Red-light panels and ketone drinks were both tested this week. Both came back null.

Two of the more heavily marketed recovery products of the past few years were tested in humans in the same issue of the same journal on 27 August. Neither did what it is sold as doing. The studies are small, and that limitation runs in both directions — but the mechanisms being tested were specific enough that a null result carries real information.

Red light: the mechanism, measured directly

Photobiomodulation — low-level laser therapy, the technology behind consumer red-light panels and masks — is marketed on a mechanistic story: light at particular wavelengths is absorbed by mitochondria, increasing their activity and, downstream, improving skin and muscle function. The authors of the first study note plainly that evidence for these proposed properties in living humans has been lacking [s1].

So they measured it. Twelve healthy adults (six men, six women; age 25±6 years; BMI 23.3±2.2 kg/m²) received photobiomodulation on one randomly assigned leg while the other leg received a sham treatment with no light emitted. Each leg went through three cycles of 5 minutes 16 seconds, delivering 5.6 kJ of light energy per cycle on the treated side. Afterwards, skin and muscle samples were taken from both legs and mitochondrial respiration was measured in permeabilised muscle fibres and minced skin tissue [s1].

The treatment unambiguously did something: skin temperature rose only in the treated leg, by 8.0±1.4 °C (P<0.001) [s1]. The energy reached the tissue.

What it did not do is change the thing the marketing claim rests on. Maximal complex I+II-linked respiration was 2.7±0.8 versus 2.6±0.7 pmol/sec/mg wet weight in skin (P=0.66) and 474±114 versus 467±81 pmol/sec/mg dry weight in muscle (P=0.71) [s1]. Mitochondrial ADP sensitivity in muscle was likewise unchanged (apparent ADP half-time 1310±180 versus 1229±240 µM ADP; P=0.14) [s1]. Of 91 metabolic genes assessed, expression differed between legs for three [s1].

The within-participant design is the strength here: each person served as their own control, which removes between-person variation that would otherwise swamp a sample of twelve. The conclusion the authors draw is narrow and matches what they measured — a single session of photobiomodulation does not increase mitochondrial respiration in skin or underlying muscle, and does not modulate muscle gene expression ex vivo [s1]. A single session. This says nothing about repeated exposure over weeks, and nothing about the wound-healing or pain applications the technique is also used for.

Ketone esters: eight days, no benefit

The second trial addressed a different claim. Ketone monoester supplementation has been proposed to enhance post-exercise recovery, preserve cognitive function, and increase both sleep quantity and quality — the case for it in multi-day endurance racing rather than in a single effort [s2].

Eighteen well-trained cyclists completed a simulated eight-day stage race in a double-blind, placebo-controlled parallel trial. Immediately after each stage and again 30 minutes before sleep, participants received either 25 g of ketone ester (n=8) or a taste-matched placebo (n=10) [s2]. Measurements spanned body composition, resting metabolic rate, subjective stress-recovery state, mechanical efficiency, a 30-minute time trial, vastus lateralis biopsies, plus daily hydration, fatigue, heart rate, power output, stage time, nutritional intake and sleep [s2].

The protocol worked as a stressor. Across both groups the race produced acute fatigue: peak heart rate fell by about 11 bpm (P for time = 0.002) and time trial performance dropped about 3% (P for time = 0.026) [s2].

The supplement did not blunt it. Neither ketone ester nor the race itself affected sleep, dietary intake or skeletal muscle markers (p>0.05) [s2]. The authors report no clear benefit on post-exercise recovery, sleep, cognitive function or endurance performance [s2].

One result points the other way. In the ketone group but not the control group, the fatigue coincided with impaired mechanical efficiency at 200 W and a 120% increase in fat oxidation rate (P for interaction = 0.028) [s2]. Higher fat oxidation is often sold as desirable; impaired mechanical efficiency at a fixed power output is not, because it means more oxygen consumed for the same work.

What the two nulls are worth

Eight participants per arm in the ketone trial and twelve in the light study are small numbers, and a small trial that finds nothing has not proven nothing exists. What it has done is bound the size of any effect: whatever photobiomodulation does to mitochondrial respiration after one session, and whatever ketone esters do across eight days of racing, it was not large enough to surface in designs built specifically to detect it.

Both papers are also unusually clean tests, because both went after a stated mechanism rather than a downstream outcome. It is easy to find a small performance difference somewhere in a large panel of measurements. It is harder to explain a product that raises tissue temperature by 8 °C without touching the respiration it is sold for [s1], or one that shifts substrate use measurably while leaving performance, sleep and recovery unmoved [s2].

Neither result is a safety finding, and neither is advice. What to watch is whether multi-session photobiomodulation trials with the same direct measurement follow — the single-session design is the main thing standing between this result and a general conclusion [s1].

Sources

• [s1] Photobiomodulation Does Not Increase Mitochondrial Respiration in Skeletal Muscle or Skin Tissue in Humans. Medicine & Science in Sports & Exercise, 27 August 2026. https://doi.org/10.1249/MSS.0000000000004120
• [s2] Ketone Ester Intake Did Not Improve Performance, Neither Cognitive Function or Sleep, During an 8-Day Simulated Cycling Race. Medicine & Science in Sports & Exercise, 27 August 2026. https://doi.org/10.1249/MSS.0000000000004119