Tart cherry juice

The active fraction is anthocyanin: cyanidin-3-glucoside and its rutinosides, a class of polyphenol with genuinely impressive antioxidant capacity in a test tube. In a human, less so, because anthocyanin bioavailability is low (often well under one percent of the ingested dose appears intact in plasma) and the compounds that circulate are largely gut-microbial and hepatic metabolites such as protocatechuic acid.

So the mechanism is probably not brute-force radical scavenging. The better hypothesis is signal modulation: attenuation of NF-kB dependent transcription, mild COX inhibition, and a downstream reduction in inflammatory cytokine output. That reframing matters, because it moves the drink from mopping up damage to turning down a signal.

Which raises the awkward question. Exercise-generated reactive oxygen species are signals, not just damage. They participate in PGC-1alpha driven mitochondrial biogenesis, in Nrf2 mediated antioxidant upregulation, and in hypertrophic signalling. Any intervention that reliably blunts the post-exercise inflammatory and oxidative response has to answer for whether it also blunts the adaptation. High-dose vitamin C and E supplementation has been shown to do exactly that.

The melatonin claim is smaller than it sounds. Tart cherries contain melatonin on the order of a few nanograms per gram, so a concentrate serving delivers vastly less than a 1 mg tablet, itself a low dose. If the sleep effect is real, the more plausible routes are tryptophan availability, polyphenol effects on tryptophan catabolism, or the fact that drinking something deliberately at 9 pm and expecting to sleep is itself a behavioural intervention. Honest answer: unresolved.

Howatson et al. 2010 is the study everyone cites: n = 20 marathon runners, eight days of concentrate, faster recovery of isometric strength and lower IL-6 and CRP. It is a well-liked study. It is also twenty people, with the cherry supply provided by the industry.

The rest of the literature runs the same direction and at the same scale. Bell et al. 2014 in cyclists, various small trials in team sport, and Vitale's 2017 review pulling them together: consistent direction, samples of ten to twenty, wildly heterogeneous dosing (30 mL of concentrate twice daily versus 240 to 480 mL of juice), and outcomes that are mostly biomarkers and soreness scales rather than competitive performance.

Sleep: Howatson et al. 2012, n = 20 healthy adults, actigraphy showing a modest increase in total sleep time and sleep efficiency. Later small trials in insomnia point the same way. The direction repeats, which is worth something. The samples remain tiny, which is worth remembering.

No tart-cherry-specific trial has yet run long enough to test whether daily use through a training block attenuates adaptation. The broader antioxidant literature says the risk is real; the cherry literature says nothing at all about it. That is an open question, not a resolved one, and it belongs in the verdict rather than in a footnote.

Score-wise this lands as underpowered rather than overstated, because the mechanism is defensible and the effects observed are plausible. There simply is not enough data of enough quality to grade it.