In the world of sports nutrition, few topics spark as much debate as the role of antioxidants in post-exercise recovery. Athletes, coaches, and nutritionists alike recognize that training—whether strength-based, endurance-focused, or sport-specific—places a physiological stress load on the body. Part of that stress involves the production of reactive oxygen species (ROS), commonly referred to as free radicals. While these molecules are often portrayed as harmful agents that damage cells and accelerate aging, the reality is far more nuanced: ROS are not simply destructive byproducts of exercise, but also act as essential signaling molecules that help the body adapt to training.

The concept of oxidative stress is central to this discussion. Oxidative stress occurs when ROS production outpaces the body’s ability to neutralize them through antioxidant defenses, leading to potential cellular damage. Exercise—particularly intense or prolonged activity—temporarily increases ROS generation through various metabolic pathways, such as mitochondrial respiration and enzyme activation. In the short term, this rise in ROS can contribute to muscle fatigue, inflammation, and micro damage to tissues. However, these same molecules also stimulate adaptive processes like mitochondrial biogenesis, improved antioxidant enzyme activity, and enhanced endurance capacity.

Enter antioxidants—substances that can neutralize ROS and restore redo balance. They exist in two primary forms:

• Endogenous antioxidants – produced by the body itself, including enzymes like superoxide dismutase (SOD), catalane, and glutathione peroxides.
• Exogenous antioxidants – obtained from the diet, such as vitamins C and E, polyphones, arytenoids, and certain minerals.

For decades, supplementation with antioxidants has been promoted as a way to reduce post-exercise muscle soreness, speed recovery, and protect against oxidative damage. The logic seems straightforward: exercise produces free radicals, antioxidants neutralize them, and therefore antioxidant supplementation should enhance recovery. But emerging research has challenged this simplistic view. Several studies have shown that high-dose antioxidant supplementation immediately after exercise may blunt some of the beneficial training adaptations by interfering with ROS-mediated signaling pathways.

This creates a complex dilemma for athletes and active individuals:

• On one hand, minimizing oxidative damage can be critical for rapid recovery between closely spaced training sessions or competitive events.
• On the other, allowing some oxidative stress appears necessary for long-term physiological adaptation and performance gains.

The central question, then, is not whether antioxidants are valuable—they clearly are—but whether consuming them immediately after a workout is always the best strategy. This article will explore the biochemical underpinnings of exercise-induced oxidative stress, the roles and types of antioxidants, the evidence both for and against immediate post-workout consumption, and practical guidelines for tailoring antioxidant intake to specific training goals and athletic profiles.

The Science of Exercise-Induced Oxidative Stress

To understand the role of antioxidants in post-exercise recovery, it is essential to first examine the biochemical events that occur during and after physical activity. Exercise-induced oxidative stress is a double-edged sword—capable of contributing both to tissue damage and to the adaptive responses that make athletes stronger, faster, and more resilient.

What Are Free Radicals and Reactive Oxygen Species (ROS)?

Free radicals are unstable molecules with one or more unpaired electrons, making them highly reactive. In biological systems, the most relevant forms are reactive oxygen species (ROS)—oxygen-containing free radicals such as:

• Superoxide anion (O₂⁻·)
• Hydroxyl radical (·OH)
• Proxy radicals (ROO·)

Additionally, non-radical derivatives like hydrogen peroxide (H₂O₂) can also contribute to oxidative stress by generating radicals through certain reactions (e.g., the Fenton reaction). Closely related are reactive nitrogen species (RNS) such as nitric oxide (NO·) and peroxynitrite (ONOO⁻), which share similar reactive properties.

Sources of ROS during Exercise

During exercise, ROS are produced through multiple pathways, including:

• Mitochondrial electron transport chain leakage – As aerobic respiration ramps up, electrons can prematurely react with oxygen, producing superoxide.
• NADPH oxidizes activation – Found in cell membranes, these enzymes generate ROS as part of immune and signaling responses.
• Xanthenes oxidize activity – Especially during high-intensity or ischemia-reperfusion scenarios.
• Auto oxidation of hemoglobin and myoglobin – Contributing to ROS in working muscles.

The rate and volume of ROS production rise significantly during prolonged endurance exercise, high-intensity interval training (HIIT), and heavy resistance training, making antioxidant defenses especially critical in these contexts.

The Beneficial Roles of ROS

While ROS are often considered harmful, they are also vital signaling molecules in the context of exercise adaptation.

• Mitochondrial biogenesis – ROS activate transcription factors such as PGC-1α, leading to increased mitochondrial content and improved aerobic capacity.
• Endogenous antioxidant enzyme up regulation – A moderate ROS increase stimulates the body to produce more antioxidant enzymes, enhancing long-term oxidative defense.
• Inflammation resolution and tissue remodeling – ROS act as triggers for cellular repair pathways, enabling muscle regeneration after micro trauma.

This paradox—ROS as both damaging agents and necessary messengers—is a key reason why indiscriminate suppression through antioxidants may sometimes hinder training outcomes.

4. Harmful Effects of Excess ROS

When ROS production exceeds the capacity of the antioxidant defense system, oxidative stress occurs, leading to:

• Lipid per oxidation – Damaging cell membranes and impairing muscle function.
• Protein oxidation – Altering enzyme activity and contractile proteins.
• DNA damage – Contributing to cellular dysfunction and aging.
  Excess oxidative stress can also prolong inflammation, delay recovery, and potentially contribute to overtraining syndromes if left unchecked.

5. The Oxidative Stress Threshold and Hermes’s

The concept of heresies is critical in sports nutrition. Hermes’s describes a dose-response relationship where low to moderate levels of a stressor (in this case, ROS) are beneficial by stimulating adaptation, but high levels are detrimental. This means:

• Too little ROS → insufficient signaling for adaptation, potentially blunted gains.
• Optimal ROS range → Strong adaptive response with minimal damage.
• Too much ROS → Cellular damage, reduced performance, slower recovery.

From a practical standpoint, this suggests that timing and dosage of antioxidant intake may determine whether supplementation helps by controlling excessive oxidative stress or hurts by interfering with beneficial ROS signaling.

Antioxidants: Types and Functions

Antioxidants are compounds that neutralize reactive oxygen species (ROS) and reactive nitrogen species (RNS), helping to maintain redo homeostasis. They achieve this by either directly scavenging free radicals, chelating metal ions that catalyze radical formation, or repairing oxidized bimolecular. In the context of exercise, antioxidants work alongside the body’s natural defenses to prevent excessive oxidative damage while allowing for the signaling processes necessary for adaptation.

Antioxidants can be broadly classified into endogenous (produced within the body) and exogenous (obtained through diet) sources.

Endogenous Antioxidants

The body has evolved a sophisticated enzymatic and non-enzymatic antioxidant system to control ROS. These defenses are dynamic and can be unregulated with regular training.

Enzymatic Antioxidants

• Superoxide dismutase (SOD): Converts superoxide anions (O₂⁻·) into hydrogen peroxide (H₂O₂). Exists in cytosolic (Cu/Zn-SOD), mitochondrial (Man-SOD), and extracellular forms.
• Catalane (CAT): Found in paroxysms, catalane converts H₂O₂ into water and oxygen.
• Glutathione peroxides (Gap): Uses reduced glutathione (GSH) to convert H₂O₂ into water, while oxidizing GSH to GSSG. Selenium is a cofactor for Gap.

Non-Enzymatic Antioxidants

• Glutathione (GSH): The most abundant intracellular antioxidant, acting as a direct ROS scavenger and a cofactor for Gap.
• Uric acid: End product of urine metabolism; scavenges peroxynitrite and hydroxyl radicals.
• Bilirubin: Byproduct of home metabolism with strong antioxidant properties at physiological concentrations.

Dietary (Exogenous) Antioxidants

Athletes rely on dietary antioxidants not only for direct free radical neutralization but also for supporting endogenous defense systems.

Vitamins

• Vitamin C (ascorbic acid): Water-soluble, scavenges a variety of ROS in the cytosol and extracellular space; regenerates oxidized vitamin E.
• Vitamin E (α-tocopherol): Fat-soluble, protects polyunsaturated fatty acids in cell membranes from lipid per oxidation.
• Vitamin A and β-carotene: Protect against singlet oxygen and lipid radicals; β-carotene also functions as a provitamin for retinol.

Minerals

• Selenium: Cofactor for glutathione peroxides.
• Zinc: Structural component of Cu/Zn-SOD; stabilizes cell membranes.
• Manganese: Cofactor for Man-SOD in mitochondria.

Polyphones and Flavonoids

• Flavonoids: Found in tea, cocoa, berries; include catechins, anthocyanins, and quercetin.
• Resveratrol: Present in grapes, red wine; exhibits both antioxidant and anti-inflammatory effects.
• Cur cumin: Turmeric-derived compound with antioxidant and signaling-modulating properties.

Arytenoids

• Lycopene: Found in tomatoes, effective against singlet oxygen.
• Lute in and zeaxanthin: Present in leafy greens; protect against light-induced oxidative damage in the retina.

Mechanisms of Antioxidant Action

Antioxidants protect cells and tissues through several key mechanisms:

• Direct radical scavenging – donating electrons or hydrogen atoms to neutralize ROS.
• Metal ion chelating – binding iron or copper to prevent Fenton-type reactions.
• Repair of oxidized molecules – regenerating oxidized vitamins and proteins.
• Up regulation of endogenous defenses – certain polyphones act as indirect antioxidants by activating transcription factors like Nrf2, which boosts antioxidant enzyme production.

Synergy between Antioxidants

Antioxidants rarely act alone. Vitamin C regenerates oxidized vitamin E, polyphones can spare glutathione, and arytenoids may work alongside flavonoids to reduce lipid per oxidation. This network effect is one reason whole-food sources of antioxidants often outperform isolated high-dose supplements.

Antioxidants and Recovery: Evidence Overview

The relationship between antioxidants and post-exercise recovery has been the subject of intensive research over the past two decades. While antioxidants are commonly believed to accelerate recovery, reduce muscle soreness, and prevent cellular damage, the scientific literature presents a more nuanced and sometimes contradictory picture. Understanding these findings is essential for athletes and active individuals aiming to optimize performance without unintentionally blunting training adaptations.

Studies Supporting Immediate Antioxidant Intake

Several investigations demonstrate that post-workout antioxidant consumption can mitigate exercise-induced oxidative stress and improve markers of recovery:

• Reduced Muscle Soreness: Vitamin C and E supplementation immediately after high-intensity resistance or endurance exercise has been associated with decreased delayed onset muscle soreness (DOMS) in some trials. By neutralizing excess ROS, antioxidants may reduce local inflammation and oxidative damage to muscle fibers.
• Lower Oxidative Stress Markers: Acute intake of polyphone-rich beverages, such as cherry juice or green tea extracts, has been shown to reduce lipid per oxidation and protein oxidation markers post-exercise. This effect is particularly evident in prolonged endurance events, where ROS generation is highest.
• Improved Recovery Kinetics: Some studies suggest that antioxidants can accelerate the replenishment of glutathione and other endogenous antioxidants, supporting faster recovery between training sessions or competitive events. For example, tart cherry juice consumed after intense cycling reduced oxidative stress markers and muscle pain, improving perceived recovery in trained athletes.

Studies Suggesting Potential Drawbacks

Contrary to the traditional view, a growing body of research indicates that immediate post-exercise antioxidant supplementation may interfere with some adaptive responses:

• Blunted Mitochondrial Biogenesis: Reactive oxygen species function as signaling molecules that trigger transcription factors like PGC-1α, which are critical for mitochondrial adaptation. High-dose vitamin C or E taken right after endurance training can attenuate these signals, potentially reducing gains in aerobic capacity over time.
• Reduced Muscle Hypertrophy Signals: In resistance-trained individuals, acute antioxidant supplementation may dampen ROS-mediated activation of motor and MAPK pathways, which are essential for muscle protein synthesis and hypertrophy.
• Variable Performance Outcomes: While antioxidants may reduce markers of oxidative damage, studies often report no significant improvement in actual strength, endurance, or sprint performance, highlighting a disconnect between biochemical markers and functional outcomes.

Neutral or Mixed Findings

Many studies fall somewhere in between, showing beneficial effects under certain conditions but negligible or adverse effects in others. Factors influencing these mixed results include:

• Dosage and Form: High-dose isolated vitamin supplements tend to produce stronger signaling interference compared to moderate, food-based antioxidant intake.
• Training Status: Novice vs. elite athletes responds differently; trained individuals often have more robust endogenous antioxidant defenses.
• Type and Intensity of Exercise: Endurance, high-intensity interval, and resistance training elicit distinct ROS profiles, which may dictate whether antioxidant intervention is helpful or detrimental.
• Timing: Immediate intake vs. delayed (e.g., a few hours post-exercise) can significantly alter outcomes.

Key Takeaways from Current Evidence

• Antioxidants can reduce oxidative stress markers and perceived muscle soreness, particularly in high-volume or endurance-based exercise.
• High-dose supplementation immediately after exercise may blunt training adaptations, especially in terms of mitochondrial biogenesis and hypertrophy.
• Food-based antioxidants appear to be safer and may offer benefits without interfering with adaptation, likely due to their moderate dosage and synergistic bioactive compounds.
• Individual factors—training experience, exercise type, and recovery goals—must guide personalized antioxidant strategies rather than a one-size-fits-all approach.

Post-Workout Window: Timing Considerations

The timing of antioxidant intake relative to exercise has emerged as a critical factor in determining whether supplementation enhances recovery or inadvertently interferes with training adaptations. While athletes often assume that “more antioxidants, immediately after exercise” is always better, recent research suggests that the post-workout window is more nuanced than previously thought.

Metabolic Changes after Exercise

Immediately after exercise, the body undergoes a series of rapid metabolic and hormonal changes that influence nutrient delivery and cellular recovery:

• Increased Blood Flow: Skeletal muscle blood flow remains elevated for up to several hours post-exercise, enhancing the delivery of glucose, amino acids, and other nutrients.
• Enhanced Insulin Sensitivity: Muscle cells are more responsive to insulin, improving the uptake of carbohydrates and amino acids necessary for glycogen resynthesis and muscle protein synthesis.
• Elevated Cellular Stress: ROS levels peak during and immediately after high-intensity or prolonged exercise, serving as key signaling molecules for adaptation.

This “window of opportunity” is sometimes referred to as the post-exercise anabolic or nutrient timing window; although it’s exact duration and significance can vary depending on training status, intensity, and type of exercise.

ROS Signaling and Adaptation

Reactive oxygen species are not solely damaging byproducts—they are also essential messengers in exercise adaptation:

• Mitochondrial Biogenesis: ROS activate transcription factors like PGC-1α, promoting the formation of new mitochondria in skeletal muscle.
• Endogenous Antioxidant Up regulation: Moderate ROS production stimulates the body’s own antioxidant defenses, increasing long-term resilience to oxidative stress.
• Inflammatory Signaling: ROS participate in controlled inflammatory responses that initiate muscle repair and remodeling.

Immediate post-workout antioxidant intake—especially in high doses—can neutralize ROS before these signaling pathways are fully activated, potentially blunting beneficial adaptations.

Timing Hypotheses for Antioxidant Intake

Researchers have proposed several strategies to balance recovery and adaptation:

• Immediate Intake (0–1 hour post-exercise): May be beneficial when rapid recovery is critical (e.g., multiple daily training sessions, tournaments, or competitions). Potential benefits include reduced oxidative damage and lower perceived muscle soreness.
• Delayed Intake (2–6 hours post-exercise): Allows ROS signaling to occur, promoting mitochondrial and hypertrophic adaptations, while still providing antioxidants to aid recovery later.
• Pre-Workout Intake: Provides baseline antioxidant protection during exercise but may have less impact on post-exercise adaptation.

Choosing the optimal timing depends on training goals and competition schedule. For example:

• Endurance athletes in multi-day events may prioritize immediate antioxidant intake to sustain performance.
• Recreational lifters focused on hypertrophy may benefit from delaying supplementation to avoid interfering with ROS-mediated anabolic signaling.

Practical Implications for Different Goals

• Strength and Hypertrophy: Delaying high-dose antioxidant supplementation or obtaining antioxidants primarily from whole foods can preserve ROS-mediated muscle growth signaling.
• Endurance and High-Volume Training: Immediate intake of moderate antioxidants may reduce oxidative stress and muscle soreness, supporting subsequent performance.
• Injury Recovery or Older Adults: Timely antioxidant intake can help mitigate excessive inflammation and oxidative stress, which may otherwise delay healing.

Whole Foods vs. Supplements

When it comes to antioxidants and post-workout recovery, the source of antioxidants can be just as important as the timing. While supplements offer convenience and precise dosing, whole foods provide a synergistic array of bioactive compounds that often enhance efficacy and safety. Understanding the distinctions between these sources can help athletes make evidence-based choices.

Synergy of Food-Based Antioxidants

Whole foods contain complex mixtures of antioxidants, vitamins, minerals, and photochemical that work together to maximize cellular protection:

• Polyphone-rich fruits: Berries, cherries, and grapes contain anthocyanins and flavonoids that scavenge ROS and up regulate endogenous antioxidant enzymes.
• Vegetables: Leafy greens, tomatoes, and cruciferous vegetables provide arytenoids, vitamin C, and other phytonutrients.
• Nuts and seeds: Provide vitamin E and polyunsaturated fatty acids that protect cell membranes from lipid per oxidation.

This network effect often results in more efficient ROS neutralization compared to single-compound supplements. For example, studies have shown that consuming tart cherry juice or mixed berry smoothies post-exercise reduces muscle soreness and oxidative stress markers without blunting adaptive signaling.

Isolated Supplements

Antioxidant supplements—such as high-dose vitamins C and E capsules—offer the advantage of controlled dosing but can carry potential drawbacks:

• High Bioavailability: Supplements often provide doses far exceeding what can be obtained from food, ensuring rapid plasma concentrations.
• Risk of Over-suppression: Excessive antioxidant intake can neutralize ROS signaling, blunting training adaptations such as mitochondrial biogenesis and muscle hypertrophy.
• Potential for Imbalance: High doses of one antioxidant may interfere with absorption or function of others, disrupting natural redo balance.

For example, research indicates that vitamin C supplementation exceeding 1,000 mg/day immediately after endurance exercise may attenuate improvements in VO₂ max and mitochondrial enzyme activity over time.

Comparative Studies

Several studies have directly compared whole foods with supplements:

• Tart Cherry Juice vs. Vitamin C Pills: Tart cherry juice reduced oxidative stress markers and improved recovery without impairing training adaptations, whereas high-dose vitamin C tablets sometimes blunted these adaptive responses.
• Mixed Berry Smoothies vs. Isolated Polyphone Extracts: Whole berries provided moderate doses of antioxidants alongside fiber, vitamins, and other phytonutrients, producing favorable outcomes in muscle recovery and inflammation.

These findings suggest that moderate, food-based antioxidant intake may offer a safer, more effective approach for most athletes than large doses of isolated supplements.

Practical Recommendations for Athletes

• Prioritize Whole Foods: Post-workout meals containing colorful fruits, vegetables, nuts, and seeds can provide antioxidants without disrupting ROS signaling.
• Use Supplements Strategically: Reserve high-dose supplements for situations where rapid recovery is critical, such as multi-day competitions or high-intensity training camps.
• Combine with Balanced Nutrition: Antioxidants work best when paired with sufficient protein, carbohydrates, and healthy fats to support overall recovery.

Conclusion

Antioxidants play a crucial role in the body’s defense against exercise-induced oxidative stress, supporting recovery and protecting cells from excessive damage. However, as research over the past two decades has demonstrated, their role in post-workout nutrition is far from straightforward. While antioxidants can reduce markers of oxidative stress, decrease muscle soreness, and aid in short-term recovery, timing, dosage, and source are critical factors that determine whether supplementation enhances or potentially hinders long-term training adaptations.

Exercise-induced reactive oxygen species (ROS) serve a dual function. On one hand, excessive ROS can damage proteins, lipids, and DNA, contributing to inflammation and delayed recovery. On the other hand, moderate ROS generation is essential for adaptive signaling, including mitochondrial biogenesis, endogenous antioxidant up regulation, and muscle hypertrophy. This hermetic effect underlines the importance of a balanced approach: suppressing ROS indiscriminately with high-dose antioxidants immediately after training may compromise the very processes that improve endurance, strength, and metabolic efficiency over time.

Evidence from the scientific literature highlights nuanced outcomes depending on the source of antioxidants. Whole-food sources, including fruits, vegetables, nuts, and seeds; provide a synergistic mix of vitamins, minerals, and polyphones that can reduce oxidative stress while preserving ROS-mediated adaptations. In contrast, isolated high-dose supplements, particularly vitamins C and E, may neutralize ROS too rapidly, potentially blunting beneficial signaling pathways. Studies comparing whole foods with supplements consistently suggest that moderate, food-based antioxidant intake is safer and more effective for recovery, particularly in recreational and elite athletes alike.

Timing also plays a pivotal role. Immediate antioxidant intake may be warranted in situations requiring rapid recovery, such as multi-day competitions or high-intensity training sessions, where minimizing muscle soreness and oxidative stress is a priority. Conversely, for athletes focused on long-term adaptations, delaying antioxidant intake by a few hours—or relying primarily on antioxidant-rich foods—may allow ROS to act as beneficial signaling molecules, supporting mitochondrial function, muscle growth, and overall training responsiveness.

Ultimately, the optimal strategy for post-workout antioxidant intake must be individualized, taking into account training goals, exercise type, intensity, and recovery needs. Emphasizing whole foods, strategically using supplements when necessary, and understanding the dual role of ROS can help athletes and active individuals maximize recovery without compromising adaptation. Rather than viewing antioxidants as a simple “repair tool,” they should be considered as part of a comprehensive, evidence-based nutrition plan that balances performance, recovery, and long-term physiological benefits.

In conclusion, antioxidants are neither universally beneficial nor harmful in the post-exercise period. Their value depends on context, timing, and source, and integrating them intelligently into a broader nutritional strategy is the key to optimizing both short-term recovery and long-term training adaptations.

SOURCES

Powers, S.K., Jackson, M.J. (2008). Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production. Physiological Reviews, 88(4), 1243–1276.

Peace, J., Suzuki, K., Combs, J.S. (2007). The influence of antioxidant supplementation on markers of inflammation and oxidative stress after exercise. Journal of Nutrition and Biochemistry, 18(6), 357–371.

Gomez-Cabrera, M.C., Salvador-Pascal, A., Cabot, H., Vine, J. (2015). Redo modulation of muscle adaptation to exercise: role of antioxidants. Free Radical Biology and Medicine, 86, 37–46.

Bristow, M., Parse K., Breach, A., et al. (2009). Antioxidants prevent health-promoting effects of physical exercise in humans. Proceedings of the National Academy of Sciences, 106(21), 8665–8670.

Bjornson, T., et al. (2019). Effects of antioxidant supplementation on exercise-induced adaptations in skeletal muscle. Redo Biology, 26, 101287.

McLeay, Y., et al. (2012). The effect of tart cherry juice on recovery and oxidative stress in marathon runners. Journal of the International Society of Sports Nutrition, 9(1), 31.

Paulsen, G., et al. (2014). Vitamin C and E supplementation alters protein signaling and muscle adaptation to strength training. Free Radical Biology and Medicine, 73, 69–79.

Bloomer, R.J., Goldfarb, A.H., Wireman, L. (2006). Effects of antioxidant supplementation on markers of oxidative stress after eccentric exercise. Journal of Strength and Conditioning Research, 20(3), 689–695.

Lushchak, V.I. (2011). Adaptive response to oxidative stress: bacteria, fungi, plants, and animals. Comparative Biochemistry and Physiology Part C, 153(2), 175–190.

Huang, D., Our, B., Prior, R.L. (2005). The chemistry behind antioxidant capacity assays. Journal of Agricultural and Food Chemistry, 53(6), 1841–1856.

Gomez-Cabrera, M.C., et al. (2008). Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance. American Journal of Clinical Nutrition, 87(1), 142–149.

Lundberg, J.O., Weisberg, E., Gladwin, M.T. (2008). The nitrate–nitrite–nitric oxide pathway in physiology and therapeutics. Nature Reviews Drug Discovery, 7(2), 156–167.

Fined, J., Lac, G., Fila ire, E. (2006). Oxidative stress: relationship with exercise and training. Sports Medicine, 36(4), 327–358.

Mastaloudis, A., et al. (2004). Antioxidant supplementation and recovery from exercise-induced oxidative stress. Nutrition, 20(5), 492–498.

Hells ten, Y., Grandson, U., Orthenblad, N. (1996). Exercise-induced free radical formation in skeletal muscle. Journal of Physiology, 495(1), 197–202.

Davies, K.J., Quintanilla, A.T., Brooks, G.A., Packer, L. (1982). Free radicals and tissue damage produced by exercise. Biochemical and Biophysical Research Communications, 107(4), 1198–1205.

Powers, S.K., Radar, Z., Jib, L.L. (2016). Exercise-induced oxidative stress: Past, present and future. Journal of Physiology, 594(18), 5081–5092.

Knees, W.L., Combs, J.S. (2006). The antioxidant paradox: ROS and adaptation to exercise. Journal of Science and Medicine in Sport, 9(4), 272–283.

Traustadóttir, T., Davies, S.S., Stock, A., et al. (2006). The effect of antioxidant supplementation on oxidative stress and muscle function in humans. Free Radical Biology and Medicine, 41(4), 451–457.

Brachium, A.J., Hopkins, W.G., Lowe, T.E. (2014). Effects of dietary antioxidants on training adaptations. International Journal of Sport Nutrition and Exercise Metabolism, 24(4), 441–451.

Close, G.L., et al. (2006). Ascorbic acid supplementation does not attenuate training adaptation in humans. Journal of Physiology, 575(1), 241–248.

Liu, J., Head, E., Garb, A.M., et al. (2002). Memory loss in aging mice: effects of antioxidant supplementation. Journal of Neuroscience, 22(23), 10117–10125.

HISTORY

Current Version
Aug 13, 2025

Written By:
ASIFA