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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The production of reactive oxygen species in skeletal muscle is linked with muscle fatigue. This study investigated the effects of the antioxidant compound N-acetylcysteine (NAC) on muscle cysteine, cystine, and glutathione and on time to fatigue during prolonged, submaximal exercise in endurance athletes. Eight men completed a double-blind, crossover study, receiving NAC or placebo before and during cycling for 45 min at 71% peak oxygen consumption (VO2 peak) and then to fatigue at 92% VO2 peak. NAC was intravenously infused at 125 mg.kg(-1).h(-1) for 15 min and then at 25 mg.kg(-1).h(-1) for 20 min before and throughout exercise. Arterialized venous blood was analyzed for NAC, glutathione status, and cysteine concentration. A vastus lateralis biopsy was taken preinfusion, at 45 min of exercise, and at fatigue and was analyzed for NAC, total glutathione (TGSH), reduced glutathione (GSH), cysteine, and cystine. Time to fatigue at 92% VO2 peak was reproducible in preliminary trials (coefficient of variation 5.6 +/- 0.6%) and with NAC was enhanced by 26.3 +/- 9.1% (NAC 6.4 +/- 0.6 min vs. Con 5.3 +/- 0.7 min; P <0.05). NAC increased muscle total and reduced NAC at both 45 min and fatigue (P <0.005). Muscle cysteine and cystine were unchanged during Con, but were elevated above preinfusion levels with NAC (P <0.001). Muscle TGSH (P <0.05) declined and muscle GSH tended to decline (P=0.06) during exercise. Both were greater with NAC (P <0.05). Neither exercise nor NAC affected whole blood TGSH. Whereas blood GSH was decreased and calculated oxidized glutathione increased with exercise (P <0.05), both were unaffected by NAC. In conclusion, NAC improved performance in well-trained individuals, with enhanced muscle cysteine and GSH availability a likely mechanism.
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PMID:N-acetylcysteine enhances muscle cysteine and glutathione availability and attenuates fatigue during prolonged exercise in endurance-trained individuals. 1519 75

It was already documented that acute hypoxemia reduces the oxidative stress following static as well as dynamic handgrip bouts in humans. Then, we examined if chronic hypoxemia could produce the same effect in patients suffering from chronic respiratory insufficiency. In rats, we studied the respective consequence of a one-month exposure to normobaric hypoxia on two muscles (soleus, SOL, and extensor digitorum longus, EDL) which have high and low aerobic metabolism, respectively. Compared to healthy humans, the resting level of erythrocyte reduced glutathione (GSH) was significantly lower in chronic hypoxemic patients, and after a handgrip contraction sustained at 50% of maximal until exhaustion the GSH level and plasma thiobarbituric acid reactive substances (TBARS) did not vary. A 20-min period of oxygen supplementation partly restored the post-handgrip oxidative stress. Compared to control rats, SOL muscle of hypoxemic animals had lower intra-muscular resting level of GSH; after a 3-min muscle stimulation (MS) leading to fatigue, TBARS did not vary in SOL and EDL and the GSH decrease was absent in SOL whereas it persisted in EDL. We concluded that chronic hypoxemia depressed the fatigue-induced oxidative stress, the effects prevailing in muscles having a high oxygen demand.
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PMID:Depressed fatigue-induced oxidative stress in chronic hypoxemic humans and rats. 1523 68

This study compares the changes in four blood markers of exercise-induced oxidative stress in response to exercise protocols commonly used to explore the global muscle performance at work (maximal incremental cycle) and endurance to fatigue of selected muscles (static handgrip and thumb adduction). Cycling and static exercises allow the muscle to work in aerobic and anaerobic conditions, respectively. Healthy adults performed an incremental cycling exercise until volitional exhaustion and, on separated days, executed infra-maximal static thumb adduction and handgrip until exhaustion. Exercise-induced oxidative stress was assessed by the increased plasma concentration of thiobarbituric acid reactive substances (TBARS), the consumption of plasma reduced ascorbic acid (RAA), and erythrocyte reduced glutathione (GSH) antioxidants, and the changes in the total antioxidant status (TAS) of plasma. Five minutes after the end of the incremental cycling exercise, we measured a peak increase in TBARS level, maximal consumption of GSH and RAA, and a modest but significant decrease in TAS concentration. In response to both static thumb adduction and handgrip, significant variations of TBARS, GSH and RAA occurred but we did not measure any significant change in TAS level throughout the 20-min recovery period of both exercise bouts. The present study shows that only the changes in TBARS, GSH and RAA explore both dynamic and static exercises. In addition, TAS measurement does not seem to represent a reliable and unique tool to explore exercise-induced oxidative stress, at least during isometric efforts that allow the muscle to work under anaerobic condition.
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PMID:Reliability of different blood indices to explore the oxidative stress in response to maximal cycling and static exercises. 1649 1

Two groups, each containing 10 young healthy male students, participated in the study. One group breathed 70% O2 after exercise (70% O2 group) while the other group breathed normal air (Normal air group) after exercise. The results of the study show the following: (1) in both groups, the Monodehydyoxygenbate (MDA) in erythrocyte (RBC) and serum, and superoxide dismutase (SOD) and glutathione Peroxidas (GSH-px) in serum were significantly higher immediately after exercise than at rest; (2) the MDA in RBC and serum were significantly higher in the Normal air group than in the 70% O2 group for 30 minutes after exercise; and (3) the SOD in serum and GSH-px in blood and serum were significantly higher in the 70% O2 group than in the Normal air group for 30 minutes after exercise. We suggest that the effects of inhaling 70% O2 could prevent fatigue from antagonizing free radicals damage, hastening removal of free radicals, which would facilitate recovery from fatigue.
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PMID:Effects of inhalation of oxygen on free radical metabolism and oxidative, antioxidative capabilities of the erythrocyte after intensive exercise. 1686 36

In previous study, we found that the reduced exercise-induced production of reactive oxygen species (ROS) reported in slow-oxidative muscle of hypoxemic rats and also in chronic hypoxemic patients did not simply result from deconditioning. In control rats and after a 3-week period of hindlimb suspension (HS), the slow-oxidative (Soleus, SOL) and fast-glycolytic skeletal muscles (Extensor digitorum longus, EDL) were sampled. We determined the response to direct muscle stimulation (twitch stimulation (TS), Maximal force (Fmax)), twitch amplitude and maximal relaxation rate, tetanic frequency, endurance to fatigue after muscle stimulation (MS), the different fibre types based on their myofibrillar adenosinetriphosphatase (ATPase) activity, and the intra-muscular redox status (Thiobarbituric Acid Reactive Sustances: TBARS, reduced glutathione: GSH, reduced ascorbic acid: RAA). After the 3-w HS period: (1) the contractile properties were modified in SOL only (reduced Fmax and twitch amplitude, increased tetanic frequency); (2) the fibre typology was modified in both muscles (in SOL: increased proportion of IIa and IIc fibres, in EDL: increased proportion of IId/x fibres but decreased proportion of IIb fibres); and (3) only in SOL, the TBARS level increased and the GSH and RAA concentrations decreased at rest and after fatiguing MS. Thus, HS accentuates the exercise-induced ROS production in slow-oxidative muscle in a direction opposite to that measured in chronic hypoxemic rats. This strongly suggests that hypoxemia reduces the ROS production independently from any muscle disuse.
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PMID:Physiological, histological and biochemical properties of rat skeletal muscles in response to hindlimb suspension. 1715 69

A state of chronic fatigue was produced in mice by subjecting them to forced swim inside a rectangular jar of specific dimensions everyday for a 6 min session for 15 days. Immobility period was recorded on alternate days. The effect of venlafaxine, a dual reuptake inhibitor of serotonin and norepinephrine was evaluated in this murine model of chronic fatigue. Venlafaxine was administered daily and on the days of testing, it was injected 30 min before forced swim session. On the 16th day i.e. 24 h after the last dose of venlafaxine, various behavioral, biochemical and neurotransmitter estimations in the brain were carried out. There was a significant increase in immobility period in vehicle treated mice on successive days, the maximum immobility score reaching on the 7th day and sustained till 15th day. Behavioral parameters revealed hyperlocomotion, anxiety response, muscle incoordination, hyperalgesia and memory deficit. Biochemical analysis showed a significant increase in lipid peroxidation, nitrite and myeloperoxidase levels and a decrease in the reduced glutathione (GSH) levels in brain homogenates. Further, there was a decrease in adrenal ascorbic acid following chronic forced swim. The neurotransmitter estimations in the brain samples revealed a decrease in norepinephrine, serotonin and dopamine levels on chronic exposure to forced swim for 15 days. Daily treatment with venlafaxine (8 and 16 mg/kg, i.p.) for 15 days produced a significant reduction in immobility period and reversed various behavioral, biochemical and neurotransmitter alterations induced by chronic fatigue. Venlafaxine could be of therapeutic potential in the treatment of chronic fatigue.
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PMID:Venlafaxine reverses chronic fatigue-induced behavioral, biochemical and neurochemical alterations in mice. 1833 91

We previously showed that the content of advanced glycation end products (AGEs) in the diet correlates with serum AGE levels, oxidant stress (OS), organ dysfunction, and lifespan. We now show that the addition of a chemically defined AGE (methyl-glyoxal-BSA) to low-AGE mouse chow increased serum levels of AGEs and OS, demonstrating that dietary AGEs are oxidants that can induce systemic OS. OS predisposes to the development of cardiovascular and chronic kidney diseases; calorie restriction (CR) is the most studied means to decrease OS, increase longevity, and reduce OS-related organ damage in mammals. Because reduction of food intake also decreases oxidant AGE s intake, we asked whether the beneficial effects of CR in mammals are related to the restriction of oxidants or energy. Pair-fed mice were provided either a CR diet or a high-AGE CR diet in which AGEs were elevated by brief heat treatment (CR-high). Old CR-high mice developed high levels of 8-isoprostanes, AGEs, RAGE, and p66(shc), coupled with low AGER1 and GSH/GSSG levels, insulin resistance, marked myocardial and renal fibrosis, and shortened lifespan. In contrast, old CR mice had low OS, p66(shc), RAGE, and AGE levels, but high AGER1 levels, coupled with longer lifespan. Therefore, the beneficial effects of a CR diet may be partly related to reduced oxidant intake, a principal determinant of oxidant status in aging mice, rather than decreased energy intake.
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PMID:Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespan. 1909 55

To gain an insight into the effects of different diets on growth and development of the domesticated silkworm at protein level, we employed comparative proteomic approach to investigate the proteomic differences of midgut, hemolymph, fat body and posterior silk gland of the silkworms reared on fresh mulberry leaves and on artificial diet. Seventy-six differentially expressed proteins were identified by MALDI TOF/TOF MS, and among them, 41 proteins were up-regulated, and 35 proteins were downregulated. Database searches, combined with GO analysis and KEGG pathway analysis revealed that some hemolymph proteins such as Nuecin, Gloverin-like proteins, PGRP, P50 and beta/-N-acetylglucosamidase were related to innate immunity of the silkworm, and some proteins identified in silkworm midgut including Myosin 1 light chain, Tropomyosin 1, Profilin, Serpin-2 and GSH-Px were involved in digestion and nutrition absorption. Moreover, two up-regulated enzymes in fat body of larvae reared on artificial diet were identified as V-ATPase subunit B and Arginine kinase which participate in energy metabolism. Furthermore, 6 down-regulated proteins identified in posterior silk gland of silkworm larvae reared on artificial diet including Ribosomal protein SA, EF-2, EF-1gamma, AspAT, ERp57 and PHB were related to silk synthesis. Our results suggested that the different diets could alter the expression of proteins related to immune system, digestion and absorption of nutrient, energy metabolism and silk synthesis poor nutrition and absorption of nutrition in silkworm. The results also confirmed that the poor nutrient absorption, weakened innate immunity, decreased energy metabolism and reduced silk synthesis are the main reasons for low cocoons yield, inferior filament quality, low survival rate of young larvae and insufficient resistance against specific pathogens in the silkworms fed on artificial diet.
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PMID:Comparative proteomic analysis between the domesticated silkworm (Bombyx mori) reared on fresh mulberry leaves and on artificial diet. 1899 23

Fatiguing exercise promotes oxidation of intracellular thiols, notably glutathione. Interventions that oppose or reverse thiol oxidation can inhibit fatigue. The reduced cysteine donor l-2-oxothiazolidine-4-carboxylate (OTC) supports glutathione synthesis and is approved for use in humans but has not been evaluated for effects on skeletal muscle. We tested the hypotheses that OTC would 1) increase reduced glutathione (GSH) levels and decrease oxidized glutathione, and 2) inhibit functional indexes of fatigue. Diaphragm fiber bundles from adult male ICR mice were incubated for 1 or 2 h at 37 degrees C with buffer (control, C) or OTC (10 mM). N-acetylcysteine (NAC; 10 mM) was used as a positive control. We measured GSH metabolites and fatigue characteristics. We found that muscle GSH content was increased after 1-h incubation with OTC or NAC but was not altered after 2-h incubation. One-hour treatment with OTC or NAC slowed the decline in force with repetitive stimulation [mean (SD) fatigue index at 300 s: OTC = 34 +/- 6% vs. C = 50 +/- 8%, P < 0.05; NAC = 55 +/- 4% vs. C = 65 +/- 8%, P < 0.05] as did the 2-h OTC treatment (OTC = 38 +/- 9% vs. C = 51 +/- 9%, P < 0.05). These results demonstrate that OTC modulates the muscle GSH pool and opposes fatigue under the current experimental conditions.
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PMID:L-2-Oxothiazolidine-4-carboxylate reverses glutathione oxidation and delays fatigue of skeletal muscle in vitro. 1940 60

Electroacupuncture (EA) and manual acupuncture (MA) have therapeutic effects on muscle fatigue in muscle disease. The deficiencies of carnitine and glutathione induce muscle fatigue. This report investigated the effects of EA and MA on carnitine and glutathione in muscle. After the mice of EA group were fixed in the animal cage, right Zusanli (ST36) and Jiexi (ST41) were acupunctured and stimulated with uniform reinforcing and reducing method by twirling the acupuncture needle for 15 min. And then, the needle handles were connected to an electric stimulator for stimulating the acupoint with dense-sparse waves. After the mice of MA group were fixed in an animal cage, right ST36 and ST41 were acupunctured and allowed for 15 min. The mice of normal control group were not acupunctured and stimulated for 15 min. The mice of all groups were killed for collecting muscle tissue 1 h after the final treatment. Carnitine and glutathione in homogenate of muscle tissue were determined with carnitine (Kainos Laboratories Co., Tokyo, Japan) and glutathione assay kit (Dojin Chemicals Co., Kumamoto, Japan). Carnitine level in muscle tissue of MA group was significantly higher than those of EA group and normal control group. Carnitine level in muscle tissue of EA group was not significantly different from that of normal control group. Glutathione levels in muscle tissue of EA group and MA group were significantly higher than that of normal control group. This report presented that carnitine in muscle is increased by MA, and not increased by EA, and that glutathione in muscle is increased by EA and MA.
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PMID:Investigation of electroacupuncture and manual acupuncture on carnitine and glutathione in muscle. 1959 78


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