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Interplay of Oxidants and Antioxidants During Exercise: Implications for Muscle Health
Abstract and Figures
Muscle contraction results in generation of reactive oxygen and nitrogen species (RONS) at a rate determined by the intensity, frequency, and duration of the exercise protocols. Strenuous exercise causes oxidation of protein, lipid, and DNA, release of cytosolic enzymes, and other signs of cell damage; however, only exhaustive exercise is detrimental. Indeed, the regulation of vascular tone, the excitation-contraction coupling, growth, and differentiation in skeletal muscle, are governed in part by RONS. This is accomplished by RONS interaction with redox-sensitive transcription factors, leading to increased gene expression of antioxidant enzymes, cytoprotective proteins, and other enzymes involved in muscle metabolic functions. However, high levels of RONS generation are known to cause oxidative stress, activate certain pathogenic pathways, and accelerate aging. This article reviews research from the past decades on the interplay of oxidants and antioxidants in skeletal muscle, with particular reference to increased contractile activity. Adaptation of muscle to increased oxidative stress and the potential mechanisms involved will be highlighted. The role of redox-controlled cell signaling in skeletal muscle health and function is also described.
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... Among the possible physiopathology of provoked vestibulodynia proposed by the scientific literature, increased tone of the PFM is known to play an important role in its setting and maintenance [7]. Muscle contraction results in generation of reactive oxygen and nitrogen species (RONS) at a rate determined by the intensity, frequency and duration of the exercise [18]. Strenuous exercise causes oxidation of protein, lipid and DNA, release of cytosolic enzymes and other signs of cell damage, mainly in exhaustive exercise. ...
... Strenuous exercise causes oxidation of protein, lipid and DNA, release of cytosolic enzymes and other signs of cell damage, mainly in exhaustive exercise. The long-lasting sustained contraction or increased tone of the PFM in PVD could generate high levels of RONS and cause oxidative stress, activating certain pathogenic pathways [18]. This cascade of events could eventually help to explain the pain mechanism of PVD and impaired sexual function. ...
Introduction and hypothesis:
To compare blood flow of the dorsal clitoral artery in women diagnosed with provoked vestibulodynia (PVD) and in healthy controls using color Doppler ultrasonography. We hypothesized that women with PVD would have a restricted blood flow compared to controls.
Methods:
This cross-sectional study evaluated the function of the dorsal clitoral artery through the spectral wave analysis of color Doppler ultrasonography (US) in 20 women diagnosed with PVD according to Friedrich's criteria and 21 healthy controls. Participants were evaluated during their follicular phase and were asked to abstain from sexual activities 24 ho prior the examination. Assessment was performed by an assessor blinded to participant diagnosis, in the morning after a 10-min rest period in a supine lying position in a room with temperature set at 22 °C. Measurements of the peak systolic velocity (PSV), time-averaged maximum velocity (TAMX), end-diastolic velocity (EDV), pulsatility (PI) and resistance index (RI) were performed at rest considering the mean value of three consecutive waveforms.
Results:
Women with PVD and healthy controls did not present any statistically different baseline characteristics. Participants with PVD presented higher values of Doppler-US PSV, TAMX, EDV and RI compared to controls (p ≤ 0.05), which are suggestive of a decrease in blood flow. However, non-significant difference was found regarding PI values between the two groups (p > 0.05).
Conclusion:
Our findings revealed decreased peripheral tissue perfusion in women with PVD compared to healthy controls using color Doppler US, based on the alteration of four of the five assessed data of US parameters.
... The concept of the damaging effects of exercise-induced oxidative stress during acute intense or prolonged exercise has been reported extensively in the literature over the years [1][2][3][4]. In terms of exercise-induced oxidative stress, there is accumulating evidence showing that there is an appropriate concentration of reactive oxygen species (ROS) with which positive physiological adaptations may occur; however, there is also evidence that ROS production can cause micromolecular structural damage or inflammation [5][6][7]. ...
High-intensity interval exercise (HIIE) is a type of structured physical training characterized by repeated bouts of high-intensity exercise interspersed with recovery periods. Although HIIE was found to improve physical performance in a relatively short period of time, there is emerging evidence suggesting that acute HIIE may induce oxidative stress. The purpose, therefore, of the present study was to examine the effect of intermittency and/or acceleration during HIIE on oxidative stress in male participants. Nine healthy males [(age: 21.0 ± 3.0 years; height: 180.0 ± 4.0 cm; body mass: 79.4 ± 7.9 kg; maximal oxygen uptake (V˙O2max) 52.0 ± 6.0 mL·kg−1·min−1)] were recruited to perform six distinct exercise protocols of various intermittency (high, medium, and low) and acceleration (high, medium, and low) while a control session was also included. Blood samples were obtained to determine oxidative stress indices (lipid hydroperoxides, superoxide dismutase, and total glutathione) at rest, 1 h, 2 h, and 24 h following exercise on a non-motorized treadmill. The intra-individual variability of participants was observed in lipid hydroperoxides at baseline, ranging from 1.80 to 20.69 μmol·L−1. No significant differences among the six different exercise protocols in any of the oxidative stress indices evaluated were observed (p > 0.05). These results suggest that the influence of various intermittency levels and acceleration patterns upon exercise-induced oxidative stress is negligible.
... The acid-base chemical reaction process will produce salt and water so that lactic acid levels in the circulation can be eliminated. Thus, the body needs important substances in the oil used during massage to prevent fatigue and muscle pain (Gomez et al., 2009). ...
... Proinflammatory factors that are released by cells during inflammation increase the production of ROS causing oxidative stress. This can either increase skeletal muscle protein degradation or decrease protein synthesis, and induce skeletal muscle mitochondrial dysfunction in CRC related cachexia [10,[33][34][35][36]. Furthermore, these pro-inflammatory factors target several signaling pathways playing a possible role in the development of cancer related cachexia by causing mitochondrial dysfunction leading to muscle loss [37,38]. ...
Up to 60% of colorectal cancer (CRC) patients develop cachexia. The presence of CRC related cachexia is associated with more adverse events during systemic therapy, leading to a high mortality rate. The main manifestation in CRC related cachexia is the loss of skeletal muscle mass, resulting from an imbalance between skeletal muscle protein synthesis and protein degradation. In CRC related cachexia, systemic inflammation, oxidative stress, and proteolytic systems lead to mitochondrial dysfunction, resulting in an imbalanced skeletal muscle metabolism. Mitochondria fulfill an important function in muscle maintenance. Thus, preservation of the skeletal muscle mitochondrial homeostasis may contribute to prevent the loss of muscle mass. However, it remains elusive whether mitochondria play a benign or malignant role in the development of cancer cachexia. This review summarizes current (mostly preclinical) evidence about the role of skeletal muscle mitochondria in the development of CRC related cachexia. Future human research is necessary to determine the physiological role of skeletal muscle mitochondria in the development of human CRC related cachexia.
... Strong evidence exists on the beneficial effect of regular moderate-to-vigorous PA/PE on human health [61,[73][74][75][76][77][78][79]. The benefits are achieved through increases of insulin sensitivity [76]; regulation of energy expenditure, insulin-like growth factor-1 (IGF-1) and insulinlike growth factor binding proteins (IGFBPs) balance; improvement of lipid and carbohydrate metabolism [77]; reduction of endothelial dysfunction [78,79]; increase of catecholamines secretion (the compounds restore the disturbed redox balance and improve insulin sensitivity); reduction of visceral adipose tissue; activation of redox-sensitive signal transduction and enhancement of expression of genes responsible for the production of antioxidant enzymes (e.g., superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx)) in muscles [71,[80][81][82]; mitochondrial biogenesis; reduction of inflammation, changes in metabolic and sex hormones metabolism; enhancement of immune system response, and up-regulating resistance to OS [40,83]. Evidence has maintained that PA of moderate to vigorous intensity produces ROS/RNS at concentrations which may be required for the proper signalling and an adaptation to excessive species production in response to training [84]. ...
Extensive research has found strongly increased generation of reactive oxygen species, free radicals, and reactive nitrogen species during acute physical exercise that can lead to oxidative stress (OS) and impair muscle function. Polyphenols (PCs), the most abundant antioxidants in the human diet, are of increasing interest to athletes as antioxidants. Current literature suggests that antioxidants supplementation can effectively modulate these processes. This overview summarizes the actual knowledge of chemical and biomechanical properties of PCs and their impact as supplements on acute exercise-induced OS, inflammation control, and exercise performance. Evidence maintains that PC supplements have high potency to positively impact redox homeostasis and improve skeletal muscle's physiological and physical functions. However, many studies have failed to present improvement in physical performance. Eleven of 15 representative experimental studies reported a reduction of severe exercise-induced OS and inflammation markers or enhancement of total antioxidant capacity; four of eight studies found improvement in exercise performance outcomes. Further studies should be continued to address a safe, optimal PC dosage, supplementation timing during a severe training program in different sports disciplines, and effects on performance response and adaptations of skeletal muscle to exercise.
Introduction. Oxidative stress is an imbalance between the production of reactive species and the body's antioxidant defense capacity. It is involved in the etiopathogenesis of many diseases such as diabetes, and neurological and cardiovascular diseases. Objective/Aims: The purpose of this article is to highlight both the beneficial effects of oxidative stress and the risks of excessive consumption of substances with antioxidant capacity Materials and Methods: Results: Free radicals alter the essential functions of cells, causing: inactivation of cellular enzymes and receptors, changes in cell permeability. If not neutralized, oxidative stress causes lipid peroxidation and DNA oxidation. Conclusion: Oxidative stress is the main subject of many studies, many of them based on the negative effects it produces in the body, both at the molecular and cellular levels, so the positive effects are ignored. Rezumat Introducere: Stresul oxidativ reprezintă un dezechilibru între producția de specii reactive și capacitatea de apărare antioxidantă a organismului. Acesta este implicat în etiopatogenia multor afecțiuni cum ar fi diabetul zaharat, bolile neurologice, cardiovasculare. Obiectiv principal al studiului: Scopul acestui articol este de a evidenția atât efectele benefice ale stresului oxidativ, cât și riscurile consumului în exces a substanțelor cu capacitate antioxidantă Material și metodă: Rezultate: Radicalii liberi modifică funcțiile esențiale ale celulelor determinând: inactivarea enzimelor și a receptorilor celulari, modificări ale permeabilității celulare. Dacă nu este neutralizat, stresul oxidativ determină peroxidarea lipidelor, oxidarea ADN-ului. Concluzii: Stresul oxidativ este subiectul principal pentru multe studii, multe dintre ele bazându-se pe efectele negative pe care le produce în organism, atât la nivel molecular cât și la nivel celular, astfel efectele pozitive sunt ignorate.
AIM: To study the effect of dihydroquercetin on the indicators of oxidative metabolism in young athletes engaged in the winter sports in the Khanty-Mansiysk Autonomous Okrug (KhMAO). MATERIAL AND METHODS: The indicators of oxidative metabolism were studied in a group of 56 male students (mean age 19.300.51 years) from the Khanty-Mansiysk boarding school of the Olympic reserve. These students were actively involved in winter sports such as cross-country skiing and biathlon. To assess the impact of the plant-derived antioxidant bioflavonoid Baikal dihydroquercetin (DHQ), the participants were administered a daily dose of 120 mg of DHQ for a period of 60 days. Measurements were taken before and after the exposure. Blood lipid peroxidation (LPO) products were studied, namely, lipid hydroperoxides (LHP) and products that react with 2-thiobarbituric acid products (PR-TBA). Additionally, we examined the indicators of the body's antioxidant defense system (ADS) through the assessment of total antioxidant activity (TAA) and thiol status (TS). To quantify the overall oxidative stress experienced by the participants, we calculated the oxidative stress coefficient (OSC) using the formula: OSC = LHP PR-TBA / TAA TS. RESULTS: The average levels of LPO values (HPL and PR-TBA) among KhMAO athletes have surpassed the upper limit of optimal values. On the other hand, the ADS parameters (TAA and TS) fall within the range of physiologically optimal values, albeit closer to the lower limit. Notably, athletes have exhibited an OSC increase that is nearly 3.5 times higher than the maximum allowable value. A quarter of the individuals examined displayed elevated HPL values, while more than 30% showed increased PR-TBA levels. A third of male athletes exhibited reduced ADS values compared to the physiologically optimal range. In total, 70.4% of skiers and biathletes in KhMAO have exceeded the OSC parameters. After two months of daily intake of 120 mg DHQ, the normalization of indicators of oxidative metabolism was observed. All parameters aligned with physiologically optimal values, except for OSC. We found a decrease in primary (LHP, 1.15 times) and secondary (PR-TBA, p=0.046) LPO indicators parallel to a significant increase in ADS indicators, specifically TAA (p=0.022) and TS (p=0.049). Conversely, there was a significant increase in ADS indicators, specifically TAA (p=0.022) and TS (p=0.049). Despite these positive changes, the OSC value, although significantly reduced (p 0.001) by 2.3 times compared to the initial value, remained above the upper limit of the physiological norm. CONCLUSION: The study demonstrated that young athletes engaged in winter sports experienced improved indicators of oxidative metabolism after a consistent two-month intake of the potent antioxidant DHQ. This led to the restoration of a balanced prooxidant-antioxidant state, enhanced overall well-being, and expedited recovery following intense physical exertion. Furthermore, our results may suggest that DHQ may contribute to prevention of non-communicable diseases in the future.
The imbalance between reactive oxygen species (ROS) production and antioxidant defense systems leads to macromolecule and tissue damage as a result of cellular oxidative stress. This phenomenon is considered a key factor in fatigue and muscle damage following chronic or high-intensity physical exercise. In the present study, the antioxidant effect of Moringa oleifera leaf extract (MOLE) was evaluated in C2C12 myotubes exposed to an elevated hydrogen peroxide (H2O2) insult. The capacity of the extract to influence the myotube redox status was evaluated through an analysis of the total antioxidant capacity (TAC), glutathione homeostasis (GSH and GSSG), total free thiols (TFT), and thioredoxin (Trx) activity, as well as the enzyme activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and transferase (GST). Moreover, the ability of MOLE to mitigate the stress-induced peroxidation of lipids and oxidative damage (TBARS and protein carbonyls) was also evaluated. Our data demonstrate that MOLE pre-treatment mitigates the highly stressful effects of H2O2 in myotubes (1 mM) by restoring the redox status (TFT, Trx, and GSH/GSSG ratio) and increasing the antioxidant enzymatic system (CAT, SOD, GPx, GST), thereby significantly reducing the TBARs and PrCAR levels. Our study provides evidence that MOLE supplementation has antioxidant potential, allowing myotubes better able to cope with an oxidative insult and, therefore, could represent a useful nutritional strategy for the preservation of muscle well-being.
Aging is multidimensional and the loss of physical activity may be an important reason in a number of age-related diseases. Exercise seems to be a required challenge for the modern urban society in order to maintain a healthy life. An individual’s capacity to utilize oxygen is an indicator of their Reactive Oxygen Species (ROS) generation rate. The common feature of all age-related disorders is the reduced quantity and quality of mitochondria due to the overproduction of ROS. Regular aerobic exercise induces the biogenesis and functionality of mitochondria via various pathways such as peroxisome proliferator-activated receptor-γ coactivator 1 alpha (PGC-1a) during aging. According to recent findings revealing that the sources of aging and exercise-induced ROS are both mitochondrial and extramitochondrial. Although going over of the physiological limits of ROS has detrimental effects, it allows the cells to adapt to exercise-induced stress within individual physiological limits. Thus, regular antioxidant supplementation might be beneficial for the elderly with regards to exercise performance. Albeit redox homeostasis is fundamentally related to aerobic type of exercise, anaerobic exercise has proven to be beneficial during aging. Regular exercise of low intensity and short duration, that targets endurance, strength, balance, and flexibility, would be effective in enhancing quality of life and aging longevity.
Contraction-induced production of reactive oxygen and nitrogen species has been shown to cause oxidative stress to skeletal muscle, heart and other organs. As an adaptive response, muscle antioxidant defense systems are upregulated in response to exercise to restore intracellular prooxidant-antioxidant homeostasis. Thus, both young and old animals and humans involved in regular exercise have shown reduced oxidative damage during acute physical exertion at accustomed or excessive intensity, or under oxidative challenges otherwise deemed detrimental. The current article provides a brief review of this exercise-induced hormesis with the emphasis on the role of redox sensitive signal transduction pathways (mainly nuclear factor κB and mitogen-activated protein kinase) that can activate the gene expression of antioxidant enzymes and proteins. Molecular mechanisms and gene targets for these signaling pathways, as well as the biological significance of the adaptations, are discussed.
Human endothelial cells exposed to H2O2 showed reduced CREP DNA binding activity, enhanced HSF activation, and no induction of NFκB binding activity. Interestingly, H2O2 was able to induce NFκB subunit p65 translocation in the nucleus. In contrast, cells exposed to TNFα showed enhanced CREP binding activity, activation of NFκB and no induction of HSE-HSF complex. Addition of H2O2, diamide and iodoacetic acid to the binding reaction mixture markedly reduced the DNA binding ability of the three transcription factors. Thus free sulfhydryls were important in DNA binding activity of CREP, NFκB and HSF, and the lack of induction of NFκB by H2O2 in intact cells was likely caused by oxidation on a thiol, and not by a deficiency in the activation pathway.
1. Oxygen is a toxic gas - an introductionto oxygen toxicity and reactive species 2. The chemistry of free radicals and related 'reactive species' 3. Antioxidant defences Endogenous and Diet Derived 4. Cellular responses to oxidative stress: adaptation, damage, repair, senescence and death 5. Measurement of reactive species 6. Reactive species can pose special problems needing special solutions. Some examples. 7. Reactive species can be useful some more examples 8. Reactive species can be poisonous: their role in toxicology 9. Reactive species and disease: fact, fiction or filibuster? 10. Ageing, nutrition, disease, and therapy: A role for antioxidants?
Oxidative cell damage can be monitored by detection of (a) photoemission of singlet molecular oxygen formed from radical interactions (so-called low-chemical chemiluminescence), (b) end products of lipid peroxidation, such as ethane, and (c) glutathione disulphide release. These methods, preferably used in a complementary fashion, provide insight into the pro-oxidant-antioxidant balance in the intact cell or organ. Recent work from this laboratory on the metabolism of hydroperoxides and aldehydes as well as on redox cycling of the quinone menadione is presented. The comparison of GSSG transport systems in liver and heart reveals a limitation of capacity in the latter, thus making GSSG export potentially critical in the heart. As part of an inter-organ feedback system between extrahepatic tissues and liver, the newly described hormone stimulation of GSH release from liver is also presented.