The Antioxidant Role of Artichoke (Cynara scolymus L.) Extract Against Exhaustive Exercise-Induced Oxidative Stress in Young Athletes

Exhaustive exercise induces systemic inflammatory responses, which are associated with exercise-induced tissue/organ damage, but the sources and triggers are not fully understood. Herein, the basics of inflammatory mediator cytokines and research findings on the effects of exercise on systemic inflammation are introduced. Subsequently, the association between inflammatory responses and tissue damage is examined in exercised and overloaded skeletal muscle and other internal organs. Furthermore, an overview of the interactions between oxidative stress and inflammatory mediator cytokines is provided. Particularly, the transcriptional regulation of redox signaling and pro-inflammatory cytokines is described, as the activation of the master regulatory factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is involved directly or indirectly in controlling pro-inflammatory genes and antioxidant enzymes expression, whilst nuclear factor-kappa B (NF-κB) regulates the pro-inflammatory gene expression. Additionally, preventive countermeasures against the pathogenesis along with the possibility of interventions such as direct and indirect antioxidants and anti-inflammatory agents are described. The aim of this review is to give an overview of studies on the systematic inflammatory responses to exercise, including our own group as well as others. Moreover, the challenges and future directions in understanding the role of exercise and functional foods in relation to inflammation and oxidative stress are discussed.

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Exercise-induced oxidative stress: glutathione supplementation and deficiency

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.5.2177 ◽

1994 ◽

Vol 77 (5) ◽

pp. 2177-2187 ◽

Cited By ~ 134

Author(s):

C. K. Sen ◽

M. Atalay ◽

O. Hanninen

Keyword(s):

Oxidative Stress ◽

Skeletal Muscle ◽

Critical Role ◽

Lipid Peroxides ◽

Thiobarbituric Acid ◽

Repeated Administration ◽

Exhaustive Exercise ◽

Relative Role ◽

Exercise Induced

Glutathione (GSH) plays a central role in coordinating the synergism between different lipid- and aqueous-phase antioxidants. We documented 1) how exogenous GSH and N-acetylcysteine (NAC) may affect exhaustive exercise-induced changes in tissue GSH status, lipid peroxides [thiobarbituric acid-reactive substances (TBARS)], and endurance and 2) the relative role of endogenous GSH in the circumvention of exercise-induced oxidative stress by using GSH-deficient [L-buthionine-(S,R)-sulfoximine (BSO)-treated] rats. Intraperitoneal injection of GSH remarkably increased plasma GSH; exogenous GSH per se was an ineffective delivery agent of GSH to tissues. Repeated administration of GSH (1 time/day for 3 days) increased blood and kidney total GSH [TGSH; GSH+oxidized GSH (GSSG)]. Neither GSH nor NAC influenced endurance to exhaustion. NAC decreased exercise-induced GSH oxidation in the lung and blood. BSO decreased TGSH pools in the liver, lung, blood, and plasma by approximately 50% and in skeletal muscle and heart by 80–90%. Compared with control, resting GSH-deficient rats had lower GSSG in the liver, red gastrocnemius muscle, heart, and blood; similar GSSG/TGSH ratios in the liver, heart, lung, blood, and plasma; higher GSSG/TGSH ratios in the skeletal muscle; and more TBARS in skeletal muscle, heart, and plasma. In contrast to control, exhaustive exercise of GSH-deficient rats did not decrease TGSH in the liver, muscle, or heart or increase TGSH of plasma; GSSG of muscle, blood, or plasma; or TBARS of plasma or muscle. GSH-deficient rats had approximately 50% reduced endurance, which suggests a critical role of endogenous GSH in the circumvention of exercise-induced oxidative stress and as a determinant of exercise performance.

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Exhaustive endurance exercise activates brain glycogen breakdown and lactate production more than insulin-induced hypoglycemia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00119.2020 ◽

2021 ◽

Author(s):

Takashi Matsui

Keyword(s):

Endurance Exercise ◽

Lactate Production ◽

Severe Hypoglycemia ◽

Exercise Group ◽

Exhaustive Exercise ◽

Endurance Capacity ◽

Brain Glycogen ◽

Insulin Group ◽

Exercise Induced

Brain glycogen localized in astrocytes produces lactate via cAMP signaling, which regulates memory functions and endurance capacity. Exhaustive endurance exercise with hypoglycemia decreases brain glycogen, although the mechanism underlying this phenomenon remains unclear. Since insulin-induced hypoglycemia decreases brain glycogen, this study tested the hypothesis that hypoglycemia mediates exercise-induced brain glycogen decrease. To test the hypothesis, the effects of insulin- and exhaustive exercise-induced hypoglycemia on brain glycogen levels were compared using the microwave irradiation method in adult Wistar rats. The insulin challenge and exhaustive exercise induced similar levels of severe hypoglycemia. Glycogen in the hypothalamus and cerebellum decreased similarly with the insulin challenge and exhaustive exercise; however, glycogen in the cortex, hippocampus, and brainstem of the exercise group were lower compared to the insulin group. Blood glucose correlated positively with brain glycogen, but the slope of regression lines was greater in the exercise group compared to the insulin group in the cortex, hippocampus, and brainstem, but not the hypothalamus and cerebellum. Brain lactate and cAMP levels in the hypothalamus and cerebellum increased similarly with the insulin challenge and exhaustive exercise, but those in the cortex, hippocampus, and brainstem of the exercise group were higher compared to the insulin group. These findings support the hypothesis that hypoglycemia mediates the exercise-induced reduction in brain glycogen, at least in the hypothalamus and cerebellum. However, glycogen reduction during exhaustive endurance exercise in the cortex, hippocampus, and brainstem is not due to hypoglycemia alone, implicating the role of exercise-specific neuronal activity in brain glycogen decrease.

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Protective Role of Polysaccharides from Gynostemma pentaphyllum Makino Supplementation against Exhaustive Swimming Exercise-Induced Oxidative Stress in Liver and Skeletal Muscle of Mice

Advanced Materials Research ◽

10.4028/www.scientific.net/amr.962-965.1231 ◽

2014 ◽

Vol 962-965 ◽

pp. 1231-1234

Author(s):

Hui Huang ◽

Bo Qi

Keyword(s):

Oxidative Stress ◽

Skeletal Muscle ◽

Protective Role ◽

Swimming Exercise ◽

Control Group ◽

High Dose ◽

Gynostemma Pentaphyllum ◽

Exercise Induced ◽

Different Doses

The objective of this study was to investigate the protective role of polysaccharide fromGynostemma pentaphyllumMakino (PGP) supplementation against exhaustive swimming exercise-induced oxidative stress. A total of 48 mice were randomly divided into four groups: control, low-dose, medium-dose, and high-dose PGP supplementation groups. The control group received distilled water and the supplementation groups received different doses of PGP (50, 100 and 200 mg/kg body weight) by gavage once a day for 28 consecutive days. After 28 days, the mice performed an exhaustive swimming exercise, and some biochemical parameters related to oxidative stress, including superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and malondialdehyde (MDA), were measured. The results showed that PGP supplementation could increase SOD, GPx and CAT contents, as well as decrease MDA contents in the liver and skeletal muscle of mice, which suggests that PGP supplementation has a protective role against exhaustive swimming exercise-induced oxidative stress.

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Antioxidant supplementation influences the neutrophil tocopherol associated protein expression, but not the inflammatory response to exercise

Open Life Sciences ◽

10.2478/s11535-007-0006-1 ◽

2007 ◽

Vol 2 (1) ◽

pp. 56-70 ◽

Cited By ~ 6

Author(s):

Antoni Sureda ◽

Pedro Tauler ◽

Antoni Aguiló ◽

Nuria Cases ◽

Isabel Llompart ◽

...

Keyword(s):

Oxidative Stress ◽

Placebo Group ◽

Inflammatory Response ◽

Exhaustive Exercise ◽

Plasma Damage ◽

Marathon Race ◽

Neutrophil Degranulation ◽

Exercise Induced ◽

Antioxidant Diet ◽

Diet Supplementation

AbstractIntense exercise induces inflammatory-like changes and oxidative stress in immune cells. Our aim was to study the effects of antioxidant diet supplementation on the neutrophil inflammatory response and on the tocopherol associated protein (TAP) expression after exhaustive exercise. Fourteen male-trained amateur runners were randomly divided in two placebo and supplemented groups. Vitamins C (152 mg/d) and E (50 mg/d) supplementation were administrated to the athletes for a month, using an almond based isotonic and energetic beverage. Non-enriched beverage was given to the placebo group. After one month, the subjects participated in a half-marathon race (21 km-run). Neutrophil TAP mRNA expression and markers of the inflammatory response were determined before, immediately after, and 3 h after finishing the half-marathon race. TAP expression increased after exercise mainly in the neutrophils of the placebo group. Exercise induced an inflammatory response in both placebo and supplemented groups, manifested with neutrophilia, increased creatine kinase and lactate dehydrogenase serum activities, neutrophil luminol chemiluminescence and myeloperoxidase release. Plasma malondialdehyde only increased in the placebo group after exercise. Diet supplementation with moderate levels of antioxidant vitamins avoids plasma damage in response to exhaustive exercise without the effects on the inflammatory process. Neutrophil degranulation and increased tocopherol associated protein could contribute to the neutrophil protection from the oxidative stress.

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