Exercise-induced Oxidative Stress Research Articles

Effect of a sulforaphane supplement on muscle soreness and damage induced by eccentric exercise in young adults: A pilot study.

ObjectiveExcessive exercise increases the production of reactive oxygen species in skeletal muscles. Sulforaphane activates nuclear factor erythroid 2‐related factor 2 (Nrf2) and induces a protective effect against oxidative stress. In a recent report, sulforaphane intake suppressed exercise‐induced oxidative stress and muscle damage in mice. However, the effect of sulforaphane intake on delayed onset muscle soreness after eccentric exercise in humans is unknown. We evaluated the effect of sulforaphane supplement intake in humans regarding the delayed onset muscle soreness (DOMS) after eccentric exercise.Research Methods & ProceduresTo determine the duration of sulforaphane supplementation, continuous blood sampling was performed and NQO1 mRNA expression levels were analyzed. Sixteen young men were randomly divided into sulforaphane and control groups. The sulforaphane group received sulforaphane supplements. Each group performed six set of five eccentric exercise with the nondominant arm in elbow flexion with 70% maximum voluntary contraction. We assessed muscle soreness in the biceps using the visual analog scale, range of motion (ROM), muscle damage markers, and oxidative stress marker (malondialdehyde; MDA).ResultsSulforaphane supplement intake for 2 weeks increased NQO1 mRNA expression in peripheral blood mononuclear cells (PBMCs). Muscle soreness on palpation and ROM were significantly lower 2 days after exercise in the sulforaphane group compared with the control group. Serum MDA showed significantly lower levels 2 days after exercise in the sulforaphane group compared with the control group.ConclusionOur findings suggest that sulforaphane intake from 2 weeks before to 4 days after the exercise increased NQO1, a target gene of Nrf2, and suppressed DOMS after 2 days of eccentric exercise.

Effect of Genistein Supplementation on Exercise-Induced Inflammation and Oxidative Stress in Mice Liver and Skeletal Muscle.

Background and objectives: The purpose of this study was to investigate the influences of oral high-dose genistein (GE) administration on exercise-induced oxidative stress, inflammatory response and tissue damage. Materials and Methods: Thirty-two mice were randomly divided into control group (Con; sedentary/0.5% CMC-Na), GE administrated group (GE; sedentary/GE dosed), exercise group (Ex; exercise/0.5% CMC-Na), or GE administrated plus exercise group (GE + Ex; exercise/GE dosed), mice in the GE and GE + Ex group were given GE orally at the dose of 200 mg/kg weight. Results: Plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, liver interleukin (IL)-6, IL-1β, superoxide dismutase 1 (SOD1), catalase (CAT), hemeoxygenase-1 (HO-1) gene expression levels and skeletal muscle IL-6, nuclear factor erythroid 2-related factor (Nrf2), and HO-1 gene expression levels increased immediately after exhaustive exercise. GE supplementation increased liver protein carbonyl concentrations. On the other hand, GE supplementation significantly decreased SOD1, CAT gene expression levels in the liver and Nrf2, and HO-1 gene expression levels in the skeletal muscles. Conclusions: Acute exercise induced organ damage, inflammation, and oxidative stress in skeletal muscles and the liver. However, a single dose of GE supplementation before exercise did not lead to favorable antioxidant and anti-inflammatory effects in this study.

Management of Oxidative Stress: Crosstalk Between Brown/Beige Adipose Tissues and Skeletal Muscles.

Exercise plays an important role in the physiology, often depending on its intensity, duration, and frequency. It increases the production of reactive oxygen species (ROS). Meanwhile, it also increases antioxidant enzymes involved in the oxidative damage defense. Prolonged, acute, or strenuous exercise often leads to an increased radical production and a subsequent oxidative stress in the skeletal muscles, while chronic regular or moderate exercise results in a decrease in oxidative stress. Notably, under pathological state, such as obesity, aging, etc., ROS levels could be elevated in humans, which could be attenuated by proper exercise. Significantly, exercise stimulates the development of beige adipose tissue and potentially influence the function of brown adipose tissue (BAT), which is known to be conducive to a metabolic balance through non-shivering thermogenesis (NST) and may protect from oxidative stress. Exercise-related balance of the ROS levels is associated with a healthy metabolism in humans. In this review, we summarize the integrated effects of exercise on oxidative metabolism, and especially focus on the role of brown and beige adipose tissues in this process, providing more evidence and knowledge for a better management of exercise-induced oxidative stress.

Proteomic Analysis of Cardiac Adaptation to Exercise by High Resolution Mass Spectrometry.

Regular exercise has many health benefits, among which is a significant reduction of cardiovascular risk. Although many beneficial effects of exercise are well described, the exact mechanisms by which exercise confers cardiovascular benefits are yet to be fully understood. In the current study, we have used high resolution mass spectrometry to determine the proteomic responses of the heart to exercise training in mice. The impact of exercise-induced oxidative stress on modifications of cardiomyocyte proteins with lipid peroxidation biomarker 4-hydroxynonenal (4-HNE) was examined as well. Fourteen male mice were randomized into the control (sedentary) group and the exercise group that was subjected to a swim exercise training program for 5 days a week for 5 months. Proteins were isolated from the left ventricular tissue, fractionated and digested for shotgun proteomics. Peptides were separated by nanoliquid chromatography and analyzed on an Orbitrap Fusion mass spectrometer using high-energy collision–induced dissociation and electron transfer dissociation fragmentation. We identified distinct ventricular protein signatures established in response to exercise training. Comparative proteomics identified 23 proteins that were upregulated and 37 proteins that were downregulated with exercise, in addition to 65 proteins that were identified only in ventricular tissue samples of exercised mice. Most of the proteins specific to exercised mice are involved in respiratory electron transport and/or implicated in glutathione conjugation. Additionally, 10 proteins were found to be modified with 4-HNE. This study provides new data on the effects of exercise on the cardiac proteome and contributes to our understanding of the molecular mechanisms underlying the beneficial effects of exercise on the heart.

Chronic L-Carnitine Supplementation on Exercise Performance, Blood Lactate, and Exercise-Induced Oxidative Stress in Resistance-Trained Males

Chronic L-Carnitine Supplementation on Exercise Performance, Blood Lactate, and Exercise-Induced Oxidative Stress in Resistance-Trained Males

Interaction Between Non-Insulin Glucose-Lowering Medication and Exercise in Type 2 Diabetes Mellitus - New Findings on SGLT2 Inhibitors.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors, which block glucose reabsorption in the kidneys, represent a novel class of non-insulin glucose-lowering medication used in the pharmacological therapy of type 2 diabetes mellitus (T2DM). They became available after the introduction of incretin-based therapies with glucagon-like peptide-1 receptor agonists (GLP-1 RAs) or dipeptidyl peptidase-4 (DPP4) inhibitors (1). All these newer drugs have multiple effects that go beyond their glucose-lowering effect (2). It has been concluded in a meta-analysis that patients with T2DM who take SGLT2 inhibitors experience fewer major adverse cardiovascular events and show reduced all-cause mortality (3). Another meta-analysis (including data from patients with T2DM, heart failure or chronic kidney disease) demonstrates that SGLT2 inhibitor use can reduce the risk of cardiac arrhythmia (4). Yet another meta-analysis shows that SGLT2 inhibitor use can reduce blood pressure in T2DM patients (5). The beneficial effects of SGLT2 inhibitors on the cardiovascular system do not only depend on the glucose-lowering effect, but are also based on other possible mechanisms, e.g. increased natriuresis and diuresis [for an overview, see (6)]. Although it is generally accepted that regular exercise also has glucose-lowering and beneficial cardiovascular effects, the combination of non-insulin glucose-lowering medication and regular exercise does not necessarily have to have additive effects on glycemic variables and/or cardiovascular health/cardiorespiratory fitness. By contrast, it has been concluded in some studies involving insulin resistant patients who take metformin, which is often recommended as the first-line medication in T2DM, that certain exercise adaptations (improvements in insulin sensitivity, peak oxygen uptake, blood pressure, lipid profile) are not further increased or can even be attenuated through metformin use (7–11). Details on the underlying molecular mechanisms of how metformin and exercise interact and affect exercise training outcomes have yet to be determined. Among others, changes in (exercise-induced) oxidative stress and/or inflammation (with effects on post-exercise cellular signals) or in (exercise-induced) autophagy have been discussed (10, 12). It should be noted, however, that not all studies report similar or blunted adaptations for all outcomes when exercise training is combined with metformin use. In the study of Viskochil et al. (13), for example, metformin and exercise training, but not exercise alone, lowered proinsulin concentrations and increased insulin clearance in adults with prediabetes. But what about the influence of SGLT2 inhibitors on training outcomes?

The effect of strength-endurance training on serum and urine metabolic profiles of female adolescent volleyball athletes.

Limited investigations on metabolic responses to exercise training in female adolescent volleyball athletes exist. The aim of this study was to obtain serum and urine metabolite markers in female adolescent volleyball athletes within 2-week strength-endurance training using a metabolomics approach coupled with biochemical analysis, which would be potential biomarkers for evaluating the physiological state of athletes. Twelve female adolescent volleyball athletes were recruited for 2-week strength-endurance training. Differential serum and urine metabolic profiles between the pre- and post-training group were obtained on gas chromatography coupled to mass spectrometry (GC-MS) and data subsequently underwent orthogonal partial least-squares analysis (OPLS). Strength-endurance training exerted a significant influence on the athletes' serum and urine metabolic profiles. The changed metabolites were primarily involved in energy metabolism, lipid metabolism and amino acids metabolism. Results support the hypothesis that female athletes displayed an increased propensity to oxidize lipids as the major energy source. Exposure to strength-endurance training also led to a significant increase in cortisol, but a decrease in testosterone, indicating disordered hormone adjustment. Exercise-induced oxidative stress occurred, as was evidenced by the decrease in reduced glutathione, and increases in blood malondialdehyde and oxidized glutathione. Since the muscle damage markers creatine kinase and lactate dehydrogenase did not show significant changes, the training might not cause cell membrane damage and the athletes did not cross the adaptive injury level. By measurement of endogenous metabolites, the metabolomics study has the potential to reveal the global physiological changes in response to exercise training.

Hypoxic Exercise Training Elevates Erythrocyte Aggregation

Pathological erythrocyte aggregation reduces capillary perfusion and oxygen transfer to tissue, which is determined by the negative surface charge on the erythrocyte membrane (intrinsic aggregability) and fibrinogen–erythrocyte interaction (extrinsic factor). Exercise-induced oxidative stress is important for rheological adaptation to training but may also cause erythrocyte senescence. This study clarifies the effects of hypoxic exercise training on intrinsic/extrinsic factors of aggregation. In total, 60 healthy sedentary males were randomly assigned to either hypoxic (HE; FIO2 = 0.15) or normoxic exercise training (NE; FIO2 = 0.21) groups for 30 min·d−1, 5 d·wk−1 for 6 weeks at 60 % of the maximum work rate or to a control group (CTL). A hypoxia exercise test (HET, FIO2 = 0.12) was performed before and after the intervention. Erythrocyte aggregation was assessed by ektacytometry, and fibrinogen binding affinity and senescence biomarkers were assessed by flow cytometry. An acute 12% oxygen HET significantly enhanced erythrocyte global aggregation through intrinsic aggregability. Resting aggregation is promoted by both intrinsic aggregability and fibrinogen binding probability and force after HE, whereas NE is mainly associated with ameliorated fibrinogen–erythrocyte interactions. The HET still facilitated global aggregation after HE because of the augmented fibrinogen-related factors, even though the intrinsic factor was suppressed. Additionally, HE further increased reticulocyte counts while reducing the expression of CD47 and CD147. Resting aggregability is promoted by both intrinsic and extrinsic factors after HE, whereas NE is mainly associated with an ameliorated affinity for fibrinogen. Although an accelerated turnover rate was observed, HE further led to erythrocyte senescence.

Effects of Vitamin E and Coenzyme Q10 Supplementation on Oxidative Stress Parameters in Untrained Leisure Horses Subjected to Acute Moderate Exercise

The effects of antioxidant supplements on exercise-induced oxidative stress have not been investigated in untrained leisure horses. We investigated the effects of 14-day supplementation with vitamin E (1.8 IU/kg/day), coenzyme Q10 (CoQ10; ubiquinone; 800 mg/day), and a combination of both (the same doses as in mono-supplementation) on the blood levels of CoQ10, vitamin E, and oxidative stress parameters in untrained leisure horses subjected to acute moderate exercise. Correlations between lipid peroxidation and muscle enzyme leakage were also determined. Forty client-owned horses were included in the study, with 10 horses in each of the antioxidant and placebo (paraffin oil) groups. Blood parameters were measured before supplementation, before and immediately after exercise, and after 24 h of rest. The differences in individual parameters between blood collection times and groups were analysed with linear mixed models (p ˂ 0.05). None of the supplemented antioxidants affected vitamin E and CoQ10 concentrations, oxidative stress parameters, or serum muscle enzymes. Lipid peroxidation occurred in horses supplemented with placebo and CoQ10 but not in horses supplemented with vitamin E or the combination of both antioxidants. These results suggest that vitamin E alone or in combination with CoQ10 prevented lipid peroxidation in untrained leisure horses subjected to acute moderate exercise.

The Effects of Beverage Intake after Exhaustive Exercise on Organ Damage, Inflammation and Oxidative Stress in Healthy Males.

Strenuous exercise induces organ damage, inflammation and oxidative stress. To prevent exercise-induced organ damage, inflammation and oxidative stress, rehydrating may be an effective strategy. In the present study, we aimed to examine whether beverage intake after exhaustive exercise to recover from dehydration prevents such disorders. Thirteen male volunteers performed incremental cycling exercise until exhaustion. Immediately after exercise, the subjects drank an electrolyte containing water (rehydrate trial: REH) or did not drink any beverage (control trial: CON). Blood samples were collected before (Pre), immediately (Post), 1 h and 2 h after exercise. Urine samples were also collected before (Pre) and 2 h after exercise. We measured biomarkers of organ damage, inflammation and oxidative stress in blood and urine. Biomarkers of muscle, renal and intestinal damage and inflammation increased in the blood and urine after exercise. However, changes in biomarkers of organ damage and inflammation did not differ between trials (p > 0.05). The biomarker of oxidative stress, thiobarbituric acid reactive substances (TBARS), in plasma, showed different changes between trials (p = 0.027). One hour after exercise, plasma TBARS concentration in REH had a higher trend than that in CON (p = 0.052), but there were no significant differences between Pre and the other time points in each trial. These results suggest that beverage intake after exercise does not attenuate exercise-induced organ damage, inflammation or oxidative stress in healthy males. However, rehydration restores exercise-induced oxidative stress more quickly.

Does vitamin C minimise exercise-induced oxidative stress?

Oxidative stress occurs when there is an imbalance between the production of free radicals and the detoxification of these reactive products. Regular exercise greatly increases the production of free radicals in humans, while excessive exercise could lead to cellular and tissue damage. This paper presents a review of studies focusing on exercise-induced oxidative stress, sufficient intensity of aerobic or anaerobic exercises, and how exercise volume and duration could increase free radicals in humans. Furthermore, this review examines the effects of chronic or acute vitamin C supplementation in minimising oxidative stress during exercise. In this regard, vitamin C is commonly consumed as an antioxidant supplement by endurance athletes to minimise exercise-induced oxidative stress, augment recovery and improve performance. However, there is still a lack of evidence regarding the antioxidant effects of vitamin C supplements during exercise. Based on the review, it could be concluded healthy, physically active individuals might not require regular intakes of non-physiological dosages of vitamin C. On the other hand, studies found that regular exercise could lead to higher antioxidant production that could be beneficial in mitigating oxidative stress and improving individuals’ health.

Pre-Exercise Carbohydrate or Protein Ingestion Influences Substrate Oxidation but Not Performance or Hunger Compared with Cycling in the Fasted State

Nutritional intake can influence exercise metabolism and performance, but there is a lack of research comparing protein-rich pre-exercise meals with endurance exercise performed both in the fasted state and following a carbohydrate-rich breakfast. The purpose of this study was to determine the effects of three pre-exercise nutrition strategies on metabolism and exercise capacity during cycling. On three occasions, seventeen trained male cyclists (VO2peak 62.2 ± 5.8 mL·kg−1·min−1, 31.2 ± 12.4 years, 74.8 ± 9.6 kg) performed twenty minutes of submaximal cycling (4 × 5 min stages at 60%, 80%, and 100% of ventilatory threshold (VT), and 20% of the difference between power at the VT and peak power), followed by 3 × 3 min intervals at 80% peak aerobic power and 3 × 3 min intervals at maximal effort, 30 min after consuming a carbohydrate-rich meal (CARB; 1 g/kg CHO), a protein-rich meal (PROTEIN; 0.45 g/kg protein + 0.24 g/kg fat), or water (FASTED), in a randomized and counter-balanced order. Fat oxidation was lower for CARB compared with FASTED at and below the VT, and compared with PROTEIN at 60% VT. There were no differences between trials for average power during high-intensity intervals (367 ± 51 W, p = 0.516). Oxidative stress (F2-Isoprostanes), perceived exertion, and hunger were not different between trials. Overall, exercising in the overnight-fasted state increased fat oxidation during submaximal exercise compared with exercise following a CHO-rich breakfast, and pre-exercise protein ingestion allowed similarly high levels of fat oxidation. There were no differences in perceived exertion, hunger, or performance, and we provide novel data showing no influence of pre-exercise nutrition ingestion on exercise-induced oxidative stress.

Effects of Dietary Strategies on Exercise-Induced Oxidative Stress: A Narrative Review of Human Studies.

Exhaustive exercise can induce excessive generation of reactive oxygen species (ROS), which may enhance oxidative stress levels. Although physiological levels are crucial for optimal cell signaling and exercise adaptations, higher concentrations have been demonstrated to damage macromolecules and thus facilitate detrimental effects. Besides single dosages of antioxidants, whole diets rich in antioxidants are gaining more attention due to their practicality and multicomponent ingredients. The purpose of this narrative review is to summarize the current state of research on this topic and present recent advances regarding the antioxidant effects of whole dietary strategies on exercise-induced oxidative stress in humans. The following electronic databases were searched from inception to February 2021: PubMed, Scope and Web of Science. Twenty-eight studies were included in this narrative review and demonstrated the scavenging effects of exercise-induced ROS generation, oxidative stress markers, inflammatory markers and antioxidant capacity, with only one study not confirming such positive effects. Although the literature is still scarce about the effects of whole dietary strategies on exercise-induced oxidative stress, the majority of the studies demonstrated favorable effects. Nevertheless, the protocols are still very heterogeneous and further systematically designed studies are needed to strengthen the evidence.

Effects of concurrent eight-week aerobic trainings and Rosa canina L. fruit hydroalcoholic extract on liver enzymes and malondialdehyde of liver in male rats following an acute aerobic exercise until exhaustion

Background: Rosa canina L. has high levels of carotenoids, flavonoids and, vitamin C antioxidant compounds that can withstand the destructive effects of exhaustive exercise-induced oxidative stress. The present study aims to investigate the effects of concurrent eight-week aerobic training and Rosa canina L. fruit hydroalcoholic extract on some liver enzymes and malondialdehyde of liver in male rats following an acute aerobic exercise until exhaustion. Methods: The present research was an experimental study. Forty male Wistar rats were randomly divided into four groups (N=10): placebo (without exercise + distilled water 2 ml supplement), supplement (without exercise + Rosa canina L extract, 100 mg/kg), exercise (8 weeks exercise + distilled water 2 ml), combined (8 weeks exercise + Rosa canina L extract, 100 mg/kg). At the end of the experiment, half of the rats were killed immediately before exhaustive exercise; while the other half were killed immediately after performing an acute exhaustive exercise on the treadmill. Serum enzymes AST, ALT, and hepatic malondialdehyde levels were measured by ELISA and thiobarbituric acid methods, respectively. Results: The results show that in all groups except the combined group serum AST, ALT, and malondialdehyde of the liver were significantly increased following an acute exhaustive exercise compared to the prior exhaustive exercise (P<0.05). Conclusion: The use of Rosa canina L Fruit hydroalcoholic extract with aerobic exercise prevented the increase of hepatic malondialdehyde and serum enzymes AST, ALT levels following an acute exhausting exercise.

Effect of Different Exercise Modalities on Oxidative Stress: A Systematic Review

Exercise-induced benefits are being increasingly recognized in promoting health and preventing diseases. However, initial adaption to exercise response can have different effects on cells, including an increase in the formation of oxidants and inflammatory mediators that ultimately leads to oxidative stress, but this scenario depends on the exercise type and intensity and training status of the individual. Therefore, we aimed to understand the effect of different types of exercise on oxidative stress. Indeed, exercise-induced minimum oxidative stress is required for regulating signaling pathways. According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, a search for relevant articles was carried out on PubMed/Medline, ISI Web of Science, and Google Scholar using a broad range of synonyms such as oxidants, reactive oxygen species (ROS), oxidative stress, exercise, physical training, aerobic exercise, and strength exercise until 2019. This study selected a total of 18 articles for assessing the oxidative damage using various parameters such as malondialdehyde (MDA), protein carbonyl (PCO), and F1-isoprostanes and enzymatic antioxidants. We observed that any type of exercise can increase the oxidative damage in an exercise type and intensity manner. Further, the training status of the individual and specific oxidative damage marker plays a crucial role in predicting earlier oxidative damage in the exercise condition. However, some of the studies that we included for review did not perform follow-up evaluations. Therefore, follow-up programs using larger numbers need to be performed to confirm our findings.

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

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.

Blood oxidative stress and post-exercise recovery are unaffected byhypobaric and hypoxic environments

ABSTRACT Hypobaria and hypoxia exert independent effects on oxidative stress during exercise, while combined effectson the post-exercise recovery period remain unclear.Accordingly, this study examined the recovery period during lab-simulated hypoxic and hypobaric conditions following exercise-induced oxidative stress. Participants (n=13) performed 60-minutes of cycling (70% watts max) in a normobaric normoxic environment followed by a four-hour recovery under three conditions; 1000m normobaric normoxia (NN, 675mmHg), 4400m normobaric hypoxia (NH, 675mmHg), or 4400m hypobaric hypoxia (HH, 440mmHg). Blood samples collected at Pre, Post, 2-Hours (2-HR), and 4-Hours (4-HR) post-exercise were analyzed fora potential increase in biochemical modifications of proteins(protein carbonyls, PC; 3-nitrotyrosines, 3NT) lipids (lipid hydroperoxides, LOOH; 8-isoprostanes, 8-ISO), and antioxidant capacity (FRAP, TEAC). Gene transcripts (EPAS, HMOX1, SOD2, NFE2L2) were quantified by qRT-PCR from muscle biopsies taken Pre and Post exercise. Hypoxia and hypobaria had no effect throughout recovery. Post-exercise TEAC (p=0.041), FRAP (p=0.013), and 8-ISO (p=0.044) increased, while PC (p=0.002) and 3-NT (p=0.032) were decreased. LOOH was lower in Post (p=0.018) NH trial samples. Exercise-dependent increases occurred in NFE2L2 (p=0.003), HMXO1 (p<0.001), SOD2 (p=0.046), and EPAS (p=0.038). Exercise recovery under conditions of NH and HH did not impact blood oxidative stress or redox-sensitive gene transcripts.

Mitochondria-targeted antioxidant supplementation improves 8\u2009km time trial performance in middle-aged trained male cyclists

BackgroundExercise increases skeletal muscle reactive oxygen species (ROS) production, which may contribute to the onset of muscular fatigue and impair athletic performance. Mitochondria-targeted antioxidants such as MitoQ, which contains a ubiquinone moiety and is targeted to mitochondria through the addition of a lipophilic triphenylphosphonium cation, are becoming popular amongst active individuals as they are designed to accumulate within mitochondria and may provide targeted protection against exercise-induced oxidative stress. However, the effect of MitoQ supplementation on cycling performance is currently unknown. Here, we investigate whether MitoQ supplementation can improve cycling performance measured as time to complete an 8 km time trial.MethodIn a randomized, double-blind, placebo-controlled crossover study, 19 middle-aged (age: 44 ± 4 years) recreationally trained (VO2peak: 58.5 ± 6.2 ml·kg− 1·min− 1, distance cycled per week during 6 months prior to study enrollment: 158.3 ± 58.4 km) male cyclists completed 45 min cycling at 70% VO2peak followed by an 8 km time trial after 28 days of supplementation with MitoQ (20 mg·day− 1) and a placebo. Free F2-isoprostanes were measured in plasma samples collected at rest, after 45 min cycling at 70% VO2peak and after completion of the time trial. Respiratory gases and measures of rating of perceived exertion (RPE) were also collected.ResultsMean completion time for the time trial was 1.3% faster with MitoQ (12.91 ± 0.94 min) compared to placebo (13.09 ± 0.95 min, p = 0.04, 95% CI [0.05, 2.64], d = 0.2). There was no difference in RPE during the time trial between conditions (p = 0.82) despite there being a 4.4% increase in average power output during the time trial following MitoQ supplementation compared to placebo (placebo; 270 ± 51 W, MitoQ; 280 ± 53 W, p = 0.04, 95% CI [0.49, 8.22], d = 0.2). Plasma F2-isoprostanes were lower on completion of the time trial following MitoQ supplementation (35.89 ± 13.6 pg·ml− 1) compared to placebo (44.7 ± 16.9 pg·ml− 1p = 0.03).ConclusionThese data suggest that MitoQ supplementation may be an effective nutritional strategy to attenuate exercise-induced increases in oxidative damage to lipids and improve cycling performance.

Effects of Exercise-Induced ROS on the Pathophysiological Functions of Skeletal Muscle.

Oxidative stress is the imbalance of the redox system in the body, which produces excessive reactive oxygen species, leads to multiple cellular damages, and closely relates to some pathological conditions, such as insulin resistance and inflammation. Meanwhile, exercise as an external stimulus of oxidative stress causes the changes of pathophysiological functions in the tissues and organs, including skeletal muscle. Exercise-induced oxidative stress is considered to have different effects on the structure and function of skeletal muscle. Long-term regular or moderate exercise-induced oxidative stress is closely related to the formation of muscle adaptation, while excessive free radicals produced by strenuous or acute exercise can cause muscle oxidative stress fatigue and damage, which impacts exercise capacity and damages the body's health. The present review systematically summarizes the relationship between exercise-induced oxidative stress and the adaptions, damage, and fatigue in skeletal muscle, in order to clarify the effects of exercise-induced oxidative stress on the pathophysiological functions of skeletal muscle.

The Effects of Curcumin Supplementation on Muscle Damage, Oxidative Stress, and Inflammatory Markers in Healthy Females with Moderate Physical Activity: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial.

Background:Exercise-induced oxidative stress, muscle damage, and inflammation represent major contributors to why athletes use ergogenic aids. Turmeric is used as a spice because of its polyphenol ingredient named curcumin. We assessed the effects of curcumin supplementation on inflammatory, oxidative stress markers, muscle damage, and anthropometric indices in women with moderate physical activity.Methods:This double-blind, placebo-controlled clinical trial was conducted on 80 women with moderate physical activity levels (defined as walking or swimming for at least 1 h per day) for 8 weeks. Mean ± SD of age (years) all participants was 21 ± 2. Participants were randomly assigned into two groups: curcumin (500 mg/day) and placebo (500 mg/day cornstarch). Serum C-reactive protein (CRP), total antioxidant capacity (TAC), malondialdehyde (MDA), lactate dehydrogenase (LDH) levels, body composition, and maximum oxygen uptake (VO2 max) were evaluated before and after an intervention.Results:Sixty-five subjects completed the 8-week intervention. Within analysis indicated a significant decrease in CRP, LDH, MDA levels, and a significant increase in VO2 max in the curcumin group after an intervention (P < 0.05). There were significant decreases in CRP (P = 0.002), LDH (P = 0.041), and MDA (P = 0.005), no significant increase in TAC, and significant increase in VO2 max (P = 0.0001) levels in the curcumin group compared with placebo group. There were no significant changes in weight, body mass index, body fat, and lean body mass between two groups.Conclusions:Our findings indicated that 8-week curcumin administration could significantly improve CRP, LDH, MDA, and VO2 max. Curcumin supplementation did not elicit significant changes in anthropometric indices in this study.