Antioxidant Supplementation and Adaptive Response to Training: A Systematic Review

Abstract

Background: Antioxidant supplementation has become a common practice among athletes to theoretically achieve a reduction in oxidative stress, promote recovery and improve performance. Objective: To assess the effect of antioxidant supplements on exercise. Methods: A systematic literature search was performed up to January 2019 in MEDLINE via EBSCO and Pubmed, and in Web of Sciences based on the following terms: “antioxidants” [Major] AND “exercise” AND “adaptation”; “antioxidant supplement” AND “(exercise or physical activity)” AND “(adaptation or adjustment)” [MesH]. Thirty-six articles were finally included. Results: Exhaustive exercise induces an antioxidant response in neutrophils through an increase in antioxidant enzymes, and antioxidant low-level supplementation does not block this adaptive cellular response. Supplementation with antioxidants appears to decrease oxidative damage blocking cell-signaling pathways associated with muscle hypertrophy. However, upregulation of endogenous antioxidant enzymes after resistance training is blocked by exogenous antioxidant supplementation. Supplementation with antioxidants does not affect the performance improvement induced by resistance exercise. The effects of antioxidant supplementation on physical performance and redox status may vary depending on baseline levels. Conclusion: The antioxidant response to exercise has two components: At the time of stress and adaptation through genetic modulation processes in front of persistent pro-oxidant situation. Acute administration of antioxidants immediately before or during an exercise session can have beneficial effects, such as a delay in the onset of fatigue and a reduction in the recovery period. Chronic administration of antioxidant supplements may impair exercise adaptations, and is only beneficial in subjects with low basal levels of antioxidants.

Glucose as a Major Antioxidant: When, What for and Why It Fails?

“…Moreover, redox modulating agents that have some health benefits when supplemented often turn out to be rather prooxidant than antioxidant, and lead to the stimulation of endogenous antioxidant defenses and the improvement of glucose metabolism. Therapeutic approaches to applying antioxidant substances in order to reduce oxidative damage and the administration of compounds with the pure purpose to provide reducing equivalents appears weak [125] in contrast to often-high in vitro activities [126], and in comparison to existing endogenous antioxidant mechanisms based on glucose as a source of reducing power for the generation of NADPH and recycling oxidized glutathione and thiols, and can in some cases be deleterious since they may interfere with redox sensors-for example protein thiol groups, and cause dysregulations.…”

Glucose as a Major Antioxidant: When, What for and Why It Fails?

“…It may be argued that the actual flow through PPP is relatively low in the brain (as it has been shown by Gaitonde M. et al [106]) and it increases substantially to approximately 20% of total glucose utilization by neurons only in case of severe oxidative stress induced by hydrogen peroxide [107] or during experimental brain injury [108]. However, a closer look into the methods used in the studies reveals that non-physiologically high concentrations of glucose were used, namely 22.3 mM in the medium and 50mM for perfusion in [107] and 23.9-26.9 mM plasma glucose after infusion in [108]). Flow of glucose into PPP is inhibited in conditions of high NADPH/NADP+ ratio, therefore as soon as the levels of NADPH are restored glucose is redirected into glycolysis or glycogen storage.…”

Glucose as a Major Antioxidant: When, What for and Why It Fails?

“…Moreover, redox modulating agents that have some health benefits when supplemented often turn to be rather prooxidant than antioxidant and lead to stimulation of endogenous antioxidant defense and improvement of glucose metabolism. Besides, therapeutic approaches to apply antioxidant substances in order to reduce oxidative damage and any administration of compounds with pure purpose to provide reducing equivalents appears weak [125] in contrast to often high in vitro activities [126] in comparison to existing endogenous antioxidant mechanisms, based on glucose as a source of reducing power for generation of NADPH and recycling oxidized glutathione and thiols and can in some cases be deleterious since they may interfere with redox sensors, for example protein thiol groups and cause dysregulations.…”