scholarly journals Exercise-Induced Regulation of Redox Status in Cardiovascular Diseases: The Role of Exercise Training and Detraining

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 13 ◽  
Author(s):  
Tryfonas Tofas ◽  
Dimitrios Draganidis ◽  
Chariklia K. Deli ◽  
Kalliopi Georgakouli ◽  
Ioannis G. Fatouros ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Exercise Training ◽  
Vascular Function ◽  
Redox Regulation ◽  
Defense Mechanism ◽  
Redox Status ◽  
Physical Conditioning ◽  
Exercise Induced ◽  
Training And Detraining

Although low levels of reactive oxygen species (ROS) are beneficial for the organism ensuring normal cell and vascular function, the overproduction of ROS and increased oxidative stress levels play a significant role in the onset and progression of cardiovascular diseases (CVDs). This paper aims at providing a thorough review of the available literature investigating the effects of acute and chronic exercise training and detraining on redox regulation, in the context of CVDs. An acute bout of either cardiovascular or resistance exercise training induces a transient oxidative stress and inflammatory response accompanied by reduced antioxidant capacity and enhanced oxidative damage. There is evidence showing that these responses to exercise are proportional to exercise intensity and inversely related to an individual’s physical conditioning status. However, when chronically performed, both types of exercise amplify the antioxidant defense mechanism, reduce oxidative stress and preserve redox status. On the other hand, detraining results in maladaptations within a time-frame that depends on the exercise training intensity and mode, as high-intensity training is superior to low-intensity and resistance training is superior to cardiovascular training in preserving exercise-induced adaptations during detraining periods. Collectively, these findings suggest that exercise training, either cardiovascular or resistance or even a combination of them, is a promising, safe and efficient tool in the prevention and treatment of CVDs.

scholarly journals How N-Acetylcysteine Supplementation Affects Redox Regulation, Especially at Mitohormesis and Sarcohormesis Level: Current Perspective

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 153
Author(s):  
Aslı Devrim-Lanpir ◽  
Lee Hill ◽  
Beat Knechtle
Keyword(s):  
Oxidative Stress ◽  
Oxidative Metabolism ◽  
Adaptive Response ◽  
Redox Regulation ◽  
Therapeutic Agent ◽  
Metabolic Effects ◽  
Metabolic Adaptations ◽  
Current Perspective ◽  
Exercise Induced ◽  
Response To Exercise

Exercise frequently alters the metabolic processes of oxidative metabolism in athletes, including exposure to extreme reactive oxygen species impairing exercise performance. Therefore, both researchers and athletes have been consistently investigating the possible strategies to improve metabolic adaptations to exercise-induced oxidative stress. N-acetylcysteine (NAC) has been applied as a therapeutic agent in treating many diseases in humans due to its precursory role in the production of hepatic glutathione, a natural antioxidant. Several studies have investigated NAC’s possible therapeutic role in oxidative metabolism and adaptive response to exercise in the athletic population. However, still conflicting questions regarding NAC supplementation need to be clarified. This narrative review aims to re-evaluate the metabolic effects of NAC on exercise-induced oxidative stress and adaptive response developed by athletes against the exercise, especially mitohormetic and sarcohormetic response.

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

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.

EFFECTS OF ONE-MONTH EXERCISE TRAINING ON EXERCISE-INDUCED OXIDATIVE STRESS IN HUMANS

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S122
Author(s):  
K Koyama ◽  
D Ando ◽  
J Yokouchi ◽  
Y Ono ◽  
M Kaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Exercise Induced

Exercise-induced brachial artery vasodilation: role of free radicals

2007 ◽  
Vol 292 (3) ◽  
pp. H1516-H1522 ◽  
Author(s):  
Russell S. Richardson ◽  
Anthony J. Donato ◽  
Abhimanyu Uberoi ◽  
D. Walter Wray ◽  
Lesley Lawrenson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Brachial Artery ◽  
Epr Spectroscopy ◽  
Vascular Function ◽  
Paramagnetic Resonance ◽  
Healthy State ◽  
Total Antioxidant ◽  
Exercise Induced

Originally thought of as simply damaging or toxic “accidents” of in vivo chemistry, free radicals are becoming increasingly recognized as redox signaling molecules implicit in cellular homeostasis. Indeed, at the vascular level, it is plausible that oxidative stress plays a regulatory role in normal vascular function. Using electron paramagnetic resonance (EPR) spectroscopy, we sought to document the ability of an oral antioxidant cocktail (vitamins C, E, and α-lipoic acid) to reduce circulating free radicals, and we employed Doppler ultrasound to examine the consequence of an antioxidant-mediated reduction in oxidative stress on exercise-induced vasodilation. A total of 25 young (18–31 yr) healthy male subjects partook in these studies. EPR spectroscopy revealed a reduction in circulating free radicals following antioxidant administration at rest (∼98%) and as a consequence of exercise (∼85%). Plasma total antioxidant capacity and vitamin C both increased following the ingestion of the antioxidant cocktail, whereas vitamin E levels were not influenced by the ingestion of the antioxidants. Brachial artery vasodilation during submaximal forearm handgrip exercise was greater with the placebo (7.4 ± 1.8%) than with the antioxidant cocktail (2.3 ± 0.7%). These data document the efficacy of an oral antioxidant cocktail in reducing free radicals and suggest that, in a healthy state, the aggressive disruption of the delicate balance between pro- and antioxidant forces can negatively impact vascular function. These findings implicate an exercise-induced reliance upon pro-oxidant-stimulated vasodilation, thereby revealing an important and positive vascular role for free radicals.

scholarly journals PCSK9 and LDL-C: The Role of Exercise

2020 ◽  
Vol 29 (4) ◽  
pp. 347-351
Author(s):  
Jaeho Jin ◽  
Wooyeon Jo ◽  
Ji Heon Noh ◽  
Sang Ki Lee
Keyword(s):  
Experimental Data ◽  
Cardiovascular Diseases ◽  
Exercise Training ◽  
Lifestyle Intervention ◽  
Ldl Receptor ◽  
Lipoprotein Cholesterol ◽  
Proprotein Convertase ◽  
Study Review ◽  
Exercise Induced

PURPOSE: Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) is a pivotal regulator of low lipoprotein-cholesterol (LDL-C) and LDL receptor (LDLR) metabolism, and the interest in PCSK9 has increased in cardiovascular diseases. Exercise reduces blood LDL-C via PCSK9-LDLR pathway in the liver and the vasculature. However, the mechanism of exercise-induced inhibition of PCSK is unclear. The aim of this review is to describe the role of exercise on PCSK9-LDLR axis in cardiovascular diseases.METHODS:This study review 34 previous studies focusing on the effect of exercise on PCSK9 in the human and animal.RESULTS:The effects of exercise and lifestyle intervention on hepatic and circulating PCSK9 are controversial. However, exercise consistently increases hepatic LDLR, and inhibits atherosclerosis via suppression of PCSK9 and LOX-1 in atherosclerotic region.CONCLUSIONS: Even though experimental data are still very limited, exercise training can improves blood LDL-C via inhibition of PCSK9 and enhancement of LDLR in liver and vasculature. The study of exercise on PCSK9 are urgently needed.

scholarly journals The DUG Pathway Governs Degradation of Intracellular Glutathione in Aspergillus nidulans

2021 ◽  
Vol 87 (9) ◽  
Author(s):  
Barnabás Csaba Gila ◽  
Heungyun Moon ◽  
Károly Antal ◽  
Márton Hajdu ◽  
Réka Kovács ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aspergillus Nidulans ◽  
Redox Regulation ◽  
Reactive Oxygen ◽  
Redox Status ◽  
Carbon Starvation ◽  
Moderate Increase ◽  
Transcriptome Data ◽  
Regulatory Pathways ◽  
Gsh Metabolism

ABSTRACT Glutathione (GSH) is an abundant tripeptide that plays a crucial role in shielding cellular macromolecules from various reactive oxygen and nitrogen species in fungi. Understanding GSH metabolism is of vital importance for deciphering redox regulation in these microorganisms. In the present study, to better understand the GSH metabolism in filamentous fungi, we investigated functions of the dugB and dugC genes in the model fungus Aspergillus nidulans. These genes are orthologues of dug2 and dug3, which are involved in cytosolic GSH degradation in Saccharomyces cerevisiae. The deletion of dugB, dugC, or both resulted in a moderate increase in the GSH content in mycelia grown on glucose, reduced conidium production, and disturbed sexual development. In agreement with these observations, transcriptome data showed that genes encoding mitogen-activated protein (MAP) kinase pathway elements (e.g., steC, sskB, hogA, and mkkA) or regulatory proteins of conidiogenesis and sexual differentiation (e.g., flbA, flbC, flbE, nosA, rosA, nsdC, and nsdD) were downregulated in the ΔdugB ΔdugC mutant. Deletion of dugB and/or dugC slowed the depletion of GSH pools during carbon starvation. It also reduced accumulation of reactive oxygen species and decreased autolytic cell wall degradation and enzyme secretion but increased sterigmatocystin formation. Transcriptome data demonstrated that enzyme secretions—in contrast to mycotoxin production—were controlled at the posttranscriptional level. We suggest that GSH connects starvation and redox regulation to each other: cells utilize GSH as a stored carbon source during starvation. The reduction of GSH content alters the redox state, activating regulatory pathways responsible for carbon starvation stress responses. IMPORTANCE Glutathione (GSH) is a widely distributed tripeptide in both eukaryotes and prokaryotes. Owing to its very low redox potential, antioxidative character, and high intracellular concentration, GSH profoundly shapes the redox status of cells. Our observations suggest that GSH metabolism and/or the redox status of cells plays a determinative role in several important aspects of fungal life, including oxidative stress defense, protein secretion, and secondary metabolite production (including mycotoxin formation), as well as sexual and asexual differentiations. We demonstrated that even a slightly elevated GSH level can substantially disturb the homeostasis of fungi. This information could be important for development of new GSH-producing strains or for any biotechnologically relevant processes where the GSH content, antioxidant capacity, or oxidative stress tolerance of a fungal strain is manipulated.

Diabetes impairs exercise training-associated thioredoxin response and glutathione status in rat brain

2009 ◽  
Vol 106 (2) ◽  
pp. 461-467 ◽  
Author(s):  
Zekine Lappalainen ◽  
Jani Lappalainen ◽  
Niku K. J. Oksala ◽  
David E. Laaksonen ◽  
Savita Khanna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Redox Status ◽  
Antioxidant Defenses ◽  
Sod Activity ◽  
Interacting Protein ◽  
Glutathione Peroxidase 1 ◽  
Thioredoxin Interacting Protein ◽  
Streptozotocin Induced Diabetes ◽  
Diabetic Brain

Regular exercise plays an important preventive and therapeutic role in oxidative stress-associated diseases such as diabetes and its complications. Thiol antioxidants including thioredoxin (TRX) and glutathione (GSH) have a crucial role in controlling cellular redox status. In this study, the effects of 8 wk of exercise training on brain TRX and GSH systems, and antioxidant enzymes were tested in rats with or without streptozotocin-induced diabetes. We found that in untrained animals, the levels of TRX-1 (TRX1) protein and activity, and thioredoxin-interacting protein (TXNip) were similar in diabetic and nondiabetic animals. Exercise training, however, increased TRX1 protein in nondiabetic animals without affecting TXNip levels, whereas diabetes inhibited the effect of training on TRX1 protein and also increased TXNip mRNA. In addition, the proportion of oxidized glutathione (GSSG) to total GSH was increased in animals with diabetes, indicating altered redox status and possibly increased oxidative stress. Glutathione peroxidase-1 (GPX1) levels were not affected by diabetes or exercise training, although diabetes increased total GPX activity. Both diabetes and exercise training decreased glutathione reductase (GRD) activity and cytosolic superoxide dismutase (Cu,Zn-SOD) levels. Nevertheless, diabetes or training had no effect on Cu,Zn-SOD mRNA, Mn-SOD protein, total SOD activity, or catalase mRNA, protein, or activity. Our findings suggest that exercise training increases TRX1 levels in brain without a concomitant rise in TXNip, and that experimental diabetes is associated with an incomplete TRX response to training. Increased oxidative stress may be both a cause and a consequence of perturbed antioxidant defenses in the diabetic brain.

scholarly journals Exercise training regulates SOD-1 and oxidative stress in porcine aortic endothelium

2003 ◽  
Vol 284 (4) ◽  
pp. H1378-H1387 ◽  
Author(s):  
James W. E. Rush ◽  
James R. Turk ◽  
M. Harold Laughlin
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Vascular Function ◽  
Aerobic Exercise Training ◽  
Heme Oxygenase 1 ◽  
Sod Activity ◽  
Aortic Endothelial Cells ◽  
Protein Levels ◽  
Markers Of Oxidative Stress

Vascular oxidative stress contributes to endothelial dysfunction. Aerobic exercise training improves vascular function. The purpose of this study was to test the hypothesis that exercise training would improve the balance of antioxidant to prooxidant enzymes and reduce markers of oxidative stress in aortic endothelial cells (AEC). Female Yucatan miniature pigs either remained sedentary (SED) or were exercise trained (EX) for 16–19 wk. EX pigs had increased AEC SOD-1 protein levels and Cu/Zn SOD activity of the whole aorta compared with SED pigs. Protein levels of other antioxidant enzymes (SOD-2, catalase) were not affected by exercise training. Protein levels of p67phox, a subunit of the prooxidant enzyme NAD(P)H oxidase, were reduced in EX vs. SED AEC. These EX adaptations were associated with lower AEC malondialdehyde levels and decreased phosphorylation of ERK-1/2. Endothelial nitric oxide synthase protein, protein nitrotyrosine content, and heme oxygenase-1 protein were not different in EX vs. SED pigs. We conclude that chronic aerobic exercise training influenced both antioxidant and prooxidant enzymes and decreased indexes of oxidative stress in AEC. These adaptations may contribute to improved endothelial function with exercise training.

Preventive and therapeutic effects of quercetin on lipopolysaccharide-induced oxidative stress and vascular dysfunction in mice

2012 ◽  
Vol 90 (10) ◽  
pp. 1345-1353 ◽  
Author(s):  
Upa Kukongviriyapan ◽  
Kwanjit Sompamit ◽  
Patchareewan Pannangpetch ◽  
Veerapol Kukongviriyapan ◽  
Wanida Donpunha
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Redox Status ◽  
Protein Carbonyl ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Vascular Responsiveness

Quercetin, a dietary antioxidant flavonoid, possesses strong anti-inflammatory and cytoprotective activities. The effects were investigated in an animal model of lipopolysaccharide (LPS)-induced endotoxaemia and vascular dysfunction in vivo. Male ICR mice were injected with LPS (10 mg/kg; i.p.). Quercetin (50 or 100 mg/kg) was intragastrically administered either before or after LPS administration. Fifteen hours after LPS injection, mice were found in endotoxaemic condition, as manifested by hypotension, tachycardia, and blunted vascular responses to vasodilators and vasoconstrictor. The symptoms were accompanied by increased aortic iNOS protein expression, decreased aortic eNOS protein expression, marked suppression of cellular glutathione (GSH) redox status, enhanced aortic superoxide production, increased plasma malodialdehyde and protein carbonyl, and elevated urinary nitrate/nitrite. Treatment with quercetin either before or after LPS preserved the vascular function, as blood pressure, heart rate, vascular responsiveness were restored to near normal values, particularly when quercetin was given as a preventive regimen. The vascular protective effects were associated with upregulation of eNOS expression, reduction of oxidative stress, and maintained blood GSH redox ratio. Overall findings suggest the beneficial effect of quercetin on the prevention and restoration of a failing eNOS system and alleviation of oxidative stress and vascular dysfunction against endotoxin-induced shock in mice.

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