45 research outputs found

    Chronic eccentric exercise and antioxidant supplementation: effects on lipid profile and insulin sensitivity

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    Eccentric exercise has been shown to exert beneficial effects in both lipid profile and insulin sensitivity. Antioxidant supplementation during chronic exercise is controversial as it may prevent the physiological training-induced adaptations. The aim of this study was to investigate: 1) the minimum duration of the eccentric exercise training required before changes on metabolic parameters are observed and 2) whether antioxidant supplementation during training would interfere with these adaptations. Sixteen young healthy men were randomized into the Vit group (1 g of vitamin C and 400 IU vitamin E daily) and the placebo (PL) group. Subjects received the supplementation for 9 weeks. During weeks 5-9 all participants went through an eccentric exercise training protocol consisting of two exercise sessions (5 sets of 15 eccentric maximal voluntary contractions) per week. Plasma triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL), low density lipoprotein (LDL), apolipoproteins (Apo A1, Apo B and Lpa) and insulin sensitivity (HOMA) were assessed before the supplementation (week 0), at weeks 5, 6, 7, 8 and 9. TG, TC and LDL were significantly lower compared to pre supplementation at both weeks 8 and 9 (P<0.05) in both groups. HDL was significantly elevated after 4 weeks of training (p < 0.005) in both groups. There was no effect of the antioxidant supplementation in any of the variables. There was no effect of either the training or the supplementation protocol in apolipoproteins levels and insulin sensitivity. A minimum duration of 3 weeks of eccentric exercise training is required before beneficial effects in lipid profile can be observed in healthy young men. Concomitant antioxidant supplementation does not interfere with the training-induced adaptations

    Random Mass Dirac Fermions in Doped Spin-Peierls and Spin-Ladder systems: One-Particle Properties and Boundary Effects

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    Quasi-one-dimensional spin-Peierls and spin-ladder systems are characterized by a gap in the spin-excitation spectrum, which can be modeled at low energies by that of Dirac fermions with a mass. In the presence of disorder these systems can still be described by a Dirac fermion model, but with a random mass. Some peculiar properties, like the Dyson singularity in the density of states, are well known and attributed to creation of low-energy states due to the disorder. We take one step further and study single-particle correlations by means of Berezinskii's diagram technique. We find that, at low energy ϵ\epsilon, the single-particle Green function decays in real space like G(x,ϵ)(1/x)3/2G(x,\epsilon) \propto (1/x)^{3/2}. It follows that at these energies the correlations in the disordered system are strong -- even stronger than in the pure system without the gap. Additionally, we study the effects of boundaries on the local density of states. We find that the latter is logarithmically (in the energy) enhanced close to the boundary. This enhancement decays into the bulk as 1/x1/\sqrt{x} and the density of states saturates to its bulk value on the scale Lϵln2(1/ϵ)L_\epsilon \propto \ln^2 (1/\epsilon). This scale is different from the Thouless localization length λϵln(1/ϵ)\lambda_\epsilon\propto\ln (1/\epsilon). We also discuss some implications of these results for the spin systems and their relation to the investigations based on real-space renormalization group approach.Comment: 26 pages, LaTex, 9 PS figures include

    Effect of body composition on redox homeostasis at rest and in response to exercise: The case of underfat women

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    Underfat individuals have been neglected as a malnourished population in terms of redox homeostasis. The aim of the present study was to evaluate the effect of body composition on redox homeostasis at rest and in response to exercise. Underfat, lean and overfat women, classified according to their BMI and body fat percentage, participated in the study and were subjected to an acute session of eccentric exercise. With regard to muscle function and damage, a significant group × time interaction was found for range of motion (P &amp;lt; .01), isometric peak torque at 90° (P &amp;lt; .01), delayed onset muscle soreness (P &amp;lt; .01) and creatine kinase (P &amp;lt; .05), with the lean group generally exhibiting faster recovery compared to the underfat and overfat groups. With regard to redox homeostasis, a significant group × time interaction was found for F2-isoprostanes, protein carbonyls and glutathione (P &amp;lt; .01 for all biomarkers), with the underfat and overfat groups exhibiting increased resting oxidative stress levels and lower exercise-induced reactive species production. In conclusively, our data underline the importance of normal body composition for redox homeostasis, since underfat and overfat women demonstrate a similar pattern of redox disturbances both at rest and in response to exercise. © 2019, © 2019 Informa UK Limited, trading as Taylor &amp; Francis Group

    N-acetylcysteine supplementation increases exercise performance and reduces oxidative stress only in individuals with low levels of glutathione

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    Most of the evidence indicates that chronic antioxidant supplementation induces negative effects in healthy individuals. However, it is currently unknown whether specific redox deficiencies exist and whether targeted antioxidant interventions in deficient individuals can induce positive effects. We hypothesized that the effectiveness of antioxidant supplements to decrease oxidative stress and promote exercise performance depends on the redox status of the individuals that receive the antioxidant treatment. To this aim, we investigated whether N-acetylcysteine (NAC) supplementation would enhance exercise performance by increasing glutathione concentration and by reducing oxidative stress only in individuals with low resting levels of glutathione. We screened 100 individuals for glutathione levels and formed three groups with low, moderate and high levels (N = 36, 12 per group). After by-passing the regression to the mean artifact, by performing a second glutathione measurement, the individuals were supplemented with NAC (2 × 600 mg, twice daily, for 30 days) or placebo using a double-blind cross-over design. We performed three whole-body performance tests (VO 2 max, time trial and Wingate), measured two systemic oxidative stress biomarkers (F 2 -isoprostanes and protein carbonyls) and assessed glutathione-dependent redox metabolism in erythrocytes (glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase, catalase and NADPH). The low glutathione group improved after NAC supplementation in VO 2 max, time trial and Wingate by 13.6%, 15.4% and 11.4%, respectively. Thirty days of NAC supplementation were sufficient to restore baseline glutathione concentration, reduce systemic oxidative stress and improve erythrocyte glutathione metabolism in the low glutathione group. On the contrary, the 30-day supplementation period did not affect performance and redox state of the moderate and high glutathione groups, although few both beneficial and detrimental effects in performance were observed. In conclusion, individuals with low glutathione levels were linked with decreased physical performance, increased oxidative stress and impaired redox metabolism of erythrocytes. NAC supplementation restored both performance and redox homeostasis. © 2017 Elsevier Inc

    Redox basis of exercise physiology

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    Redox reactions control fundamental processes of human biology. Therefore, it is safe to assume that the responses and adaptations to exercise are, at least in part, mediated by redox reactions. In this review, we are trying to show that redox reactions are the basis of exercise physiology by outlining the redox signaling pathways that regulate four characteristic acute exercise-induced responses (muscle contractile function, glucose uptake, blood flow and bioenergetics) and four chronic exercise-induced adaptations (mitochondrial biogenesis, muscle hypertrophy, angiogenesis and redox homeostasis). Based on our analysis, we argue that redox regulation should be acknowledged as central to exercise physiology. © 202

    Transition-state theory model for the diffusion coefficients of small penetrants in glassy polymers

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    Previous molecular dynamics simulations have shown that the diffusion of a penetrant in a glassy polymer involves occasional jumps between cavities through the opening of a "neck", and thus, because this is a rare event, the diffusion coefficient can be estimated using transition-state theory. We treat this process as a unimolecular rearrangement and develop semiempirical means of estimating the activation energy, frequency factor and jump length. The activation energy is obtained by treating the polymer as a continuous solid and calculating the energy required to expand a neck in that continuum. The model for the frequency factor uses the result from simulations that the distribution of frequencies of the modes in the transition is very similar to that distribution for the reactant state. The frequency factor is estimated by considering only the motion of the penetrant. These motions are treated as harmonic oscillators. The jump length is obtained from simple geometric considerations of the polymer chain. The ibility. The model reproduces experimental trends semiquantitatively and could be used to interpolate and extrapolate experimental diffusion data

    Antioxidants in personalized nutrition and exercise

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    The present review highlights the idea that antioxidant supplementation can be optimized when tailored to the precise antioxidant status of each individual. A novel methodologic approach involving personalized nutrition, the mechanisms by which antioxidant status regulates human metabolism and performance, and similarities between antioxidants and other nutritional supplements are described. The usefulness of higherlevel phenotypes for data-driven personalized treatments is also explained. We conclude that personally tailored antioxidant interventions based on specific antioxidant inadequacies or deficiencies could result in improved exercise performance accompanied by consistent alterations in redox profile. © 2018 American Society for Nutrition. All rights reserved

    Eccentric exercise per se does not affect muscle damage biomarkers: early and late phase adaptations

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    Purpose: Acute high-intensity unaccustomed eccentric exercise performed by naive subjects is accompanied by disturbances in muscle damage biomarkers. The aim of the study was to investigate whether a causal relationship indeed exists between eccentric exercise and muscle damage. Methods: Twenty-four men randomly assigned into a concentric only or an eccentric-only training group and performed 10 weeks of isokinetic resistance exercise (one session/week of 75 maximal knee extensors actions). Physiological markers of muscle function and damage (i.e., range of motion, delayed onset muscle soreness, isometric, concentric and eccentric peak torque) were assessed prior to and 1–3 and 5 days post each session. Biochemical markers of muscle damage (creatine kinase) and inflammation (C-reactive protein) were measured prior and 2 days post each session. Results: After the first bout, eccentric exercise induced greater muscle damage compared to concentric exercise; however, during the nine following sessions, this effect progressively diminished, while after the 10th week of training, no alterations in muscle damage biomarkers were observed after either exercise protocol. Additionally, strength gains at the end of the training period were comparable between the two groups and were mode-specific. Conclusion: (1) eccentric exercise per se does not affect muscle damage biomarkers; (2) muscle damage occurs as a result of muscle unaccustomedness to this action type; (3) exercise-induced muscle damage is not a prerequisite for increased muscle strength. Collectively, we believe that muscle unaccustomedness to high-intensity eccentric exercise, and not eccentric exercise per se, is the trigger for muscle damage as indicated by muscle damage biomarkers. © 2020, Springer-Verlag GmbH Germany, part of Springer Nature
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