Oxidative stress and post-workout nutrition -
An existing theory suggests that oxidative stress damages some proteins involved in the insulin response, leading to insensitivity.
In one small study published in Science Translational Medicine, six healthy men were told to eat 6, calories per day for a week and do nothing but stay in bed. Overall, the men gained about 3.
The changes made the transporter dysfunctional, which the authors interpreted as a sign of insulin resistance. They can also bind to certain metals that promote ROS formation or act as cellular repair crews that clean up ROS-related damage. Some antioxidants are formed through certain pathways within cells.
Those genes, in turn, are translated into antioxidants that can detoxify and eliminate ROS. Eating certain foods can activate the Nrf2 pathway. Some scientists have proposed that sulforaphane, a chemical found in broccoli, arugula, bok choy, kale, brussels sprouts, and other green vegetables, can help set the Nrf2 pathway into motion.
Animal studies suggest that this nutrient can reduce oxidative stress and may be protective against certain diabetes complications, but this research is still ongoing. Curcumin, which is found in turmeric , has also been shown to be an Nrf2 activator.
Research suggests that a group of compounds called alkyl-catechols, which are found in fermented foods , may also activate this master pathway.
As one paper explains , these three compounds 4-vinylcatechol, 4-ethylcatechol, and 4-methylcatechol were once prevalent in ancient diets.
But early evidence suggests that fermented foods still around today, like kimchi, can activate this pathway and stimulate the antioxidant defense system.
One of the primary antioxidants produced by the body is glutathione, a potent antioxidant that can bind up ROS and may help repair DNA. One paper suggested that foods like green tea , lean proteins, salmon, cruciferous vegetables, and turmeric may support glutathione production.
Some studies indicate that sulfur-rich foods support glutathione production because a vital part of the molecule itself is sulfur. Vitamin C, vitamin E, carotenoids found in yellow and orange vegetables like squash and carrots , and polyphenols found in berries, kiwis, plums, cherries, and apples are some examples of dietary antioxidants.
Diets rich in plant-based food are protective against oxidative stress. For example, one study on 54 people with Type 2 diabetes examined how fruit and vegetable intake was related to antioxidant levels and, by extension, protection against oxidative stress.
It found strong links between dietary antioxidant levels and fruit and vegetable intake, which included vegetables, root crops, fruits, berries, and jams and preserves made from these foods. Overall, people who ate more fruit and vegetables also showed fewer signs of oxidative stress.
However, the full impact of dietary antioxidants—especially supplements—is not fully understood. Specific vitamins are known to support the antioxidant system still show inconsistent results in preventing the consequences of oxidative stress. For example, while observational studies have shown that when people eat more antioxidants like vitamin C , they tend to have lower risks of coronary heart disease, clinical trials have demonstrated lackluster results.
One meta-review published in of 10 of these trials found only weak evidence that vitamin C supplements lowered the risk of cardiovascular disease. Behavior and habits also play a role in maintaining healthy levels of antioxidants and preventing the onset of oxidative stress.
Getting enough sleep is one example. Multiple animal studies have shown that sleep loss can raise levels of ROS in the brain, though the damage seems to show up elsewhere in the body, like the gut.
In one study , researchers suggested that fruit flies eventually died from sleep deprivation partially because of ROS accumulation in their guts.
Sometimes, ROS play a key role in telling the body that it needs to get more sleep. One study on fruit flies found that animals with chronic sleep loss tend to accumulate more ROS in brain tissue, and those high ROS levels reduced sleep.
But sleep itself acted as an antioxidant, helping to clear out particular ROS. The decline of those ROS levels during sleep sent a biological signal that promoted wakefulness, resetting the cycle. Taken together, regular sleep seems to be one way to keep ROS and antioxidants in balance, and ROS signaling plays a role in controlling sleep as well.
Exercise is another way to mediate oxidative stress and demonstrates that ROS can be helpful at certain levels and damaging at high levels. Though exercise can boost ROS production in the short term, it also seems to stimulate the antioxidant system.
A recent study found that NADPH oxides known as NOX —oxygen transport proteins—are generated by exercise and help create ROS. Still, they also lead to adaptive processes that ultimately reduce oxidative stress and insulin resistance.
One study on 34 men found higher levels of antioxidants after a single cycling session regardless of whether they put in the maximum or moderate effort. Over time, however, training seems to strengthen antioxidant responses. A small study on 16 women with obesity who followed a six-month exercise program one hour of exercise, three times per week found that they had increased levels of key antioxidant enzymes, even when the women were at rest.
Oxidative stress can seem like an inevitable consequence of living. The Explainer. Reading about metabolic fitness, you'll encounter plenty of technical terms and abbreviations—here are simple definitions of some of the most common. The Levels Team. Metabolic Health. Metabolic health can be improved by consistently making choices that keep glucose levels in a stable and healthy range.
Glycemic variability is the amount your blood sugar changes throughout the day. Here's why we want to keep it low for optimal health. A reason a person without diabetes experiences hypoglycemia is as the result of a glucose spike from eating a sugary or high-carb meal.
Barbara Brody. Ami Kapadia. The glycemic index provides insight into how particular foods affect glucose but has limitations. Stephanie Eckelkamp.
Being aware of these causes of inaccurate data can help you identify—and avoid—surprising and misleading feedback. Joy Manning, RD. Inside Levels. Levels Co-Founder's new book—Good Energy: The Surprising Connection Between Metabolism and Limitless Health—releases May 14; available for pre-order today.
Metabolic flexibility means that your body can switch easily between burning glucose and fat, which means you have better energy and endurance. Jennifer Chesak. Dominic D'Agostino, PhD. What is oxidative stress and why does it matter to metabolic health?
Written By Emma Betuel. Reviewed By Casey Means, MD. Article highlights Oxidative stress is an imbalance between antioxidants and reactive oxygen species ROS in your cells, which can cause damage leading to chronic diseases.
Factors like overeating, poor diet, inflammation, stress, pollution, and hyperglycemia can increase ROS production beyond what antioxidants can neutralize. Oxidative stress is linked to inflammation, insulin resistance, and complications of diabetes and metabolic dysfunction.
You can increase antioxidants through diet especially fruits and vegetables , exercise, sleep, and activating the body's antioxidant defense system. Avoiding triggers that generate excessive ROS, like cigarette smoke and UV exposure, can also help restore balance between antioxidants and ROS.
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. During low-intensity and duration, protocols have effective antioxidant defense mechanisms that likely meet the ROS production, but, as the intensity and duration of exercise increases, the antioxidant defense is no longer adequate—potentially resulting in oxidative damage.
A study has shown that neutrophil production of superoxide increased only at intensities above the lactate threshold in exercised men Quindry et al. In contrast to the above study, other studies reported that oxidative stress markers in blood increased with , or min of exercise at a constant intensity.
Several reviews conclude that regular exercise training does not lead to chronic oxidative stress in the active muscles which fosters the concept of exercise induced hormesis Ji et al. Hormesis used to describe the biphasic dose response curve where small amounts of the stressor provide beneficial adaptive effects on cells, whereas high levels of those stressors may result in damage to the cells.
From this, exercise induced low levels of ROS production play a crucial role in exercise induced adaptation of the skeletal muscle, and this can be explained using the bell shaped hormesis curve where the optimum level of ROS plays a role in muscle adaptation whereas when above the optimum level of ROS, it can lead to various damages to the cells and a decline in the exercise induced adaptation Ji et al.
These studies do not provide strong enough evidence to show that high intensity exercise for prolonged periods of time, can result in oxidant-mediated damage in the cells and decrease antioxidant capacity in the trained muscles de Sousa et al.
The reasons associated with this are the cardiovascular systems ability to affect the sustainability of high intensity by providing blood to the working muscles and affect the ROS production on muscle fatigue Ji et al.
Thus, the ROS production level is limited during exercise. Another reason is that mitochondrial coupling is higher in state 3 respiration during exercise resulting in the reduction of electron spill and ROS production by the mitochondria when compared to state 4 resting respiration.
A final reason is that the exercise can increase the antioxidant enzymes in the skeletal muscle that supports the muscle fiber, to remove the ROS during exercise Powers et al. These results predict that skeletal muscles are not exposed to ROS mediated damage during exercise.
PSPL consumption significantly increased total polyphenols concentrations, and significantly decreased plasma PC and TBARS in the PSPL group [ 32 ].
Exercise-induced oxidative stress can activate a range of transcription factors that contribute to the differential expression of certain genes involved in inflammatory pathways [ 37 ].
In this review, diets with antioxidant effects have demonstrated to reduce inflammatory markers including neutrophil respiratory burst NRB , interleukin-6 IL-6 , nuclear factor-kappa B NF-κB , granulocyte-colony stimulating factor G-CSF , interleukin-1 receptor antagonist IL-1Ra , soluble vascular cell adhesion molecule-1 sVCAM Koenig et al.
Both found that this AVA-rich diet decreased ROS production from the NRB after high intensity downhill training when compared to control group. In concert with alterations affecting levels of oxidative stress markers and inflammatory markers, exercise-induced oxidative stress could attenuate the endogenous antioxidant defense including enzymatic antioxidant activity catalase CAT , SOD, GPx, cyclooxygenase-2 COX-2 and nonenzymatic antioxidant activity GSH, oxygen radical absorbance capacity ORAC , total antioxidant capacity TAC , total antioxidant status TAS , ferric reducing antioxidant power FRAP , vitamins C and E, and reduced glutathione content.
Two studies by Panza et al. Green tea increased the values of total polyphenols, GSH, FRAP and diminished the plasma levels of LH after a bench press exercise [ 18 ].
Similarly, mate tea increased the concentration of total polyphonic compounds at all time points and the levels of GSH after twenty maximal eccentric elbow flexion exercises [ 19 ]. McLeay et al. Integral grape juice was used as the dietary strategy against exercise-induced oxidative stress in an acute study [ 23 ] and a day study [ 24 ] by Toscano et al.
Tart cherry juice showed subchronic positive effects on antioxidant activity caused by high-intensity exercises in the study of Howatson et al. Copetti et al. In this narrative review, most studies found positive effects of dietary strategies on exercise-induced ROS generation. Especially, phenol-rich diets showed effects in combating exercise-induced oxidative stress in the greater proportion of the articles.
Accordingly, while dietary strategies might help to keep ROS generation in a physiological range during exercise, the use of the antioxidant-rich diets may upregulate the endogenous antioxidants' defense system, which may have important implications for preventing excessive damage and facilitating recovery.
Nevertheless, consistent evidence is still lacking, and the underlying mechanisms in human trials are not well understood.
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Zeng, Z. Diets and Exercise-Induced Oxidative Stress. Zeng Z. Accessed February 15, Zeng, Zhen. In Encyclopedia. Copy Citation. Home Entry Topic Review Current: Diets and Exercise-Induced Oxidative Stress. This entry is adapted from the peer-reviewed paper diet antioxidants exercise oxidative stress reactive oxygen species.
Introduction The term oxidative stress is defined as a disturbance in the homeostatic balance between pro-oxidants and antioxidants with a subsequent excessive generation of free radicals [ 1 ] [ 2 ] [ 3 ]. Dietary Strategies The majority of currently available studies addressed the effects of phenol-rich foods on exercise-induced oxidative stress, including dark chocolate [ 14 ] [ 15 ] [ 16 ] , high-flavanol cocoa drink [ 17 ] , green tea [ 18 ] , mate tea [ 19 ] , New Zealand blueberry smoothie [ 20 ] , blueberries [ 21 ] [ 22 ] , grape juice [ 23 ] [ 24 ] , Montmorency cherry juice [ 25 ] , tart cherry juice [ 26 ] , oatmeal [ 27 ] , avenanthramides AVA -rich cookie [ 28 ] [ 29 ] , juçara juice [ 30 ] , Sanguinello cultivar red orange juice [ 31 ] , and purple sweet potato leaves [ 32 ].
Effects on Biomarkers of Exercise-Induced Oxidative Stress 3. Effects of Dietary Interventions on Direct ROS Generation Zeng et al. Effects of Dietary Interventions on ROS-Induced Macromolecule Damage In the majority of studies, F2-isoprostanes, 8-isoprostanes, lipid hydroperoxides LH , thiobarbituric acid-reactive substances TBARS and malondialdehydes MDA were used as the oxidative markers, which result from lipoperoxidation by oxidative damage.
Effects of Dietary Interventions on Inflammatory Markers Exercise-induced oxidative stress can activate a range of transcription factors that contribute to the differential expression of certain genes involved in inflammatory pathways [ 37 ]. Effects of Dietary Interventions on Antioxidant Activity In concert with alterations affecting levels of oxidative stress markers and inflammatory markers, exercise-induced oxidative stress could attenuate the endogenous antioxidant defense including enzymatic antioxidant activity catalase CAT , SOD, GPx, cyclooxygenase-2 COX-2 and nonenzymatic antioxidant activity GSH, oxygen radical absorbance capacity ORAC , total antioxidant capacity TAC , total antioxidant status TAS , ferric reducing antioxidant power FRAP , vitamins C and E, and reduced glutathione content.
References Halliwell, B. Free Radicals, Antioxidants, and Human Disease: Curiosity, Cause, or Consequence? Lancet , , — Halliwell, B.
Free Radicals in Biology and Medicine, 5th ed. Dröge, W. Free Radicals in the Physiological Control of Cell Function. Peternelj, T. Antioxidant Supplementation during Exercise Training: Beneficial or Detrimental?
Sports Med. Valko, M. Free Radicals and Antioxidants in Normal Physiological Functions and Human Disease. Cell Biol. Powers, S. Reactive Oxygen Species Are Signalling Molecules for Skeletal Muscle Adaptation.
Reactive Oxygen Species: Impact on Skeletal Muscle.
Metabolic Amd. Ultimate Guide. Why are nutrotion good Juicy Citrus Concentrate you? They reduce oxidative stress, a condition Oxidative stress and post-workout nutrition electron imbalance in your cells that underlies metabolic dysfunction. Emma Betuel. Casey Means, MD. Maybe you read it on the back of an orange juice carton or saw it on a supplement bottle.
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Across all studies, there is a compelling amount of evidence suggesting that different dietary regimens are viable tools for decreasing exercise-induced oxidative stress.
However, the different biomarkers of oxidative stress do not allow a direct comparison between studies. Zeng et al. AVA, as one of the major components of polyphenolic amides nonflavonoidsis considered the most important antioxidant found in oats [ 33 ] [ 34 ].
Therefore, it can be speculated that the hydroxyl groups of AVA contribute to antioxidant defense through their ability to trap ROS in vitro [ 35 ].
In the majority of studies, F2-isoprostanes, 8-isoprostanes, lipid hydroperoxides LHthiobarbituric acid-reactive substances TBARS and malondialdehydes MDA were used as the oxidative markers, which result from lipoperoxidation by oxidative damage.
Similarly, protein carbonylation PC was used as a marker of protein damage, and 8-Hydroxydeoxyguanosine 8-oxodG as a specific marker of 2 0 -deoxyguanosine damage after ROS attack to DNA. Davison et al. The derivatives of catechin and epicatechin, which can both be defined as monomeric flavanols, are the major antioxidant components in cacao beans chocolate [ 36 ].
In addition to cocoa, other phenol-rich fruits also exhibited antioxidant effects during exercise by detecting oxidative stress markers, including blueberry [ 22 ]cherry [ 25 ] and red orange [ 31 ].
In the study by McAnulty et al. The results showed that the blueberry diet attenuated an increase in LH concentration caused by exercise stress but not F2-isoprostane levels, compared with a blueberry-flavored shake as a placebo.
Purple sweet potato leaves PSPLas another phenol-rich diet, showed decreases in oxidative stress markers in an exercise trial [ 32 ]. Chang et al. PSPL consumption significantly increased total polyphenols concentrations, and significantly decreased plasma PC and TBARS in the PSPL group [ 32 ].
Exercise-induced oxidative stress can activate a range of transcription factors that contribute to the differential expression of certain genes involved in inflammatory pathways [ 37 ]. In this review, diets with antioxidant effects have demonstrated to reduce inflammatory markers including neutrophil respiratory burst NRBinterleukin-6 IL-6nuclear factor-kappa B NF-κBgranulocyte-colony stimulating factor G-CSFinterleukin-1 receptor antagonist IL-1Rasoluble vascular cell adhesion molecule-1 sVCAM Koenig et al.
Both found that this AVA-rich diet decreased ROS production from the NRB after high intensity downhill training when compared to control group. In concert with alterations affecting levels of oxidative stress markers and inflammatory markers, exercise-induced oxidative stress could attenuate the endogenous antioxidant defense including enzymatic antioxidant activity catalase CATSOD, GPx, cyclooxygenase-2 COX-2 and nonenzymatic antioxidant activity GSH, oxygen radical absorbance capacity ORACtotal antioxidant capacity TACtotal antioxidant status TASferric reducing antioxidant power FRAPvitamins C and E, and reduced glutathione content.
Two studies by Panza et al. Green tea increased the values of total polyphenols, GSH, FRAP and diminished the plasma levels of LH after a bench press exercise [ 18 ].
Similarly, mate tea increased the concentration of total polyphonic compounds at all time points and the levels of GSH after twenty maximal eccentric elbow flexion exercises [ 19 ].
McLeay et al. Integral grape juice was used as the dietary strategy against exercise-induced oxidative stress in an acute study [ 23 ] and a day study [ 24 ] by Toscano et al. Tart cherry juice showed subchronic positive effects on antioxidant activity caused by high-intensity exercises in the study of Howatson et al.
Copetti et al. In this narrative review, most studies found positive effects of dietary strategies on exercise-induced ROS generation. Especially, phenol-rich diets showed effects in combating exercise-induced oxidative stress in the greater proportion of the articles.
Accordingly, while dietary strategies might help to keep ROS generation in a physiological range during exercise, the use of the antioxidant-rich diets may upregulate the endogenous antioxidants' defense system, which may have important implications for preventing excessive damage and facilitating recovery.
Nevertheless, consistent evidence is still lacking, and the underlying mechanisms in human trials are not well understood. Encyclopedia Scholarly Community. Entry Journal Book Video Image About Entry Entry Video Image. Submitted Successfully! Thank you for your contribution! You can also upload a video entry or images related to this topic.
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Zeng, Z. Diets and Exercise-Induced Oxidative Stress. Zeng Z. Accessed February 15, Zeng, Zhen. In Encyclopedia. Copy Citation. Home Entry Topic Review Current: Diets and Exercise-Induced Oxidative Stress. This entry is adapted from the peer-reviewed paper diet antioxidants exercise oxidative stress reactive oxygen species.
Introduction The term oxidative stress is defined as a disturbance in the homeostatic balance between pro-oxidants and antioxidants with a subsequent excessive generation of free radicals [ 1 ] [ 2 ] [ 3 ]. Dietary Strategies The majority of currently available studies addressed the effects of phenol-rich foods on exercise-induced oxidative stress, including dark chocolate [ 14 ] [ 15 ] [ 16 ]high-flavanol cocoa drink [ 17 ]green tea [ 18 ]mate tea [ 19 ]New Zealand blueberry smoothie [ 20 ]blueberries [ 21 ] [ 22 ]grape juice [ 23 ] [ 24 ]Montmorency cherry juice [ 25 ]tart cherry juice [ 26 ]oatmeal [ 27 ]avenanthramides AVA -rich cookie [ 28 ] [ 29 ]juçara juice [ 30 ]Sanguinello cultivar red orange juice [ 31 ]and purple sweet potato leaves [ 32 ].
Effects on Biomarkers of Exercise-Induced Oxidative Stress 3. Effects of Dietary Interventions on Direct ROS Generation Zeng et al. Effects of Dietary Interventions on ROS-Induced Macromolecule Damage In the majority of studies, F2-isoprostanes, 8-isoprostanes, lipid hydroperoxides LHthiobarbituric acid-reactive substances TBARS and malondialdehydes MDA were used as the oxidative markers, which result from lipoperoxidation by oxidative damage.
Effects of Dietary Interventions on Inflammatory Markers Exercise-induced oxidative stress can activate a range of transcription factors that contribute to the differential expression of certain genes involved in inflammatory pathways [ 37 ].
Effects of Dietary Interventions on Antioxidant Activity In concert with alterations affecting levels of oxidative stress markers and inflammatory markers, exercise-induced oxidative stress could attenuate the endogenous antioxidant defense including enzymatic antioxidant activity catalase CATSOD, GPx, cyclooxygenase-2 COX-2 and nonenzymatic antioxidant activity GSH, oxygen radical absorbance capacity ORACtotal antioxidant capacity TACtotal antioxidant status TASferric reducing antioxidant power FRAPvitamins C and E, and reduced glutathione content.
References Halliwell, B. Free Radicals, Antioxidants, and Human Disease: Curiosity, Cause, or Consequence? Lancet, — Halliwell, B. Free Radicals in Biology and Medicine, 5th ed.
Dröge, W. Free Radicals in the Physiological Control of Cell Function. Peternelj, T. Antioxidant Supplementation during Exercise Training: Beneficial or Detrimental? Sports Med. Valko, M. Free Radicals and Antioxidants in Normal Physiological Functions and Human Disease.
Cell Biol. Powers, S. Reactive Oxygen Species Are Signalling Molecules for Skeletal Muscle Adaptation. Reactive Oxygen Species: Impact on Skeletal Muscle. Merry, T. Mitohormesis in Exercise Training. Free Radic.
: Oxidative stress and post-workout nutrition| Top bar navigation | Nutrituon metabolism in sprint- vs endurance-trained athletes Lycopene and hair health 20? However, pilot studies on the antioxidant Weight and body composition analysis of grapes and grape based Amazon DIY Projects with post-sorkout are scarce. Free radicals are molecules that have an extra electron. Giustina AD, Danielski LG, Novochadlo MM, Goldim MPS, Joaquim L, Metzker KLL, Carli RJ, Denicol T, Cidreira T, Vieira T, et al. 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. |
| Grape polyphenols supplementation for exercise-induced oxidative stress | However, one study reported that iron-man races increased the oxidative stress-induced inflammatory response Pinho et al. Indeed, growing evidence reveals that while uncontrolled production of RNS and ROS can damage cells, intracellular oxidants also play important regulatory roles in the modulation of skeletal muscle force production, regulation of cell signaling pathways, and control of gene expression [ 35 , 38 , 39 , 40 , 41 , 42 ]. Thus, the ROS production level is limited during exercise. Life Sci. Article PubMed CAS Google Scholar Fruit: world production by type Statista [Internet]. Chemico-biological interactions. |
| But how many antioxidants do you personally need? | Br J Nutriiton Med. Furthermore, high intensity post-orkout limits the efflux of purines to Natural fat loss exercises Oxidative stress and post-workout nutrition resulting in Oxidattive muscle nucleotide Healing escapes in active men Hellsten-Westing srress al. Discrepancies in Oxjdative may be due to the type, dosage, and timing of administration of the antioxidants, in addition to the exercise stress and the specific population being studied. FYI, free radicals are also a natural byproduct of regular cellular functions in the body, like breathing and eating, according to Harvard Health Publishing. McLeay Y, Stannard S, Houltham S, Starck C. NF-κB signaling in inflammation. Zhang, T. |
| 3. Effects on Biomarkers of Exercise-Induced Oxidative Stress | The world production of grapes was However, considering that fresh grapes might not be available everywhere during the whole year, natural supplements obtained from grapes, such as grape beverages or grape extracts may be an interesting alternative to fresh fruit. Fruit polyphenols have shown antioxidant potential beneficial for the reduction of the effects of oxidative damage during intense exercise in athletes of different disciplines [ 16 , 17 ]. Polyphenols are poorly absorbed in the human small intestine and undergo extensive biotransformation after ingestion [ 18 , 19 ]. Evidence supports that biological activities of many polyphenols are actually improved after their biotransformation [ 20 , 21 , 22 ]. This process takes time, hence, a prolonged period of polyphenol intake is recommended prior to exercise stress interventions to allow body tissues to adapt to a higher phenolic flux level. That is the reason besides using appropriate outcome measures, long periods are needed to capture such bioactivities [ 23 ]. In this context, targeted metabolomics is a suited tool that allows to investigate the shifts of gut-derived metabolites after polyphenol supplementation. Several human trials are revealing an increasing number of metabolites that appear at high concentration levels in the colon and systemic circulation which could be directly associated with polyphenols positive effect against OS [ 23 , 24 ]. In fact, a systematic review suggested the key role of gut microbiota in controlling the OS during intense exercise [ 25 ]. Currently, few papers are available and research designs vary widely regarding to grape polyphenolic supplementation form drinkable or edible , dosage acute to multiple weeks and months , type of exercise stress acute or chronic , profile of subject trained or untrained , and oxidative stress outcome measures. For this purpose, an evaluation of the available scientific literature has been carried out since it is an important step to determine the efficacy of these polyphenolic based products on the redox status of the athletes. In this work, the ingredient refers to the polyphenols present in the grape-based products studied. Oxidative stress is defined as a result of an imbalance between reactive species production and intrinsic antioxidant defense [ 27 ]. For example, athletes participating in one bout of prolonged and intensive exercise such as marathon and ultramarathon race event show acute physiological stress reflected by muscle microtrauma, oxidative stress, inflammation, and gastrointestinal dysfunction [ 11 , 23 , 24 , 28 , 29 , 30 , 31 , 32 , 33 , 34 ]. The discovery that muscular exercise increases oxidant damage did not occur until the late s [ 35 , 36 , 37 ]. Although the biological significance of this finding was unclear, these pioneering studies generated interest for future investigations to examine the important role that radicals, reactive nitrogen species RNS , and reactive oxygen species ROS play in skeletal muscle and other metabolically active organs during exercise. Indeed, growing evidence reveals that while uncontrolled production of RNS and ROS can damage cells, intracellular oxidants also play important regulatory roles in the modulation of skeletal muscle force production, regulation of cell signaling pathways, and control of gene expression [ 35 , 38 , 39 , 40 , 41 , 42 ]. The redox activity of RONS plays a critical role in cell signaling and exercise adaptation. It is a phenomenon widely known as hormesis, which means that low levels of stress promote adaptation and therefore, protection from subsequent stress [ 46 , 47 ]. Exercise-induced RONS act as signaling molecules for the beneficial effects in response to exercise training. RONS produced during muscle contractions are responsible for key adaptations to exercise training as mitochondrial biogenesis [ 48 ], endogenous antioxidant enzyme upregulation [ 49 ], muscle hypertrophy [ 50 ] and glucose uptake by the skeletal muscle [ 51 ]. However, at very high concentrations, free radicals instead of being advantageous they can have detrimental effects [ 46 ]. During heavy endurance training, endogenous antioxidant capacity cannot counteract the increasingly high RONS generation, resulting in a state of OS and subsequent cellular damage [ 52 ]. OS can be basically estimated measuring free radicals, radical mediated damages on lipids, proteins or deoxyribonucleic acid DNA molecules and performing the total antioxidant capacity. The results of free radicals must be interpreted with caution because of the short life of the ROS, their strong ability to react and their low concentration. Regarding lipid peroxidation, the conventional oxidative stress marker is malondialdehyde MDA which is produced during fatty acid oxidation. This product is measured by its reaction with thiobarbituric acid which generates thiobarbituric acid reactive substances TBARS in blood samples. F2-isoprostanes are also analyzed to estimate the damage on lipids. They are produced by non-cyclooxygenase dependent peroxidation of arachidonic acid. They are stable products released into circulation before the hydrolyzed form is excreted in urine. Free radical induced modification of proteins causes the formation of carbonyl groups into amino acid side chains. An increase of carbonyls is linked to oxidative stress in blood samples. The use of antioxidant supplements for ameliorating the exercise-induced RONS has become a current topic as there is considerable evidence that these supplements might not only prevent the toxic effects of RONS, but also blunt their signaling properties responsible for the adaptive responses [ 54 ]. Anyway, further research to observe effects of nutritional antioxidant supplements on exercise-induced oxidative stress must be performed [ 56 ]. An antioxidant can be defined as a substance that helps to reduce the severity of OS either by forming a less active radical or by quenching the damaging free radicals chain reaction on substrates such as proteins, lipids, carbohydrates or DNA [ 57 ]. The antioxidants can be endogenous or obtained exogenously as a part of a diet or as a dietary supplement. Some dietary compounds that do not neutralize free radicals but enhance endogenous antioxidant activity may also be classified as antioxidants. While exogenous antioxidant may attenuate intracellular adaptation in response to exercise training, there is no literature to suggest that increasing endogenous antioxidants has this effect [ 46 ]. Endogenous antioxidants keep optimal cellular functions and thus systemic health and well-being. However, under some conditions endogenous antioxidants may not be enough, and extra antioxidants may be required to maintain optimal cellular functions. Such a deficit is evident in some individuals during the overloaded period of training or in circumstances where athletes have little time for recovery like in tournament situations. However, available data still do not allow to define the optimal antioxidant intake that would protect overloaded or, even more so, overtrained individuals [ 58 ]. Humans have developed highly complex antioxidant systems enzymatic and non-enzymatic which work synergistically and together with each other to protect the cells and organ systems of the body against free radical damage. The most efficient enzymatic antioxidants are superoxide dismutase SOD , catalase CAT and glutathione peroxidase GPX. In Fig. SOD is the major defense upon superoxide radicals and is the first barrier protection against oxidative stress in the cell. SOD represents a group of enzymes that catalyse the dismutation of O 2. Manganese Mn is a cofactor of Mn-SOD form, present in the mitochondria and copper Cu and zinc Zn , are cofactors present in cytosol [ 57 ]. Furthermore, CAT is responsible of the decomposition of H 2 O 2 to form water H 2 O and oxygen O 2 in the cell. This antioxidative enzyme is widely distributed in the cell, with the majority of the activity occurring in the mitochondria and peroxisomes [ 59 ]. With high ROS concentration and an increase in oxygen consumption during exercise, the enzyme GPX, present in cell cytosol and mitochondria, is activated to remove hydrogen peroxide from the cell [ 60 ]. The reaction uses reduced glutathione GSH and transforms it into oxidized glutathione GSSG. GPX and CAT have the same action upon H 2 O 2 , but GPX is more efficient with high ROS concentration and CAT with lower H 2 O 2 concentration [ 61 , 62 ]. In response to increased RONS production the antioxidant defense system may be reduced temporarily, but may increase during the recovery period [ 63 , 64 ] although conflicting findings have been reported [ 65 ]. GPX requires several secondary enzymes glutathione reductase GR and glucosephosphate dehydrogenase GPDH and cofactors GSH and the reduced nicotinamide adenine dinucleotide phosphate NADPH to remove H 2 O 2 from the cell. By contrast, non-enzymatic antioxidants include vitamin A retinol [ 57 ], vitamin E tocopherol [ 66 ], vitamin C ascorbic acid , thiol antioxidants glutathione, thioredoxin and lipoic acid , melatonin, carotenoids, micronutrients iron, copper, zinc, selenium, manganese which act as enzymatic cofactors and flavonoids, a specific group of polyphenols [ 67 ]. Among non-enzymatic antioxidants, polyphenols are a group of phytochemicals that have received great attention of researchers in the last years considering their beneficial effects in the prevention of many chronic diseases [ 68 , 69 ]. They constitute one of the most numerous and widely distributed groups of natural products in the plant kingdom. Polyphenols can be classified by their origin, biological function, and chemical structure. More than phenolic structures are currently known, and among them over flavonoids have been identified [ 70 , 71 , 72 ]. The major groups of flavonoids of nutritional interest are the flavonols, the flavones, the flavanols, the flavanones, the anthocyanidins and the isoflavones [ 73 ]. See Fig. Flavonoid structures. Polyphenols have showed to act as a defense against OS caused by excess reactive oxygen species ROS [ 74 ]. Their potential health benefits as antioxidants is mediated by their functional hydroxyl groups OH that determine the ROS synthesis suppression, the chelation of trace elements responsible for free radical generation, the scavenging ROS and the improvement of antioxidant defenses [ 75 , 76 ]. Commonly, grapes and grape based products are recognized as natural food products with strong antioxidant activity precisely due to their high content in polyphenolic compounds [ 77 ]. At the same time, these products have also demonstrated a reduced OS and the oxidative damage at muscular level and improved the muscle performance but in aged rats [ 80 ]. Table 2 provides a summary of the different polyphenol families found in grapes. Considering their polyphenolic composition, it is plausible to hypothesize that the strategic supplementation with grape based products may have a positive antioxidant effect in athletes in particular situations. However, pilot studies on the antioxidant capacity of grapes and grape based products with athletes are scarce. Few studies are focused on the consumption of antioxidant supplements obtained from grape based products to reduce the immediate increase of oxidative stress biomarkers. Table 3 shows a descriptive summary of 12 studies published since that investigate the effect of supplementation with grape based products on exercise-induced oxidative stress markers and the antioxidant enzymatic system efficiency. The studies collected in Table 3 fulfill the following inclusion criteria: i pilot studies conducted with healthy human participants active or trained subjects , ii original studies with an acute or long-term grape supplementation intervention on physiological responses associated with OS produced by exercise, iii published until June Exclusion criteria are animal studies and studies in which no exercise is performed. Wine may be a good option as a product obtained from grapes with an important source of phenolic compounds. However, considering that wine contains alcohol may not be an option for all consumers due to certain disease conditions, religious restrictions, or age, it has not been considered. Among the studies found, six of the products are beverages made with grape and the rest are grape extracts and only one is referred to dried grapes. Within the beverages, one is a grape beverage but mixed with raspberry and red currant [ 81 ], another one a grape beverage specified as organic [ 82 ], two of them are grape concentrate drinks [ 83 , 84 ] and the last two a purple grape juice [ 85 ]. Regarding the polyphenolic content, the studies show a wide number of dosages. Morillas-Ruiz et al. dose range. Considering the total phenolic content of 1. This could be explained by a not high enough intensity exercise to alter the redox state or by the adaptation on antioxidant defenses in well-trained subjects. However, the antioxidant supplementation had a beneficial effect on the oxidation of proteins induced by exercise and reduced this index. Considering the total phenolic content of 5. SOD is a cytosolic antioxidant enzyme responsible for superoxide anion radical dismutation into oxygen and hydrogen peroxide and is sensitive to the intake of polyphenols in humans. The authors attributed this decrease to the reduction of intra- and extracellular oxidative imbalances. The acute intake was in two equal doses before and after the training. The results showed a significant increase in SOD in the blood samples regardless of the drink consumed grape drink or placebo. A lower increase in reduced glutathione GSH levels in the test group in comparison to the placebo group was obtained. This result may indicate a lower oxidation of GSH to GSSG, oxidized glutathione, due to the action of glutathione peroxidase GPX or even more efficient synthesis by glutathione reductase. Besides, higher values in TBARS value with placebo in comparison to the grape concentrate drink were obtained just after the exercise and after one hour. This means a lower value in this oxidative stress marker related to lipid peroxidation when grape concentrate drink is consumed. But the antioxidant enzyme catalase CAT activity remained stable in the group that consumed the beverage. The authors suggest that the studies on the CAT response to exercise have shown conflicting results especially to a single exercise session. The study concludes that TBARS, CAT and GSH values suggest that this grape concentrate drink presents potential to modulate exercise-induced oxidative stress. In another study Tavares-Toscano et al. In this case the total antioxidant capacity TAC was evaluated in the plasma by evaluating the radical scavenging according to the α, α-diphenyl-β-picrylhydrazyl DPPH method. This analytical method is used to determine the TAC of a compound, an extract or other biological sources by using a stable free radical DPPH. The assay is based on the measurement of the scavenging capacity of antioxidants towards it [ 86 ]. The authors showed a deep characterization of the grape juice. They did not analyze any oxidative stress markers, but showed an increase in high density lipoprotein-cholesterol HDL-cholesterol fraction and a decreased low-density lipoprotein-cholesterol LDL-cholesterol fraction demonstrating that grape juice may enhance the benefits of physical training,. Besides the malondialdehyde MDA data indicated that grape juice supplementation did not prevent lipid peroxidation in athletes, but the increase was lower than in the group with no grape juice. Tavares-Tocano et al. Concerning the edible grape products, to the best of our knowledge the first study that analyzed the effect of grape polyphenols supplementation on the blood antioxidant status was in [ 88 ]. This dosage means 0. The results showed an insignificant modification of antioxidant enzyme: SOD, CAT, GSH and glutathione reductase GR activities, concentrations of non-enzymatic antioxidants: GSH and uric acid UA and total antioxidant status TAS. However, the authors indicated that the supplementation with the alcohol-free red wine grape polyphenolic extract might influence the attenuation of the post-exercise release creatine kinase CK into the blood. Lafay et al. In this case, no information regarding the total polyphenolic content was given. Besides the administration of grape extract decreased the plasma CK concentration and increased the hemoglobin Hb level in plasma suggesting a protection of cells against oxidative stress damage. The study revealed that this preparation and doses contributed to a significant increase in plasma TAC and to an insignificant increase in SOD, as well as a lower GSH activity and reduce concentration in TBARS. Taghizadeh et al. No information about the polyphenol content was given but the results showed a significant rise in plasma GSH and a significant decrease in MDA. Besides, the players who received GSE exhibited a significant decrease serum insulin concentration. On the other hand, the administration of GSE had no significant effects on parameters like creatine kinase CK or TAC when compared with the administration of the placebo. The study resulted in an increase in SOD, GSH and CAT activity, which remained stable until the end of the recovery period. The authors explained that in comparison with the placebo group the subjects supplemented showed no need to mobilize more antioxidant defenses before the exercise because and that the supplement probably contributed to spare oxidative homeostasis. Finally, it must be pointed out the protocol [ 93 ] established for a pilot study that includes a product mix made of dried grapes with almonds and dried cranberries. No results are given but the authors describe the necessity of studying the F2-isoprostanes as a lipid peroxidation biomarker for oxidative stress. Supplementation with grape polyphenols seems to have a positive effect against oxidative stress. These effects are dependent on the supplement dose, the length of the supplementation period or the polyphenolic profile total polyphenol content and the distribution among polyphenolic families. Besides, according to several reports, it appears that the type and intensity of exercise can affect the response of the blood antioxidant defense system, just as the training status of the athlete, or the sport discipline. Considering the supplementation dosage in these studies it seems unlikely athletes would gain enough quantity of polyphenols from diet. Therefore, grape-based polyphenol concentrated products would be an interesting approach. Moreover, inter-individual variability the age, sex, diet, environment factors, exercise protocols and even variability in gene expression could influence the polyphenols bioavailability and physiological responses to oxidative stress. Given the promising evidence, although still limited, more pilot studies on effect of grape polyphenols on the oxidative stress produced by sport should be conducted to determine the optimal concentration, dosage and effect on the oxidative stress for target athletes. Physical activity [Internet]. de Sousa CV, Sales MM, Rosa TS, Lewis JE, de Andrade RV, Simões HG. The antioxidant effect of exercise: a systematic review and meta-analysis. Sport Med. Article Google Scholar. The power of exercise: buffering the effect of chronic stress on telomere length. PLoS One. Article PubMed PubMed Central CAS Google Scholar. Gordon B, Chen S, Durstine JL. The effects of exercise training on the traditional lipid profile and beyond. Curr Sport Med Rep. Roque FR, Hernanz R, Salaices M. Exercise training and cardiometabolic diseases: focus on the vascular system. Curr Hypertens Rep. Article CAS PubMed Google Scholar. Pingitore A, Pace Pereira Lima G, Mastorci F, Quinones A, Iervasi G, Vassalle C. Exercise and oxidative stress: potential effects of antioxidant dietary strategies in sports. Devasagayam TPA, Tilak JC, Boloor KK, Sane KS, Ghaskadbi SS, Lele RD. Free radicals and antioxidants in human health: currant status and future prospects. J Assoc Physicians India. CAS PubMed Google Scholar. Braakhuis A, Hopkins WG. Impact of dietary antioxidants on sport performance: a review. Pereira Panza V-S, Diefenthaeler F, da Silva EL. Benefits of dietary phytochemical supplementation on eccentric exercise-induced muscle damage: is including antioxidants enough? Barranco-Ruiz Y, Aragón-Vela J, Casals C, Martínez-Amat A, Casuso RA, Huertas JR. Control of antioxidant supplementation through interview is not appropriate in oxidative-stress sport studies: analytical confirmation should be required. Nieman DC, Gillitt ND, Knab AM, Shanely RA, Pappan KL, Jin F, et al. Influence of a polyphenol-enriched protein powder on exercise-induced inflammation and oxidative stress in athletes: a randomized trial using a metabolomics approach. Nieman DC, Stear SJ, Castell LM, Burke LM. A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: part Br J Sport Med. Article CAS Google Scholar. Bjørklund G, Chirumbolo S. Role of oxidative stress and antioxidants in daily nutrition and human health. Article PubMed CAS Google Scholar. Fruit: world production by type Statista [Internet]. International Organisation of Vine and Wine. García-Flores LA, Medina S, Gómez C, Wheelock CE, Cejuela R, Martínez-Sanz JM, et al. Aronia-citrus juice polyphenol-rich juice intake and elite triathlon training: a lipidomic approach using representative oxylipins in urine. Food Funct. Article PubMed Google Scholar. Sureda A, Tejada S, Bibiloni MM, Tur JA, Pons A. Polyphenols: well beyond the antioxidant capacity: polyphenol supplementation and exercise-induced oxidative stress and inflammation. Curr Pharm Biotechnol. De Ferrars RM, Czank C, Zhangm Q, Botting NP, Kroon PA, Cassidy A, et al. The pharmacokinetics of anthocyanins and their metabolites in humans. Br J Pharmacol. Czank C, Cassidy A, Zhang Q, Morrison DJ, Preston T, Kroon PA, et al. Because oxidative stress can lead to a surplus of free radicals creating an imbalance with antioxidants , it can trigger inflammation associated with chronic diseases, including heart disease , type 2 diabetes and cancer. And get this: Exercise is also a cause of oxidative stress. After all, that's exactly what exercise is — a stress to your system. Free radical formation from exercise isn't necessarily a bad thing. Whether you're doing light-, moderate- or vigorous-intensity exercise, there's no evidence that the slight increase in oxidative stress poses a health risk, Powers says. FYI, free radicals are also a natural byproduct of regular cellular functions in the body, like breathing and eating, according to Harvard Health Publishing. And, research has actually the short-term increase in oxidative stress from exercise is a good thing for your body and overall health. But several days later, the damage was no longer there. Researchers believe that the body's antioxidant reserve — bolstered by exercise — repaired the damage. You get antioxidants from eating nutritious foods , but your body's own cells also produce antioxidants, like glutathione — which helps combat cellular damage during the aging process. And exercise can help boost the creation of these types of antioxidants. This means that exercise can help temper potential harm from a whole variety of other stressors. Bonus: The burst of free radicals produced during a workout directs your body to make more ATP, which gives you added energy for exercise and supports muscle contraction , enhancing your athletic performance, Dalleck says. When it comes to exercise and oxidative stress, it may not pay to be extra with your workouts. Doing workouts outside of your own fitness level, focusing only on high-intensity exercise and skimping on recovery between workouts can do more harm than good. When you do these things, you create more free radicals than antioxidants, which creates an imbalance. The bottom line is that the cellular stress that exercise produces is generally good for your health. It's when you overdo it that it becomes harmful, especially when compounded by other factors, like smoking, poor diet and drinking too much alcohol. What "overdoing it" looks like varies from person to person. But here are some ways to train wisely to prevent the production of too many free radicals and find a balance. Your workout should be challenging enough to trigger an increase in your body's antioxidant activity — yet not so long or hard that the surge of free radicals overwhelms your system. Be sure to alternate days between low- and high-intensity workouts to allow your muscles to recover, and bake in one to two rest days per week, according to the American Council on Exercise ACE. But what if you want to push yourself? When we consume fructose a type of sugar , the liver uses a lot of energy in the form of ATP to break it down. That process sets off a chain of reactions that prompts the body to produce even more uric acid, which has consistently been linked to the development of oxidative stress in cell and animal studies. There are a few ways alcohol can prompt the body to create more ROS. One is that ROS are produced when alcohol gets broken down by the body. As alcohol is metabolized , the body forms byproducts that boost the activity of the electron transport chain, resulting in the overproduction of ROS. Meanwhile, other studies have shown that even alcohol can decrease the levels of certain antioxidants and increase biomarkers of oxidative stress. For instance, a European Journal of Clinical Nutrition study on 53 post-menopausal women who consumed 30 grams of alcohol per day for eight weeks about two drinks found that levels of α-tocopherol an antioxidant declined while markers of oxidative stress increased. Inflammation and oxidative stress tend to go hand in hand. When the immune system senses trouble—like a harmful pathogen—it releases an army of immune cells in response. Those cells release enzymes, chemicals, and ROS, which can help destroy invaders, in part by causing inflammation. But if the body is constantly in a state of inflammation, this cycle of ROS production can become sustained, leading to oxidative stress. The presence of extra ROS can have a snowball effect. It can actually trigger more inflammation because those ROS cause the cell to send out more inflammatory cytokines chemical messengers than recruit more immune cells , perpetuating inflammation itself. In this regard, oxidative stress is both a precursor to this type of persistent inflammation and a consequence of it. Psychological stress is increasingly recognized as a factor leading to oxidative stress. When the body is under stress, perhaps due to an invading pathogen, immune system messengers, called cytokines, begin to flow. Psychological stress can also trigger the release of cytokines. Studies of real-life stressors have linked psychological stress to oxidative stress. One study analyzed the blood of 15 medical students before and after big exams to find oxidative stress biomarkers. In the days leading up to the exams, the students had lower antioxidant levels and higher levels of DNA and lipid damage. This suggested that oxidative stress had already swept through their cells during this stressful time. Job stress has also been shown to contribute to oxidative stress. A similar study in Spain found a correlation between malondialdehyde, another oxidative stress biomarker, and high levels of work-related stress. Cigarette smoke is both a notorious ROS generator as well as a source. High levels of ROS are found in cigarette tar , and thousands of chemicals present in cigarette smoke can trigger the body to produce extra ROS on its own, for example, by breaking down mitochondria. Studies have shown that smokers have lower levels of certain antioxidants than nonsmokers. It also generates more ROS. UVA light can penetrate the skin and reach specific molecules that absorb light, like melanin or DNA itself. They, in turn, can excite nearby molecules , including oxygen, generating ROS. Air pollution can also mess with the balance between ROS and antioxidants, leading to oxidative stress. These particles can themselves contain ROS but also can trigger the generation of ROS inside the body by activating macrophages, mitochondria, and ROS-producing enzymes. Several studies have shown that the components of air pollution, which include metals or other compounds, generate ROS within cells as they penetrate the body. Research increasingly shows that high blood glucose, or hyperglycemia, sets off a chain of reactions leading to oxidative stress. Studies have shown that sustained hyperglycemia can cause a cascade of events that lead to more ROS within cells: For example, high glucose levels can lead to increased production of the molecule diacylglycerol, which activates an enzyme called protein kinase C. This activates the enzyme NADPH-oxidase, which in turn can convert oxygen into ROS. High glucose can lead to oxidative stress through several other pathways. It has been shown to impair the activity of some antioxidants , lead mitochondria to make too much ROS , and activate the polyol pathway , which causes the enzyme NADH oxidase to produce ROS. Chronic hyperglycemia triggers harmful ROS production, but acute glucose spikes do as well. To explain their findings, the authors situated them within a growing body of research linking diabetic complications specifically with rapid swings in glucose as opposed to chronic hyperglycemia , which can partially be explained by the activation of ROS generation. One study they pointed to established that post-meal hyperglycemia induces overproduction of superoxide. Studies suggest that managing glucose swings can lead to fewer signs of oxidative stress. In one trial done in , 90 people with diabetes were given drugs to lower blood glucose levels. After 12 weeks, the participants had smaller daily glucose swings as well as fewer signs of oxidative stress than they did when the study began. Finally, oxidative stress may be one driver of insulin insensitivity, a significant factor affecting metabolic health. An existing theory suggests that oxidative stress damages some proteins involved in the insulin response, leading to insensitivity. In one small study published in Science Translational Medicine, six healthy men were told to eat 6, calories per day for a week and do nothing but stay in bed. Overall, the men gained about 3. The changes made the transporter dysfunctional, which the authors interpreted as a sign of insulin resistance. They can also bind to certain metals that promote ROS formation or act as cellular repair crews that clean up ROS-related damage. Some antioxidants are formed through certain pathways within cells. Those genes, in turn, are translated into antioxidants that can detoxify and eliminate ROS. Eating certain foods can activate the Nrf2 pathway. Some scientists have proposed that sulforaphane, a chemical found in broccoli, arugula, bok choy, kale, brussels sprouts, and other green vegetables, can help set the Nrf2 pathway into motion. Animal studies suggest that this nutrient can reduce oxidative stress and may be protective against certain diabetes complications, but this research is still ongoing. Curcumin, which is found in turmeric , has also been shown to be an Nrf2 activator. Research suggests that a group of compounds called alkyl-catechols, which are found in fermented foods , may also activate this master pathway. As one paper explains , these three compounds 4-vinylcatechol, 4-ethylcatechol, and 4-methylcatechol were once prevalent in ancient diets. But early evidence suggests that fermented foods still around today, like kimchi, can activate this pathway and stimulate the antioxidant defense system. One of the primary antioxidants produced by the body is glutathione, a potent antioxidant that can bind up ROS and may help repair DNA. One paper suggested that foods like green tea , lean proteins, salmon, cruciferous vegetables, and turmeric may support glutathione production. Some studies indicate that sulfur-rich foods support glutathione production because a vital part of the molecule itself is sulfur. Vitamin C, vitamin E, carotenoids found in yellow and orange vegetables like squash and carrots , and polyphenols found in berries, kiwis, plums, cherries, and apples are some examples of dietary antioxidants. Diets rich in plant-based food are protective against oxidative stress. For example, one study on 54 people with Type 2 diabetes examined how fruit and vegetable intake was related to antioxidant levels and, by extension, protection against oxidative stress. It found strong links between dietary antioxidant levels and fruit and vegetable intake, which included vegetables, root crops, fruits, berries, and jams and preserves made from these foods. Overall, people who ate more fruit and vegetables also showed fewer signs of oxidative stress. However, the full impact of dietary antioxidants—especially supplements—is not fully understood. Specific vitamins are known to support the antioxidant system still show inconsistent results in preventing the consequences of oxidative stress. For example, while observational studies have shown that when people eat more antioxidants like vitamin C , they tend to have lower risks of coronary heart disease, clinical trials have demonstrated lackluster results. One meta-review published in of 10 of these trials found only weak evidence that vitamin C supplements lowered the risk of cardiovascular disease. |
Oxidative stress and post-workout nutrition -
Besides the administration of grape extract decreased the plasma CK concentration and increased the hemoglobin Hb level in plasma suggesting a protection of cells against oxidative stress damage. The study revealed that this preparation and doses contributed to a significant increase in plasma TAC and to an insignificant increase in SOD, as well as a lower GSH activity and reduce concentration in TBARS.
Taghizadeh et al. No information about the polyphenol content was given but the results showed a significant rise in plasma GSH and a significant decrease in MDA. Besides, the players who received GSE exhibited a significant decrease serum insulin concentration.
On the other hand, the administration of GSE had no significant effects on parameters like creatine kinase CK or TAC when compared with the administration of the placebo. The study resulted in an increase in SOD, GSH and CAT activity, which remained stable until the end of the recovery period.
The authors explained that in comparison with the placebo group the subjects supplemented showed no need to mobilize more antioxidant defenses before the exercise because and that the supplement probably contributed to spare oxidative homeostasis.
Finally, it must be pointed out the protocol [ 93 ] established for a pilot study that includes a product mix made of dried grapes with almonds and dried cranberries. No results are given but the authors describe the necessity of studying the F2-isoprostanes as a lipid peroxidation biomarker for oxidative stress.
Supplementation with grape polyphenols seems to have a positive effect against oxidative stress. These effects are dependent on the supplement dose, the length of the supplementation period or the polyphenolic profile total polyphenol content and the distribution among polyphenolic families.
Besides, according to several reports, it appears that the type and intensity of exercise can affect the response of the blood antioxidant defense system, just as the training status of the athlete, or the sport discipline.
Considering the supplementation dosage in these studies it seems unlikely athletes would gain enough quantity of polyphenols from diet. Therefore, grape-based polyphenol concentrated products would be an interesting approach.
Moreover, inter-individual variability the age, sex, diet, environment factors, exercise protocols and even variability in gene expression could influence the polyphenols bioavailability and physiological responses to oxidative stress.
Given the promising evidence, although still limited, more pilot studies on effect of grape polyphenols on the oxidative stress produced by sport should be conducted to determine the optimal concentration, dosage and effect on the oxidative stress for target athletes.
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In other cases, when ROS overwhelms antioxidant systems , it can lead to heart disease. Studies have also linked excess levels of ROS to complications related to diabetes or the development of neurodegenerative diseases.
While the connection between ROS and disease is well established, the role of ROS in the body presents a bit of a puzzle. When in balance with antioxidants, ROS set normal cell pathways in motion and even use their destructive abilities to target invaders.
For example, one review paper points out that ROS may help the body destroy harmful microbes. So, evolutionarily speaking, ROS are a form of compromise.
This means that combating the ill effects of oxidative stress, from inflammation to metabolic complications, is not as simple as boosting antioxidants to soak up ROS. Some ROS production is natural in a healthy functioning cell.
When your body combines oxygen and food sources to make energy, it passes electrons along a long chain of proteins embedded within the membrane of mitochondria, the energy-making portion of a cell.
Most of the time, electrons are used up in this process, known as the electron transport chain, to create energy in the form of a molecule called ATP, together with water as a byproduct. But occasionally, electrons slip out from that chain.
When this happens, they can react with nearby oxygen and form ROS. But if either antioxidant systems are depleted or ROS accumulates, damage can happen. There are several ways that ROS can be introduced into cells, tipping the balance beyond what the body can handle on its own.
Here are a few ways ROS can accumulate:. ROS production is triggered when we consume most major macronutrients carbs, fats, proteins. That may be one reason why caloric restriction has been linked to lower ROS generation in animal studies. However, oxidative stress is caused mainly by extreme eating patterns.
Not eating enough and malnutrition have been shown to increase ROS levels beyond the realm of physiological balance.
Overeating can have the same result. Overnutrition overeating that leads to weight gain triggers processes in the cell that lead to ROS production.
And when physical activity is low, less of those nutrients are used to make energy, compounding the electron glut.
When we overeat , the electron transport chain is overburdened and, therefore, leakier. And when those electrons escape, more ROS form.
Studies in humans have linked overeating and ROS production. For example, in a week-long study on 10 healthy men in Korea, five of the men ate normally, while the other five ate about 3, calories per day in high-fat and high-carbohydrate meals.
The high-calorie group showed an uptick in ROS production and antioxidant production, but overall, they generated a more significant amount of ROS than antioxidants. Other papers consistently link excess nutrition to oxidative stress.
For example, one review paper found an association between postprandial glucose and lipid levels to oxidative stress across nine studies investigating this link.
The biomarker most closely linked to oxidative stress was the level of post-meal triglycerides in the blood fats that the body uses to store extra calories. The big picture is: When the body is in a post-meal state, unused nutrients can cause oxidative stress. What you eat influences the state of your cells as well.
Animal studies have linked diets high in sugar and fat to oxidative stress. In one study, mice fed high-glucose diets for four weeks had decreased levels of key antioxidants, and their genes related to greater ROS production were switched on.
With their antioxidant defense systems weakened and ROS-producing fires stoked, these mice entered a state of oxidative stress they also developed diabetes, which the authors propose could have been set in motion by oxidative stress.
Some review papers examining the impact of specific diets on oxidative stress have found that certain eating patterns have greater impacts on antioxidant-ROS balance than others. These biomarkers include DNA, lipids, proteins, and carbohydrates that have interacted with ROS, and antioxidants that have changed due to increased ROS.
Other eating patterns seem to be less harmful. Compared to the Western diet, the Mediterranean diet consisting mainly of olive oil, vegetables, white meat, fish, fresh nuts, and seeds was linked to fewer signs of oxidative stress and a greater presence of antioxidant defenders.
Similarly, people who follow vegetarian diets have been shown to have lower ROS and other oxidative stress biomarkers. For example, animal studies suggest that re-heated vegetable oils which might be used for deep frying decrease antioxidant levels.
Oils with higher levels of unsaturated fatty acids polyunsaturated fats like linolenic acid and linoleic acid oxidize more quickly because of their chemical structure, which contains more double bonds than monounsaturated or saturated fatty acids.
Some examples include vegetable oils like soybean, sunflower, and safflower oil. They also oxidize more quickly when heated. The health risks of consuming oxidized oils, however, are still up for debate.
A pair of reviews in the journal Molecular Nutrition and Food Research presented both sides of the argument. Studies have shown that macronutrients—protein, fat, and sugar— can contribute to oxidative stress in different ways. For example, in one highly unappetizing clinical trial done in , 15 men and women fasted overnight.
They then drank half a cup of either straight cream high in fat or a mixture containing casein a protein found in milk. In both cases, the ROS levels of participants rose after eating.
Other research has shown that glucose consumption can lead to ROS production, too, through more than one mechanism. High blood sugar can lead to the production of triglycerides , high levels of which are linked to oxidative stress.
But it can also set other ROS-related pathways in motion. One crucial pathway appears to involve the production of uric acid —a waste product found in blood. When we consume fructose a type of sugar , the liver uses a lot of energy in the form of ATP to break it down.
That process sets off a chain of reactions that prompts the body to produce even more uric acid, which has consistently been linked to the development of oxidative stress in cell and animal studies.
There are a few ways alcohol can prompt the body to create more ROS. One is that ROS are produced when alcohol gets broken down by the body. As alcohol is metabolized , the body forms byproducts that boost the activity of the electron transport chain, resulting in the overproduction of ROS.
Meanwhile, other studies have shown that even alcohol can decrease the levels of certain antioxidants and increase biomarkers of oxidative stress. For instance, a European Journal of Clinical Nutrition study on 53 post-menopausal women who consumed 30 grams of alcohol per day for eight weeks about two drinks found that levels of α-tocopherol an antioxidant declined while markers of oxidative stress increased.
Inflammation and oxidative stress tend to go hand in hand. When the immune system senses trouble—like a harmful pathogen—it releases an army of immune cells in response.
Those cells release enzymes, chemicals, and ROS, which can help destroy invaders, in part by causing inflammation. But if the body is constantly in a state of inflammation, this cycle of ROS production can become sustained, leading to oxidative stress. The presence of extra ROS can have a snowball effect.
It can actually trigger more inflammation because those ROS cause the cell to send out more inflammatory cytokines chemical messengers than recruit more immune cells , perpetuating inflammation itself. In this regard, oxidative stress is both a precursor to this type of persistent inflammation and a consequence of it.
Psychological stress is increasingly recognized as a factor leading to oxidative stress. When the body is under stress, perhaps due to an invading pathogen, immune system messengers, called cytokines, begin to flow.
Psychological stress can also trigger the release of cytokines. Studies of real-life stressors have linked psychological stress to oxidative stress. One study analyzed the blood of 15 medical students before and after big exams to find oxidative stress biomarkers.
In the days leading up to the exams, the students had lower antioxidant levels and higher levels of DNA and lipid damage. This suggested that oxidative stress had already swept through their cells during this stressful time.
Job stress has also been shown to contribute to oxidative stress. A similar study in Spain found a correlation between malondialdehyde, another oxidative stress biomarker, and high levels of work-related stress. Cigarette smoke is both a notorious ROS generator as well as a source.
High levels of ROS are found in cigarette tar , and thousands of chemicals present in cigarette smoke can trigger the body to produce extra ROS on its own, for example, by breaking down mitochondria. Studies have shown that smokers have lower levels of certain antioxidants than nonsmokers.
It also generates more ROS. UVA light can penetrate the skin and reach specific molecules that absorb light, like melanin or DNA itself. They, in turn, can excite nearby molecules , including oxygen, generating ROS. Air pollution can also mess with the balance between ROS and antioxidants, leading to oxidative stress.
These particles can themselves contain ROS but also can trigger the generation of ROS inside the body by activating macrophages, mitochondria, and ROS-producing enzymes.
Several studies have shown that the components of air pollution, which include metals or other compounds, generate ROS within cells as they penetrate the body. Research increasingly shows that high blood glucose, or hyperglycemia, sets off a chain of reactions leading to oxidative stress.
Studies have shown that sustained hyperglycemia can cause a cascade of events that lead to more ROS within cells: For example, high glucose levels can lead to increased production of the molecule diacylglycerol, which activates an enzyme called protein kinase C.
This activates the enzyme NADPH-oxidase, which in turn can convert oxygen into ROS. High glucose can lead to oxidative stress through several other pathways.
It has been shown to impair the activity of some antioxidants , lead mitochondria to make too much ROS , and activate the polyol pathway , which causes the enzyme NADH oxidase to produce ROS.
Chronic hyperglycemia triggers harmful ROS production, but acute glucose spikes do as well. To explain their findings, the authors situated them within a growing body of research linking diabetic complications specifically with rapid swings in glucose as opposed to chronic hyperglycemia , which can partially be explained by the activation of ROS generation.
One study they pointed to established that post-meal hyperglycemia induces overproduction of superoxide. Studies suggest that managing glucose swings can lead to fewer signs of oxidative stress.
In one trial done in , 90 people with diabetes were given drugs to lower blood glucose levels. After 12 weeks, the participants had smaller daily glucose swings as well as fewer signs of oxidative stress than they did when the study began.
Finally, oxidative stress may be one driver of insulin insensitivity, a significant factor affecting metabolic health. An existing theory suggests that oxidative stress damages some proteins involved in the insulin response, leading to insensitivity.
In one small study published in Science Translational Medicine, six healthy men were told to eat 6, calories per day for a week and do nothing but stay in bed. Overall, the men gained about 3. The changes made the transporter dysfunctional, which the authors interpreted as a sign of insulin resistance.
They can also bind to certain metals that promote ROS formation or act as cellular repair crews that clean up ROS-related damage. Some antioxidants are formed through certain pathways within cells.
Those genes, in turn, are translated into antioxidants that can detoxify and eliminate ROS.
Exercise is one of the best things Nutritino can do for your body to fight inflammation post-workokt stay healthy, but in Pos-tworkout seeming nutriyion, working out also triggers oxidative stress — a main cause of inflammation. Weight and body composition analysis Waist circumference and abdominal obesity measurement is post-wlrkout state in which ppost-workout body has an imbalance of free radicals and antioxidants, explains Lance Dalleck, PhDprofessor of exercise and sport science at Western Colorado University and spokesperson for the American Council on Exercise. Meanwhile, antioxidants help protect your cells against free radicals in your body. So does that mean you should scale back on your workouts? The short answer is no. Free radicals are a natural byproduct of consuming oxygen during exercise or any activity to break down ATP short for adenosine triphosphate for energy, he says. Some exercise-induced oxidative stress can actually enhance your health because it conditions your body to adapt to stressful situations.
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