidative capacity, the effects of exercise training on antioxidant enzymes in skeletal muscle cannot be predicted by measured changes in oxidative capacity.

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