Dtress authors read and approved of strese final manuscript. Consumption of foods rich in antioxidants in the diet during or after Outsource resupply needs plays a Oxidative stress and post-workout nutrition role in reducing this damage. They reported to the lab in the morning following an eight hour fast. Nutr Rev. Manganese Mn is a cofactor of Mn-SOD form, present in the mitochondria and copper Cu and zinc Znare cofactors present in cytosol [ 57 ].

Oxidative stress and post-workout nutrition -

No subject was a vegetarian or a smoker, nor did they use tobacco products, anti-inflammatory drugs, or antioxidant supplements before for a minimum of six months or during the study period.

Characteristics of subjects who completed the study are provided in Table 1. All experimental procedures were performed in accordance with the Helsinki Declaration and the policy statement of the American College of Sports Medicine on research with human subjects. The University of Memphis Human Subjects Committee approved all experimental procedures.

All subjects provided both verbal and written consent prior to participating in this investigation. Subjects were initially assigned to perform either a prior bout of eccentric exercise as described below, or no prior exercise. In both conditions, subjects consumed two capsules per day one soft gel and one powder to provide the above dosage, for 14 days prior to performing the eccentric exercise protocol as described below, and during two days of recovery.

The use of the selected antioxidants, as well as the dosage and time of administration was based on our previous work demonstrating benefits in relation to muscle injury [ 7 ] and oxidative stress [ 9 , 22 ]. We have recently shown that the 14 day pretreatment period significantly elevates both plasma levels of vitamin C and vitamin E [ 22 ].

Both the soft gel soybean oil and powder cellulose placebos were identical in appearance to the antioxidants packaged in typical one gram capsules. All group assignment was randomized and double-blinded. Subjects reported to the laboratory on several occasions as shown in Table 2.

During visit one, anthropometric measurements were obtained, concentric bench press one-repetition maximum 1RM was determined, and practice was provided for the isometric and dynamic muscle performance tests. For the 1RM testing, the ProSpot ® self spotting system was used, which "catches" the barbell at the top portion of the lift and lowers it back to the starting position, thereby negating the eccentric component.

This system was used in order to avoid any additional familiarization associated with eccentric work. An additional practice session was performed 48—72 hours after this initial visit. The 1RM testing as well as practice sessions did not induce any degree of muscle soreness in our sample of resistance trained men.

Therefore, we do not believe that these sessions interfered with our outcome variables, as they might have if we had included previously non-resistance trained subjects.

Following this second practice session, subjects received their group assignment. Those subjects not performing a prior bout of eccentric exercise started their assigned treatment for the 14 day period. Those subjects assigned to perform prior exercise exactly as described below for the eccentric exercise protocol were scheduled to do so within 48—72 hours following their second practice session.

These subjects began their assigned treatment 72—96 hours following their prior exercise bout, for the 14 day period. During the 14 day pretreatment supplementation period, all subjects were instructed to resume their normal patterns of resistance training, with the exception of refraining from strenuous physical activity during the 48 hours preceding the eccentric exercise protocol.

The 14 day period between the initial and second eccentric bout for subjects in the prior exercise group was chosen to allow for complete recovery from the initial bout, while allowing for any protection afforded by the preconditioning bout to remain present, as such adaptations have been reported to appear for periods up to months following the initial bout [ 5 ], at least for markers of muscle damage.

There are presently no data in relation to attenuation of oxidative stress biomarkers and the repeated bout effect. During the two days preceding the eccentric exercise protocol subjects were asked to avoid strenuous physical activity.

They reported to the lab in the morning following an eight hour fast. To ensure subject safety and for ease of administration, a Smith-machine was chosen for this exercise.

The barbell was lowered for five seconds at which time it came in contact with their chest at the end of the five second period. This continued until all 10 repetitions were performed. Subjects were provided seconds rest between each set and were provided water ad libitum.

Through pilot testing, we found that the load and rest interval length used here were sufficient to induce considerable muscle soreness and loss of muscle force, and realistic to complete.

Therefore, even though use of a protocol inclusive of greater loads may have induced more injury, and thus potentially a greater degree of adaptive protection, it simply was not realistic for subjects to perform.

The actual load used during the protocol was used in this equation, accounting for any potential decrease in load due to fatigue. Rating of perceived exertion RPE using the 6—20 Borg scale and heart rate Polar A5 monitors was also assessed at the completion of each set and the average value over 10 sets was calculated.

The dependent variables in this investigation are commonly used in the study of exercise-induced muscle injury and oxidative stress [ 23 ]. The variables described below with the exception of antioxidant reducing capacity — measured only pre exercise; and lactate — measured only pre and immediately after exercise were measured pre, immediately after, 24 and 48 hours after the eccentric exercise protocol.

The order of data collection was as follows. For each time point, approximately 15 mL of blood was collected into vacutainer tubes via antecubetal venipuncture. The pre exercise sample was taken following a minute quiet rest period.

Blood from tubes containing EDTA was placed on ice and immediately used for analysis of whole blood lactate Accutrend; Roche Diagnostics, Mannheim, Germany. The remainder of blood was immediately processed by centrifugation to obtain plasma. Blood collected into vacutainer tubes containing no additive was allowed to clot at room temperature for 30 minutes and then processed by centrifugation to obtain serum.

Both plasma and serum samples were stored in multiple aliquots at °C until analyzed for markers described below. All assays were performed in duplicate on first thaw. As a marker of sarcolemma disruption, serum creatine kinase activity was measured spectrophotometrically using commercially available reagents StanBio Labs, Boerne, TX.

The coefficient of variation for this assay was 4. As a marker of systemic inflammation, serum C-reactive protein was measured using an ultra-sensitive sandwich ELISA procedure Diagnostic Systems Laboratories, Inc. The coefficient of variation for this assay was 5. Plasma antioxidant reducing capacity represented as uric acid equivalents was determined as a marker of blood antioxidant capacity using commercially available reagents Northwest Life Science Specialties, Vancouver, WA.

The coefficient of variation for this assay was 6. As markers of oxidative stress, plasma protein carbonyls were measured using an ELISA according to the procedures recommended by the manufacturer Zentech Technology, Dunedin, New Zealand , and plasma total peroxides were measured using a colorimetric assay with hydrogen peroxide as the standard, as described by the reagent manufacturer Pierce Biotechnology, Inc.

The coefficient of variation for these assays was 3. To ensure quality control, both high and low calibrated controls were used in each ELISA procedure.

Using a 10 cm visual analog scale where "0" represents no pain and "10" represents intense pain subjects reported their perceived muscle soreness following the performance of two concentric-eccentric repetitions of the barbell bench press exercise using a standard 20 kg barbell.

Subjects were familiarized to these procedures prior to the day of the eccentric protocol. Maximal isometric force in a bench press position was measured using a customized force plate and power rack design. This power rack had one-inch hole spacing for individual bar height adjustments.

The upper arm was fixed parallel to the floor with a 90° angle about the elbow joint and the bar was in line with the mid-sternum.

From this position, the corresponding grip width and fixed bar height were recorded and reproduced for all testing sessions. Calibration of the force plate was performed daily according to manufacturer's recommendations Rice Lake Weighing Systems; Rice Lake, WI. Subjects were given instruction to contract as hard and as fast as possible.

Data were sampled at Hz and channeled though a bit analog-to-digital converter DASJr; Measurement Computing, Middleboro, MA. Data were smoothed using a 4 th -order recursive Butterworth digital filter cutoff frequency 30 Hz and analyzed for peak force using Datapac 2k2 v3.

The movement began with the bar against the subjects' chest in line with the mid-sternum. When given the command from the investigator, subjects attempted to throw the bar for maximal height.

Grip widths corresponding to those of the isometric test were maintained throughout testing. Subjects were also instructed to keep their entire body in contact with the bench and force plate.

Data were sampled as described previously, except that a 20 Hz cutoff frequency was used for velocity. For both the isometric and dynamic tests, the higher of two values for each measure was used in the analyses. All subjects were instructed to maintain their normal diet during the study period and completed daily food records for the two days before testing, the day of testing, and the day following testing.

Records were analyzed for total kilocalories, protein, carbohydrate, fat, vitamin C, vitamin E, and vitamin A using commercially available software Diet Analysis Plus, ESHA Research, Salem, OR. The data for all dependent variables were analyzed using a 4 group × 4 time repeated measures ANOVA.

Significant interactions and main effects were analyzed using Tukey's post hoc test. As sample sizes were relatively small amongst groups, we performed the Kolmogorov-Smirnov and Mauchly tests to confirm normality and homogeneity of variances, respectively.

From our dependent variables, we identified creatine kinase activity and C-reactive protein as those not following a normal distribution and were subsequently log transformed for analysis.

The Mauchly test confirmed sphericity of our data. Subject characteristics, dietary variables, and antioxidant reducing capacity data were compared between subject groups using a one-way ANOVA. Pairwise correlations for all dependent variables were generated.

Effect size calculations were performed using Cohen's D. All analyses were performed using JMP statistical software SAS Institute, Cary, NC.

The data for dependent variables are presented as mean ± SEM. Subject characteristics, exercise related measures e. work, RPE, heart rate, and lactate , and dietary data are presented as mean ± SD.

Characteristics of these 30 subjects are included in Table 1. Six subjects did not complete all aspects of the study due to personal reasons e. lack of time, problems with blood donation, injury resulting from accident unrelated to study. No differences were observed between NoP, NoA, ExP, or ExA for total work ± ; ± ; ± ; ± kJ , RPE 16 ± 2; 18 ± 1; 17 ± 1; 16 ± 2 , heart rate ± 15; ± 16; ± 21; ± 12 bpm , or blood lactate 7.

Dietary data are shown in Table 3. Neither creatine kinase activity nor C-reactive protein followed a normal distribution and therefore, data were log transformed prior to analysis.

However, for ease of comparison to other published studies using these biomarkers, the original values are included in Figure 1.

Data for bloodborne variables are shown in Figure 1. Creatine kinase activity A , C-reactive protein B , protein carbonyls C and peroxides D before and following an acute bout of eccentric resistance exercise in trained men. Values remained below pre exercise at 48 hours post exercise for maximal isometric force but recovered by 24 hours post exercise for peak velocity.

Data for muscle soreness and function are shown in Figure 2. Muscle soreness A , maximal isometric force B , peak velocity C , and maximal dynamic force D before and following an acute bout of eccentric resistance exercise in trained men.

The only exceptions to the finding of small effect sizes occurred for creatine kinase activity and C-reactive protein at both 24 and 48 hours post exercise, where effect size calculations ranged from 0.

The findings of the present study partially refute our initial hypotheses. That is, no effect was observed for the combination of prior exercise and antioxidant supplementation in our sample of resistance trained subjects. Based on these data, there appears to be no independent or combined effect of prior exercise or antioxidant supplementation as provided here on markers of muscle injury or oxidative stress following muscle damage-inducing exercise.

Due to the novelty of our chosen exercise model we initially believed that the performance of a preconditioning session would allow for an adaptation in accordance with the repeated bout effect, which is quite evident for non-resistance trained subjects, as described by McHugh [ 4 ].

Despite the fact that our subjects were resistance trained, no individual used eccentric exercise exclusively, especially using the high volume-load employed in the present study.

Therefore, we believed that the novelty of such a prior bout would lend protection against the subsequent bout in relation to muscle injury and oxidative stress.

However, this was not the case, and we need to reject our initial hypothesis. While creatine kinase activity, muscle soreness, maximal isometric force and peak velocity were altered in response to the exercise bout, indicative of a muscle injury response, there were no group differences noted for any variable.

It is possible that a pro-oxidant effect was apparent in this group, although other markers did not appear to differ greatly between this group and the others.

Free radicals damage our cells and our DNA and have been linked as a possible cause of cancer and visible ageing. However, if we keep our intake of antioxidants high then these vitamins can combat the production of free radicals and keep our body at an optimum level. Well, as we said before, exercising puts our body under physical stress and it ramps up the production of free radicals.

Therefore, if we are not preloading with an adequate amount of antioxidant-containing foods then we are at risk of suffering from cell damage, which is not good.

A recent study on people with type 2 diabetes suggests that fruit and vegetable intake may decrease oxidative stress and inflammation. An increased intake of fruit and vegetables can therefore be beneficial for patients with type 2 diabetes, since these patients are documented to have raised oxidative stress and inflammation.

Although the study is focused on people suffering from diabetes, their levels of stress and inflammation are far higher than people without, due to the imbalance of their blood glucose levels. Diet becomes important because many people today live on a diet made up of many processed foods and sugar, which are counterproductive to combatting free radicals and oxidative stress.

By simply adjusting the way that you eat, you could maintain that healthy balance in the body that is necessary to live a healthy life. Learn what lifestyle-related diseases are and how to take small steps in your daily life to proactively prevent disease by downloading our Proactive Health Management Playbook.

Your body produces antioxidants on its own, but it is not enough to combat the effects of free radicals that are caused as a result of your environment and lifestyle. Your genetics play a big role in determining your inherent need for antioxidants and how well your body utilises these vitamins.

By doing a DNA test you will receive information based on your own individual profile pertaining to your antioxidant need, which will guide you in knowing the amount of antioxidants you should be including in your diet; although whatever your profile you should be consciously including antioxidant-rich foods in your diet regardless as they are crucial for a healthy life.

Another route that people go is to supplement rather than focusing on foods. At DNAfit we are all about promoting a food first approach because foods that are high in antioxidants are also rich in other vitamins such as vitamin E, vitamin C, selenium, zinc and beta carotene.

Moderate exercise can increase the antioxidant's level which facilitates an optimal level of ROS, whereas high intensity exercise can induce ROS formation, giving the maximum cellular adaptation Powers and Jackson, Additionally, assessing the oxidative damage is unequivocal during exercise because oxidative damage is varied according to the intensity and duration.

This can ultimately bring into question the exact role of ROS and exercise performance Knechtle and Nikolaidis, ROS can induce several adaptive signaling pathways in the skeletal muscle Powers and Jackson, However, the mechanism by which it can induce those pathways that signal for improved exercise performance is poorly understood.

Furthermore, the ROS steady state level may significantly contribute to such an effect instead of an elevated level of ROS. Steady-state concentrations of ROS are well-balanced by several enzymatic regulations. For example, superoxide dismutase SOD lowers the steady state level of superoxide and decreases the rate of H2O2 production Liochev and Fridovich, , Further, this can maintain the activities of catalase and peroxidase.

These studies exposed the fact that superoxide radicals inactivated the catalase and peroxidase, and SOD is the reason for this. In the exercise condition, steady state and ROS levels are determined by both the rate of ROS production and the rate of ROS scavenging.

Oxidative stress is not only a phenomenon that refers to elevated levels of ROS that damage lipids, proteins, and DNA, but it also plays a significant role in physiological changes through the interaction with cysteine Cys residues of proteins.

Therefore, it is important to consider the measurement of oxidative stress before it causes damage to the cells by affecting several physiological functions. However, measurement of oxidative stress in the cells has several limitations in terms of biomarker selection.

This should run down the exact status of oxidative stress. Therefore, focusing on the underlying mechanism of adaptive signaling induced by ROS and selecting suitable biomarkers may facilitate runners that compete in long distance running by preventing ROS-induced damages in the skeletal muscles.

Running in events like a marathon or ultra-marathon can result in muscle injury, and the main factors that induce muscle injury are the activation of inflammatory cascades and oxidative stress, but measurement of oxidative stress has no particular suitable biomarkers as stated above Niemelä et al.

Therefore, this kind of sport may be a useful platform to find applicable biomarkers that can exactly predict the oxidative stress status in the cells. Moreover, there have been several arguments on whether extreme training sessions like ultra-marathons may increase the health benefits of physical exercise.

The level of oxidation response ROS level which improves the exercise performance or increases the exercise-induced benefits is ambiguous Mrakic-Sposta et al. Measuring the oxidative damage by selecting suitable biomarkers, nutrition, individual physical condition, type, and intensity of running exercise among the runners Mrakic-Sposta et al.

However, no studies have firmly established these aspects in terms of improving running exercise performance and the benefits. Therefore, the aim of this study was to present a systematic overview of published articles and to find the suitable biomarkers that predict oxidative stress among long-distance runners.

To avoid the risk of missing relevant articles, additional papers were searched on the gray literature i. One author AT ran the search and screened the initial titles after duplicates were removed.

Two authors AT and GY independently examined potentially relevant articles in depth. We included only papers published in peer-reviewed journals which reported findings from experimental controlled studies, i.

We excluded articles not available in English, unpublished papers, and conference posters, or those reporting findings of non-experimental studies e.

First author's name, year of publication, sample of intervention and control group, design and duration of the study, topic, type of intervention, outcome, assessment, and results were recorded using an electronic spreadsheet. II The runners had to be competitive, and participants that required medical support were omitted.

III Search outputs included only articles that were peer-reviewed and published in English language journals. IV Only running programs like half marathons, marathons, and ironman races were included as types of interventions.

Only parameters that were related to oxidative damage and some studies on inflammatory responses that induce oxidative stress were included as types of outcome measures. The abstracts of the articles were further narrowed down using the following criteria: Inclusion criteria: We included prospective cohort studies, cross sectional studies, and randomized clinical trials.

Exclusion criteria: We excluded different sport activities other than running programs. The risk of bias assessment was performed independently by two authors based on the Cochrane Risk of Bias Assessment Tool. A third author was consulted in case of any disagreements.

For each study, the study characteristics e. All the parameters were evaluated in blood samples collected during or after the running program. Disagreements were resolved through discussions with other authors. After evaluating titles and abstracts, articles were identified as potentially relevant from initial data base searches Figure 1.

After screening was performed using titles and relative keywords, articles were excluded. The remaining 34 potential articles full texts were carefully evaluated, and 22 articles were excluded.

The full texts of the remaining 12 articles were retrieved and reviewed, which were then included for systematic analysis. A total of 12 studies were included in this study. Study population, the number of participants, mean age and SD, intervention, and main outcomes are outlined in Table 1.

This study selected 12 articles to assess the effect of running exercise protocols on oxidative stress parameters. Fourteen articles were identified by searching databases and two were identified by the article's reference for inclusion in the analysis.

All the records used in this study were based on human subjects. From the 12 included studies, at least six studies had risk of bias. Three studies had high risk in random sequence generation and allocation concealment.

Four studies had a high risk in incomplete outcome data and two studies had high risk in other biases. Six studies had unclear risk in randomization and allocation concealment.

Three studies had low risk in randomization and allocation concealment. Eleven studies had low risk in blinding of participants, and four studies had high risk in blinding of outcome assessment. All the studies had low risk in selective reporting Table 2.

Four studies had low risk in other biases and six studies had unclear risk in other biases Figure 2. After the first study that suggests exercise increases oxidative stress by Dillard et al. in , a plethora of reports have shown that exercise increases oxidative stress in humans or animals.

These studies mostly used cycle ergometer or treadmill exercises in which the participants used maximal or submaximal exercise in a climate-controlled laboratory.

This compromises the prediction of the oxidative stress status among the exercised people. Therefore, to predict oxidative stress, it is important to assess suitable oxidative damage markers in various running platforms.

One study showed neutrophilia and enhanced PMN capacity to generate oxygen radicals after running. This is the point where the oxygen radicals are established in the runner's blood and are evidenced by increased levels of LPO and GSSG as well as decreased level of SOD and GSH-Px Hessel et al.

Another study showed that a single bout of endurance exercise increases TRAP and some of its components like uric acid, but this was due to an adaptive mechanism against running-induced oxidative stress. The intense endurance exercise increased MDA which may react physiologically with several nucleosides to form adducts to deoxyguanosine and deoxyadenosine, and increased exercise intensity may increase the purine oxidation which results in an increase in the formation of uric acid UA.

This may be due to an adaptive mechanism against running-induced oxidative stress. Further, endurance training increases the high rate of ATP hydrolysis compared to its resynthesis which further stimulates the myokinase reaction and adenosine monophosphate deaminase reaction. Consequently, the adenine nucleotide pool decreased.

Inosine-5'-monophosphate IMP , hypoxanthine Hx , xanthine X , and UA are exercise related products of adenine nucleotide degradation that accumulate in the skeletal muscle or efflux into the blood which ultimately decreases the adenine nucleotide pool precursors Zieliński et al.

However, adenine nucleotide pool restoration may be slow and energy consuming, and de novo synthesis from the purine Hx is the only compound that may be reconverted and reutilized into the adenine nucleotide pool after being catalyzed by hypoxanthine-guanine phosphoribosyltransferase HGPRT.

Intense exercise increases the Plasma Hx significantly. Therefore, it is considered as an index of exercise intensity Rychlewski et al. Furthermore, high intensity exercise limits the efflux of purines to the plasma resulting in reduced muscle nucleotide loss in active men Hellsten-Westing et al.

Six weeks of high intensity exercise decreased the level of Hx both at rest and after the exercise, and this may be due to muscle adaptation that leads to a reduced adenine nucleotide Hellsten-Westing et al. Further, this study showed that a reduced level of thiol content was efficiently utilized by the ROS after the race Liu et al.

An additional study showed that prolonged ultra-endurance exercise causes an increase in ROS production and oxidative stress, but it is dependent on specific biomarkers and the exercise duration Vezzoli et al.

A different study investigated the effect of running on oxidative modification of nucleic acid, and it was found that marathon participation immediately induced an inflammatory response, but it did not increase the oxidative modification of nucleic acid, instead, it decreases the oxidatively generated nucleic acid modifications, suggesting an adaptive antioxidant effect following running Radák et al.

One study showed that even after the running, the oxidative stress lasted for up to 3 days. Additionally, this study showed that capacity oxidation-reduction potential cORP , and GSH are the most effective markers for analyzing running-induced oxidative stress Spanidis et al.

Two studies investigated the ironman triathlon's effect in inducing oxidative damage. From those two studies, one study showed that there is no persistent oxidative stress in response to an iron-man race Wagner et al.

Another study showed that increased oxidative stress regulates the inflammatory process during heavy exertion Nieman et al. Another study showed that heavy endurance exercise increased the lipid peroxidation Mastaloudis et al.

One study showed that exhaustive and prolonged exercise induces oxidative stress and inflammation Mrakic-Sposta et al. This systematic review analyzed the effect of different running programs on oxidative stress with the aim of determining suitable biomarkers that predict the early oxidative stress status in runners.

From the 12 selected and systematically reviewed articles, running exercises do not elicit a response to specific biomarkers of oxidative stress, instead, oxidative stress markers like ROS induced end products of lipids, proteins, and various enzymatic and non-enzymatic antioxidants expressed according to the training status of the individual.

Although it is known that exercises like running can induce oxidative stress, the methods that potentially measure the oxidative damage are limited because some of the methods have failed to reflect the exact status of oxidative stress in the cells. Consequently, the measurement of oxidative stress is required and is a more promising approach in different physiological conditions induced by exercise.

Measurement of cellular ROS is one of the direct ways to determine the oxidative stress. For example, fluorogenic probes are used as a direct method to measure superoxide radicals, hydrogen peroxide, hydroxyl radicals, and peroxyl radicals Debowska et al.

Other ways to assess the oxidative stress include ROS derived metabolites D-ROMS. However, these measurements are compromised in predicting its accuracy because the radicals that are assessed using direct measurements are relatively short lived and highly reactive Denicola et al.

Additionally, different ROS have different degrees of reactivity toward cellular components, and the free iron availability is considered crucial for ROS toxicity due to the role it plays in the Fenton reaction to produce hydroxyl radicals. Therefore, indirect measurement could be a useful platform to determine ROS induced oxidative stress.

For example, ROS induced damage to lipids, proteins, and nucleic acids and its further end product assessment could be a promising approach to assess the oxidative stress in the samples of people that exercise.

For example, all the studies that we selected with the aim of finding the suitable biomarkers, have assessed the ROS induced end products like PC, MDA, TBARS, 8-OH-dG, and F2-isoprostanes, but no studies firmly reported the suitable biomarkers to measure the oxidative damage because sample type, collection of sample timing, and exercise duration and type may frequently change the reaction time of the ROS, which may compromise the prediction of ROS induced oxidative stress.

Further, measuring the level of antioxidant compounds such as enzymatic, non-enzymatic compounds, and some low molecular mass compounds are useful candidates for evaluating oxidative stress in the samples.

However, frequent changes in ROS concentration due to duration, intensity, and type of exercise may mispredict the expression level of those enzymatic and non-enzymatic antioxidants. For example, one study reported that the GSH level increased after the race whereas the CAT level was not significantly increased Spanidis et al.

Another study reported that the CAT level increased after the race Pinho et al. These contradicting results may be because the concentration of ROS differed in different running statuses such as in distance and the time in which the race was completed.

Regarding exercise, different types of exercises influence the level of ROS induced end products based on the training status Hadžović-Džuvo et al. Furthermore, studies have shown that endurance exercise increased ROS and induced damage to lipids, proteins, DNA and antioxidant levels Kanter et al.

However, direct evidence on those oxidative damage markers is limited in reflecting oxidative stress, and some studies only observe a few markers that are increased during endurance training as well as some markers do not show signs of any increment Alessio et al.

Vezzoli et al. observed that prolonged ultra-endurance running increased the PC, TBARS, TAC, and 8-OH-dG Vezzoli et al. Spanidis et al.

reported that there were no changes observed during or after running in TBARS, PC, and TAC, suggesting that these outcomes are dependent on training status and specific biomarkers that are assessed during running Spanidis et al. Further, this study reported that GSH and cORP are the most effective biomarkers to analyze running-induced oxidative stress.

In addition, this study showed that these markers existed up to 3 days after the race, which is possibly due to the exercise intensity and total caloric expenditure.

Indeed, several studies have shown that the oxidative stress response is altered in relation to exercise intensity Alessio et al. From these results, we conclude that assessing the oxidative damage markers in response to exercise running may vary according to exercise intensity, duration, and individual antioxidant capacity.

No persistent results were observed in all the selected studies with regards to oxidative stress biomarkers. However, most of the studies used oxidative damage markers and individual antioxidant capacity such as PC, MDA, TBARS, CAT, and GSH for the measurement of oxidative stress, suggesting that assessing oxidative damage markers and individual antioxidant capacity could be a promising method to reflect the potentiality of methods on oxidative stress compared to the direct method that assesses the ROS.

The national institutes of health define the word biomarker as the process of both normal and abnormal processes in the biological system. Since there is no specific biomarker to predict the accurate status of oxidative stress, inflammatory markers could also be a useful candidate to assess the oxidative stress in exercise conditions.

An exercise induced inflammatory response has long-term effects on human health, but ROS could be the driving factor for inflammation Suzuki, ROS induce several signaling events that are directly involved in inducing inflammation during exercise, such as nuclear factor kappa-light-chain-enhancer of activated B cells NFkB and activator protein-1 AP-1 Biswas, ; Liu et al.

Studies observed that running exercises increased the inflammatory response, but did not increase nucleic acid modifications by ROS, bringing into questioning the above statement of whether ROS could be a driving factor for inflammatory response or whether exercise-induced adaptive antioxidant effects could only detoxify the ROS without affecting inflammatory cascades Radák et al.

However, one study reported that iron-man races increased the oxidative stress-induced inflammatory response Pinho et al. In contrast, another study observed that no consistent changes were observed in oxidative stress parameters and inflammatory responses, suggesting that different exercise modalities have different effects on oxidative stress parameters and inflammatory responses Wagner et al.

For example, high-intensity prolonged running exercise induced the oxidative stress and inflammation, but even moderate continuous exercise increased the oxidative stress compared to discontinuous high-intensity exercise Mastaloudis et al. However, this moderate exercise-induced oxidative stress effect could be changed with duration.

These varying results show the uncertainty of the argument that inflammatory markers cannot be used for assessing the oxidative stress. More research is therefore required to confirm the effect of inflammatory markers as an effective strategy to assess oxidative stress in exercise conditions.

ROS generation depends on exercise intensity and duration, as exercise types differ in their energy requirements, level of oxygen consumption, and the mechanical stress imposed on tissues.

Journal of the Outsource resupply needs Post-woorkout of Sports Nutrittion volume 18Article number: 3 Cite Outsource resupply needs article. Metrics details. Redox activity of Amazon Baby Products species plays pot-workout important and a positive role on exercise adaptation, but these species at very high concentrations have detrimental effects. As a result, the use of antioxidant supplements for reducing oxidative stress can be an effective health strategy to maintain an optimal antioxidant status. In this sense, grapes are an important source of natural antioxidants due to their high content in polyphenols. Posst-workout Basics. Ultimate Guide. Why are antioxidants good Oxidative stress and post-workout nutrition you? They reduce oxidative stress, a condition of electron imbalance in your cells that underlies metabolic dysfunction. Emma Betuel. Casey Means, MD.