Antioxidants, training and the food–supplement distinction
In this investigation
More antioxidant activity is not a performance goal by itself
My food choices include fruit, a red pepper and nuts. Their vitamins and other compounds are interesting, but “antioxidant” is a chemical description, not a score that should be maximized. Exercise-generated oxidants can participate in adaptation as well as cause damage. The research question is whether an intervention improves an outcome that matters, with acceptable tradeoffs, in the relevant training context.
Most of the concern discussed here comes from isolated, high-dose vitamins C and E taken together. Those trials do not establish that I should remove raspberries, oranges, peppers or walnuts. They also cannot isolate the effect of one vitamin from the combination, or establish the effect of every food polyphenol, juice or botanical extract.
A change in cell signaling is not automatically a worse athlete
In 54 young adults, eleven weeks of endurance training with 1,000 mg vitamin C plus 235 mg vitamin E daily blunted some mitochondrial-protein changes relative to placebo. Yet VO₂max improved about 8% in both groups, and improvements in running performance did not significantly differ. This is evidence of altered cellular adaptation without demonstrated overall performance impairment in that experiment. Paulsen et al., 2014 endurance trial.
A separate 32-person resistance-training trial used the same vitamin combination for ten weeks. It altered signaling after exercise and hampered some strength gains, particularly the biceps curl, but did not significantly reduce muscle hypertrophy or the acute protein-synthesis response. The endpoints did not all agree, so “antioxidants stop muscle growth” would misstate the result. Paulsen et al., 2014 strength trial.
A newer sprint study sharpens the same distinction
A 2025 trial in 22 recreationally active young men compared the same C/E doses with placebo during three weeks of four to six 30-second all-out cycling efforts, three times weekly. Vitamins blunted changes in muscle proteins, particularly in type 2 fibers and mitochondrial energy-production pathways. They did not significantly change the improvement in maximal cycling performance. Wyckelsma et al., 2025.
The authors suggest that diminished mitochondrial adaptation could impair submaximal endurance gains. That is a physiological inference, not a measured slower submaximal time trial in this report. The short duration, small groups and different intervals also matter when relating it to my ten-second running efforts. The study supports caution about routine high-dose supplementation, with a narrower conclusion than a headline about ruined sprint training.
The pooled functional evidence is less dramatic
A systematic review of randomized trials searched through June 2019 and required at least four weeks of supervised training. It included nine trials in the aerobic analyses and nine in the resistance-training analyses. It found no significant pooled attenuation of VO₂max, endurance performance, lean mass or strength with C and/or E. The authors still called for larger, adequately powered studies. Clifford et al., 2020.
This synthesis predates the 2025 sprint study and would exclude its three-week duration. It does not prove equivalence or universal safety, but it is important counterevidence to claiming that every athlete will lose measurable gains. Molecular signals and functional outcomes should be presented separately.
There are also positive recovery-marker findings
In a crossover study of 15 elite endurance athletes, six weeks of 1,000 IU natural vitamin E plus 1,000 mg vitamin C daily attenuated the rise in creatine kinase after a 40-minute steady run. This is a positive signal in a different population and protocol. The measured endpoint was a blood marker associated with muscle membrane leakage, not faster race times, fewer injuries or demonstrated tendon healing. Gillam et al., 2022.
A smaller biomarker rise is not automatically better long-term adaptation. Conversely, a concerning signaling change does not automatically negate every potential use during unusually demanding competition or recovery. Those uses need trials with the corresponding functional outcome rather than an assumption that one marker settles both questions.
What this changes for my diet
The current pattern already includes ordinary sources of C and E, and the food record does not establish a reason for routine high-dose C/E supplementation. Keep the fruit, pepper and nuts that I enjoy. Correcting a verified deficiency is a different clinical question from trying to exceed adequate intake for performance.
If a supplement is evaluated, record its actual dose, timing, reason and measurable outcome. “Less oxidation” is not sufficient evidence of better recovery. Evidence about C/E tablets should also not be generalized to every herb, cocoa, tea or berry; each specific intervention has its own dose, food matrix and endpoint. For now, consistently eating the food I like and sleeping well has a clearer practical role than adding a high-dose antioxidant stack.