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Antioxidant supplements and endurance exercise: Current evidence and mechanistic insights.

ABSTRACT: Antioxidant supplements are commonly consumed by endurance athletes to minimize exercise-induced oxidative stress, with the intention of enhancing recovery and improving performance. There are numerous commercially available nutritional supplements that are targeted to athletes and health enthusiasts that allegedly possess antioxidant properties. However, most of these compounds are poorly investigated with respect to their in vivo redox activity and efficacy in humans. Therefore, this review will firstly provide a background to endurance exercise-related redox signalling and the subsequent adaptations in skeletal muscle and vascular function. The review will then discuss commonly available compounds with purported antioxidant effects for use by athletes. N-acetyl cysteine may be of benefit over the days prior to an endurance event; while chronic intake of combined 1000 mg vitamin C + vitamin E is not recommended during periods of heavy training associated with adaptations in skeletal muscle. Melatonin, vitamin E and α-lipoic acid appear effective at decreasing markers of exercise-induced oxidative stress. However, evidence on their effects on endurance performance are either lacking or not supportive. Catechins, anthocyanins, coenzyme Q10 and vitamin C may improve vascular function, however, evidence is either limited to specific sub-populations and/or does not translate to improved performance. Finally, additional research should clarify the potential benefits of curcumin in improving muscle recovery post intensive exercise; and the potential hampering effects of astaxanthin, selenium and vitamin A on skeletal muscle adaptations to endurance training. Overall, we highlight the lack of supportive evidence for most antioxidant compounds to recommend to athletes.

SUBMITTER: Mason SA

PROVIDER: S-EPMC7284926 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Cancer immunotherapy, especially immune checkpoint blockade (ICB), has revolutionized oncology. However, only a limited number of patients benefit from immunotherapy, and some cancers that initially respond to immunotherapy can ultimately relapse and progress. Thus, some studies have investigated combining immunotherapy with other therapies to overcome resistance to monotherapy. Recently, multiple preclinical and clinical studies have shown that tumor vasculature is a determinant of whether immunotherapy will elicit an antitumor response; thus, vascular targeting may be a promising strategy to improve cancer immunotherapy outcomes. A successful antitumor immune response requires an intact "Cancer-Immunity Cycle," including T cell priming and activation, immune cell recruitment, and recognition and killing of cancer cells. Angiogenic inducers, especially vascular endothelial growth factor (VEGF), can interfere with activation, infiltration, and function of T cells, thus breaking the "Cancer-Immunity Cycle." Together with immunostimulation-regulated tumor vessel remodeling, VEGF-mediated immunosuppression provides a solid therapeutic rationale for combining immunotherapy with antiangiogenic agents to treat solid tumors. Following the successes of recent landmark phase III clinical trials, therapies combining immune checkpoint inhibitors (ICIs) with antiangiogenic agents have become first-line treatments for multiple solid tumors, whereas the efficacy of such combinations in other solid tumors remains to be validated in ongoing studies. In this review, we discussed synergies between antiangiogenic agents and cancer immunotherapy based on results from preclinical and translational studies. Then, we discussed recent progress in randomized clinical trials. ICI-containing combinations were the focus of this review because of their recent successes, but combinations containing other immunotherapies were also discussed. Finally, we attempted to define critical challenges in combining ICIs with antiangiogenic agents to promote coordination and stimulate collaboration within the research community.

Project description:BACKGROUND:Hepcidin is an iron regulating hormone, and exercise-induced hepcidin elevation is suggested to increase the risk of iron deficiency among athletes. OBJECTIVE:We compared serum hepcidin responses to resistance exercise and endurance (cycling) exercise. METHODS:Ten males [mean ± standard error: 172 ± 2 cm, body weight: 70 ± 2 kg] performed three trials: a resistance exercise trial (RE), an endurance exercise trial (END), and a rest trial (REST). The RE consisted of 60 min of resistance exercise (3-5 sets × 12 repetitions, 8 exercises) at 65% of one repetition maximum, while 60 min of cycling exercise at 65% of [Formula: see text] was performed in the END. Blood samples were collected before exercise and during a 6-h post-exercise (0h, 1h, 2h, 3h, 6h after exercise). RESULTS:Both RE and END significantly increased blood lactate levels, with significantly higher in the RE (P < 0.001). Serum iron levels were significantly elevated immediately after exercise (P < 0.001), with no significant difference between RE and END. Both the RE and END significantly increased serum growth hormone (GH), cortisol, and myoglobin levels (P < 0.01). However, exercise-induced elevations of GH and cortisol were significantly greater in the RE (trial × time: P < 0.001). Plasma interleukin-6 (IL-6) levels were significantly elevated after exercise (P = 0.003), with no significant difference between the trials. Plasma hepcidin levels were elevated after exercise (P < 0.001), with significantly greater in the RE (463 ± 125%) than in the END (137 ± 27%, P = 0.03). During the REST, serum hepcidin and plasma IL-6 levels did not change significantly. CONCLUSION:Resistance exercise caused a greater exercise-induced elevation in hepcidin than did endurance (cycling) exercise. The present findings indicate that caution will be required to avoid iron deficiency even among athletes in strength (power) types of events who are regularly involved in resistance exercise.

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Antioxidant supplements and endurance exercise: Current evidence and mechanistic insights.

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