scholarly journals Dietary Supplementation with the MicroalgaGaldieria sulphuraria(Rhodophyta) Reduces Prolonged Exercise-Induced Oxidative Stress in Rat Tissues

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Simona Carfagna ◽  
Gaetana Napolitano ◽  
Daniela Barone ◽  
Gabriele Pinto ◽  
Antonino Pollio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Acute Exercise ◽  
Ischemia Reperfusion ◽  
Dietary Supplementation ◽  
Peroxyl Radicals ◽  
Antioxidant Enzyme Activities ◽  
Rat Tissues ◽  
Lipid Hydroperoxides ◽  
Exercise Induced

We studied the effects of ten-day 1%Galdieria sulphurariadietary supplementation on oxidative damage and metabolic changes elicited by acute exercise (6-hour swimming) determining oxygen consumption, lipid hydroperoxides, protein bound carbonyls in rat tissue (liver, heart, and muscle) homogenates and mitochondria, tissue glutathione peroxidase and glutathione reductase activities, glutathione content, and rates of H2O2mitochondrial release. Exercise increased oxidative damage in tissues and mitochondria and decreased tissue content of reduced glutathione. Moreover, it increased State 4 and decreased State 3 respiration in tissues and mitochondria.G. sulphurariasupplementation reduced the above exercise-induced variations. Conversely, alga supplementation was not able to modify the exercise-induced increase in mitochondrial release rate of hydrogen peroxide and in liver and heart antioxidant enzyme activities. The alga capacity to reduce lipid oxidative damage without reducing mitochondrial H2O2release can be due to its high content of C-phycocyanin and glutathione, which are able to scavenge peroxyl radicals and contribute to phospholipid hydroperoxide metabolism, respectively. In conclusion,G. sulphurariaability to reduce exercise-linked oxidative damage and mitochondrial dysfunction makes it potentially useful even in other conditions leading to oxidative stress, including hyperthyroidism, chronic inflammation, and ischemia/reperfusion.

Intermittent hypoxic training: implications for lipid peroxidation induced by acute normoxic exercise in active men

2001 ◽  
Vol 101 (5) ◽  
pp. 465-475 ◽  
Author(s):  
Damian M. BAILEY ◽  
Bruce DAVIES ◽  
Ian S. YOUNG
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Acute Exercise ◽  
Mass Action ◽  
Lipid Hydroperoxides ◽  
Double Blind ◽  
Intermittent Hypoxic Training ◽  
Hypoxic Conditions ◽  
Hypoxic Training ◽  
Exercise Induced

Oxidant generation during regular physical exercise training may influence the adaptive responses that have been shown to confer protection against oxidative stress induced by subsequent acute exercise. To examine this, we randomly assigned 32 males to either a normoxic (n = 14) or a hypoxic (n = 18) group. During the acute phase, subjects in the hypoxic group performed two maximal cycling tests in a randomized double-blind fashion: one under conditions of normoxia and the other under hypoxic conditions (inspired fraction of O2 = 0.21 and 0.16 respectively). During the intermittent phase, the normoxic and hypoxic groups each trained for 4 weeks at the same relative exercise intensity, under conditions of normoxia and hypoxia respectively. During acute exercise under hypoxic conditions, the venous concentrations of lipid hydroperoxides and malondialdehyde were increased, despite a comparatively lower maximal oxygen uptake (o2max) (P < 0.05 compared with normoxia). The increases in lipid hydroperoxides and malondialdehyde were correlated with the exercise-induced decrease in arterial haemoglobin oxygen saturation (r =-0.61 and r =-0.50 respectively; P < 0.05), but not with o2max. Intermittent hypoxic training attenuated the increases in lipid hydroperoxides and malondialdehyde induced by acute normoxic exercise more effectively than did normoxic training, due to a selective mobilization of α-tocopherol (P < 0.05). The latter was related to enhanced exercise-induced mobilization/oxidation of blood lipids due to a selective increase in o2max (P < 0.05 compared with normoxic group). We conclude that lipid peroxidation induced by acute exercise (1) increases during hypoxia; (2) is not regulated exclusively by a mass action effect of o2; and (3) is selectively attenuated by regular hypoxic training. Oxidative stress may thus be considered as a biological prerequisite for adaptation to physical stress in humans.

scholarly journals Effects of grape seed extract supplementation on exercise-induced oxidative stress in rats

2011 ◽  
Vol 108 (2) ◽  
pp. 249-256 ◽  
Author(s):  
Muaz Belviranlı ◽  
Hakkı Gökbel ◽  
Nilsel Okudan ◽  
Kemal Başaralı
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Acute Exercise ◽  
Grape Seed Extract ◽  
Grape Seed ◽  
Seed Extract ◽  
Antioxidant Enzyme Activities ◽  
Chronic Exercise ◽  
Exercise Induced

The aim of the present study was to investigate the effects of grape seed extract (GSE) supplementation on exercise performance and oxidative stress in acutely and chronically exercised rats. A total of sixty-four male rats were used in the study. Rats were divided into six groups: control, chronic exercise control, acute exercise control (AEC), GSE-supplemented control, GSE-supplemented chronic exercise and GSE-supplemented acute exercise groups. Chronic exercise consisted of treadmill running at 25 m/min, 45 min/d, 5 d a week for 6 weeks. Rats in the acute exercise groups were run on the treadmill at 30 m/min until exhaustion. GSE were given at 100 mg/kg of body weight with drinking water for 6 weeks. Plasma was separated from blood samples for the analysis of oxidative stress markers. There was no significant difference in time of exhaustion between the acute exercise groups. Plasma malondialdehyde (MDA) levels were higher in the acute exercise groups and lower in the chronic exercise groups. GSE supplementation decreased MDA levels. Xanthine oxidase and adenosine deaminase activities were higher in the AEC group compared to all the other groups. NO levels were increased with both chronic exercise and GSE supplementation. Superoxide dismutase and glutathione peroxidase activities were lower in the acute exercised groups and higher in the chronic exercised groups. GSE supplementation caused an increase in antioxidant enzyme activities. In conclusion, GSE supplementation prevents exercise-induced oxidative stress by preventing lipid peroxidation and increasing antioxidant enzyme activities.

scholarly journals Effects of glutamine supplementation on oxidative stress-related gene expression and antioxidant properties in rats with streptozotocin-induced type 2 diabetes

2011 ◽  
Vol 107 (8) ◽  
pp. 1112-1118 ◽  
Author(s):  
Pei-Hsuan Tsai ◽  
Jun-Jen Liu ◽  
Chui-Li Yeh ◽  
Wan-Chun Chiu ◽  
Sung-Ling Yeh
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Amino Acid ◽  
Oxidative Damage ◽  
Antioxidant Capacity ◽  
Enzyme Activities ◽  
Antioxidant Enzyme Activities ◽  
Related Gene ◽  
Gene Expressions ◽  
Oxidative Stress Related Gene

There are close links among hyperglycaemia, oxidative stress and diabetic complications. Glutamine (GLN) is an amino acid with immunomodulatory properties. The present study investigated the effect of dietary GLN on oxidative stress-relative gene expressions and tissue oxidative damage in diabetes. There were one normal control (NC) and two diabetic groups in the present study. Diabetes was induced by an intraperitoneal injection of nicotinamide followed by streptozotocin (STZ). Rats in the NC group were fed a regular chow diet. In the two diabetic groups, one group (diabetes mellitus, DM) was fed a common semi-purified diet while the other group received a diet in which part of the casein was replaced by GLN (DM-GLN). GLN provided 25 % of total amino acid N. The experimental groups were fed the respective diets for 8 weeks, and then the rats were killed for further analysis. The results showed that blood thioredoxin-interacting protein (Txnip) mRNA expression in the diabetic groups was higher than that in the NC group. Compared with the DM group, the DM-GLN group had lower glutamine fructose-6-phosphate transaminase 1, a receptor of advanced glycation end products, and Txnip gene expressions in blood mononuclear cells. The total antioxidant capacity was lower and antioxidant enzyme activities were altered by the diabetic condition. GLN supplementation increased antioxidant capacity and normalised antioxidant enzyme activities. Also, the renal nitrotyrosine level and Txnip mRNA expression were lower when GLN was administered. These results suggest that dietary GLN supplementation decreases oxidative stress-related gene expression, increases the antioxidant potential and may consequently attenuate renal oxidative damage in rats with STZ-induced diabetes.

scholarly journals Alternative Interventions to Prevent Oxidative Damage following Ischemia/Reperfusion

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Simón Quetzalcoatl Rodríguez-Lara ◽  
Ernesto German Cardona-Muñoz ◽  
Ernesto Javier Ramírez-Lizardo ◽  
Sylvia Elena Totsuka-Sutto ◽  
Araceli Castillo-Romero ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Therapeutic Approaches ◽  
Alternative Interventions ◽  
Stress States ◽  
The Relationship ◽  
Irreparable Damage

Ischemia/reperfusion (I/R) lesions are a phenomenon that occurs in multiple pathological states and results in a series of events that end in irreparable damage that severely affects the recovery and health of patients. The principal therapeutic approaches include preconditioning, postconditioning, and remote ischemic preconditioning, which when used separately do not have a great impact on patient mortality or prognosis. Oxidative stress is known to contribute to the damage caused by I/R; however, there are no pharmacological approaches to limit or prevent this. Here, we explain the relationship between I/R and the oxidative stress process and describe some pharmacological options that may target oxidative stress-states.

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

scholarly journals Exercise-Induced Oxidative Stress, Nitric Oxide and Plasma Amino Acid Profile in Recreational Runners with Vegetarian and Non-Vegetarian Dietary Patterns

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1875 ◽  
Author(s):  
Josefine Nebl ◽  
Kathrin Drabert ◽  
Sven Haufe ◽  
Paulina Wasserfurth ◽  
Julian Eigendorf ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Amino Acid ◽  
Acute Exercise ◽  
Amino Acid Profile ◽  
Post Exercise ◽  
Stable Isotope Dilution ◽  
Amino Acid Profiles ◽  
Recreational Runners ◽  
Exercise Induced

This study investigated the exercise-induced changes in oxidative stress, nitric oxide (NO) metabolism and amino acid profile in plasma of omnivorous (OMN, n = 25), lacto-ovo-vegetarian (LOV, n = 25) and vegan (VEG, n = 23) recreational runners. Oxidative stress was measured as malondialdehyde (MDA), NO as nitrite and nitrate, and various amino acids, including homoarginine and guanidinoacetate, the precursor of creatine. All analytes were measured by validated stable-isotope dilution gas chromatographic-mass spectrometric methods. Pre-exercise, VEG had the highest MDA and nitrate concentrations, whereas nitrite concentration was highest in LOV. Amino acid profiles differed between the groups, with guanidinoacetate being highest in OMN. Upon acute exercise, MDA increased in the LOV and VEG group, whereas nitrate, nitrite and creatinine did not change. Amino acid profiles changed post-exercise in all groups, with the greatest changes being observed for alanine (+28% in OMN, +21% in LOV and +28% in VEG). Pre-exercise, OMN, LOV and VEG recreational runners differ with respect to oxidative stress, NO metabolism and amino acid profiles, in part due to their different dietary pattern. Exercise elicited different changes in oxidative stress with no changes in NO metabolism and closely comparable elevations in alanine. Guanidinoacetate seems to be differently utilized in OMN, LOV and VEG, pre- and post-exercise.

A Soccer Match’s Ability to Enhance Lymphocyte Capability to Produce ROS and Induce Oxidative Damage

2009 ◽  
Vol 19 (3) ◽  
pp. 243-258 ◽  
Author(s):  
Miguel David Ferrer ◽  
Pedro Tauler ◽  
Antoni Sureda ◽  
Pedro Pujol ◽  
Franchec Drobnic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Coenzyme Q ◽  
Training Period ◽  
Antioxidant Vitamin ◽  
Antioxidant Enzyme Activities ◽  
Double Blind ◽  
Soccer Match ◽  
Before And After ◽  
Soccer Training

Soccer-associated oxidative stress has barely been studied. The aims of this study were to establish the effect of a soccer training match and the effect of a diet supplementation with a multivitamin complex and coenzyme Q during 3 months of soccer training on the pro-oxidant and antioxidant status of lymphocytes. In a randomized, double-blind trial, 19 male preprofessional soccer players were treated with either an antioxidant nutrient cocktail or placebo for 90 days. After this period the athletes played a soccer match lasting 60 min. All determinations were made under basal conditions before and after the training period and after the match. Basal lymphocyte hydrogen peroxide (H2O2) production did not change after the 3 months of training. Catalase activity decreased (about 50%) after the 3 months, whereas glutathione reductase increased its activity (150–200%) both with placebo and in the supplemented group. Basal ascorbate levels were maintained during the training period, whereas α-tocopherol and MDA decreased (about 40%) in both groups. The match increased H2O2 production (180%) in both groups when the lymphocytes were stimulated with phorbol myristate acetate, and it also increased MDA levels (150%). Antioxidant enzyme activities and antioxidant vitamin levels were maintained before and after the match. Regular soccer training modifies the lymphocyte strategy to eliminate ROS and increases protection against oxidative damage. A friendly soccer match raises lymphocyte capacity to produce ROS and oxidative damage, but it is not enough to induce a defensive response, thus leading to a situation of postexercise oxidative stress. Supplementation with low doses of antioxidant vitamins and coenzyme Q does not modify the endogenous antioxidant response to training.

scholarly journals Exercise protects against doxorubicin-induced oxidative stress and proteolysis in skeletal muscle

2011 ◽  
Vol 110 (4) ◽  
pp. 935-942 ◽  
Author(s):  
Ashley J. Smuder ◽  
Andreas N. Kavazis ◽  
Kisuk Min ◽  
Scott K. Powers
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Oxidative Damage ◽  
Muscle Fibers ◽  
Muscular Exercise ◽  
Protease Activation ◽  
Exercise Induced

Doxorubicin (Dox) is a potent antitumor agent used in cancer treatment. Unfortunately, Dox is myotoxic and results in significant reductions in skeletal muscle mass and function. Complete knowledge of the mechanism(s) by which Dox induces toxicity in skeletal muscle is incomplete, but it is established that Dox-induced toxicity is associated with increased generation of reactive oxygen species and oxidative damage within muscle fibers. Since muscular exercise promotes the expression of numerous cytoprotective proteins (e.g., antioxidant enzymes, heat shock protein 72), we hypothesized that muscular exercise will attenuate Dox-induced damage in exercise-trained muscle fibers. To test this postulate, Sprague-Dawley rats were randomly assigned to the following groups: sedentary, exercise, sedentary with Dox, or exercise with Dox. Our results show increased oxidative stress and activation of cellular proteases (calpain and caspase-3) in skeletal muscle of animals treated with Dox. Importantly, our findings reveal that exercise can prevent the Dox-induced oxidative damage and protease activation in the trained muscle. This exercise-induced protection against Dox-induced toxicity may be due, at least in part, to an exercise-induced increase in muscle levels of antioxidant enzymes and heat shock protein 72. Together, these novel results demonstrate that muscular exercise is a useful countermeasure that can protect skeletal muscle against Dox treatment-induced oxidative stress and protease activation in skeletal muscles.

Abstract 100: Delta Opioid Receptor Blockade Abolishes Exercise-Induced Cardioprotection Against Ischemia-Reperfusion Injury In Vivo

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Juliana P Borges ◽  
Marina Tristao ◽  
Eduardo V Tibiriçá ◽  
Marcos A Lessa
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Acute Exercise ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Receptor Subtype ◽  
Kappa Receptor ◽  
Exercise Induced ◽  
Delta Receptor ◽  
And Control

Introduction: Recent studies showed that exercise enhances myocardial tolerance to ischemia-reperfusion (I-R) injury via an opioid receptor-dependent mechanism. However, the specific subtype of opioid receptor involved in this response remains to be determined. Methods: Male Wistar rats were first divided into 2 groups: exercised and control. The exercised group underwent 4 consecutive days of treadmill training (60 min at 70% of maximal oxygen consumption). The exercised group was then divided into 4 subgroups: exercised (Exe; n = 10); exercised + kappa receptor antagonist (Exe + K; n=4); exercised + delta receptor antagonist (Exe + D; n=4); exercised + mu receptor antagonist (Exe + M; n=4). Control group was also divided into 2 groups: control (Ctr; n = 10) and control sham (Sham; n = 10). To induce I-R injury, anesthetized animals were submitted to a left thoracotomy and a 30 min interventricular coronary occlusion followed by 60 min of reperfusion. The hemodynamic parameters were recorded and infarct size was post-mortem determined by double staining using TTC/Evans blue and expressed as a percentage of the area at risk. Results: As shown in the figure, Sham group showed no infarct, Exe group showed a significant reduction in the infarcted area (27.6%) when compared to Ctr group (42.0%). The pretreatment with mu and kappa receptor antagonist did not alter the cardioprotective effect of exercise. However, the pretreatment with delta receptor antagonist prevented the exercise-induced cardioprotection. Conclusions: Endogenous opioid system is involved in cardioprotection conferred by acute exercise, and delta receptor subtype seems to play an important role in this response.

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