REF-1773 · Aussieker et al., 2026 · Medicine and Science in Sports and Exercise · Paper · PubMed

After one session of photobiomodulation on one leg, with a sham emitting no light on the other, mitochondrial respiration did not differ significantly between legs in skin (2.7 ± 0.8 vs 2.6 ± 0.7 pmol/s/mg wet weight, P = 0.66) or in the muscle beneath (474 ± 114 vs 467 ± 81 pmol/s/mg dry weight, P = 0.71) in 12 healthy adults, though it warmed the skin by 8.0 °C; a resting mechanistic study of the proposed mechanism, no exercise or performance outcome

Main caveat: 12 participants and a single session at rest; no training period, no exercise, no performance outcome.
limited, mixed evidenceMeasured on non-athletes to trained athletesRead from the abstract only

Aussieker and colleagues tested the claim that photobiomodulation directly raises mitochondrial activity in skin and muscle in living humans. Twelve healthy adults (6 men, 6 women) received PBM on one randomly assigned leg and a sham treatment with no light emitted on the other. Each leg got three cycles of 5 min 16 s, with 5.6 kJ of light energy per cycle on the PBM leg.

Skin temperature was measured before and after, and skin and muscle samples were then taken from both legs. Mitochondrial respiration was measured in permeabilised muscle fibres and minced skin with an Oroboros Oxygraph-O2k, and 91 metabolic genes were assessed in muscle. Skin temperature rose only on the PBM leg, by 8.0 °C.

Maximal complex I+II-linked respiration did not differ between legs in skin or in muscle, muscle mitochondrial ADP sensitivity did not differ, and only 3 of 91 genes differed in expression. The authors conclude that a single PBM session does not increase mitochondrial respiration in skin or underlying muscle, and does not modulate muscle gene expression measured ex vivo.

Participants

12 healthy adults, 6 M / 6 F; age 25 ± 6 years; BMI 23.3 ± 2.2 kg/m².
Not in the abstract: training status, physical activity level.

Protocol

Design: within-participant; one leg randomised to PBM, the other to sham (CON, no light emitted).
What was applied: three cycles of PBM, 5 min 16 s each, 5.6 kJ of light energy per cycle, on one leg at rest; the sham leg got the same cycles with no light. The device type (the abstract uses "low-level laser therapy" as another name for PBM), wavelengths, irradiance, area treated and the exact site on the leg are not in the abstract. No exercise was involved.
Measures: skin temperature before and after treatment; after treatment, skin and muscle samples from both legs (time from treatment to sampling not in the abstract); maximal complex I+II-linked respiration in permeabilised muscle fibres and minced skin (Oroboros Oxygraph-O2k); muscle mitochondrial ADP sensitivity; expression of 91 metabolic genes on custom microfluidic cards.

Key Results

MeasurePBM legSham legP
Skin temperature change+8.0 ± 1.4 °Crose only in the PBM leg< 0.001
Skin maximal complex I+II respiration (pmol/s/mg wet weight)2.7 ± 0.82.6 ± 0.70.66
Muscle maximal complex I+II respiration (pmol/s/mg dry weight)474 ± 114467 ± 810.71
Muscle ADP sensitivity, apparent ADP half-time (µM ADP)1310 ± 1801229 ± 2400.14
Muscle gene expression3 of 91 genes differed between legs
Values are mean ± SD as given; no confidence intervals for the differences are in the abstract. Which 3 genes differed, and in which direction, is not stated.

Practical Application

In living humans, after one session of photobiomodulation on the leg, mitochondrial respiration in the skin and in the muscle under it did not differ significantly from the sham leg (12 healthy adults, P = 0.66 and 0.71); the mechanism proposed for red-light benefits was not seen after a single session. No exercise or performance outcome was measured.
To "does red light boost my mitochondria?": say one sham-controlled human study measured it directly in muscle and skin samples and found no significant difference after one session; repeated sessions over weeks were not tested, so a cumulative effect is not ruled out by this study.
The light warmed the skin by 8.0 °C, so the tissue did receive energy. Inference, not tested here: participants could likely tell which leg was treated, though respiration in tissue samples is hard for expectation to move; and any benefit felt after a session may come from warmth rather than from mitochondria.
Mitochondrial respiration measured ex vivo is a marker (PHYS-44); adaptation comes from repeated training signals plus recovery (PHYS-18).

Limitations

12 participants and a single session at rest; no training period, no exercise, no performance outcome.
One dose and one (unreported in the abstract) wavelength set; other doses or wavelengths are not tested.
The sham emitted no light and the treated leg warmed by 8.0 °C, so participants were probably not blinded to the leg; the tissue outcomes limit how much this matters.
Means ± SD with P values; no intervals for the leg differences and no stated smallest effect the study could detect, so a small increase cannot be excluded from what the abstract reports.
Training status, device details and the time from treatment to sampling are not in the abstract; funding and conflicts of interest are not in the abstract.
Written from the abstract and the PubMed record; full text not read.
How this entry was checked and changed
Why this level

a within-participant comparison of 12 (B, as for a crossover under 15) one step down because it is a mechanistic study whose outcomes are tissue markers with no performance outcome (rule 3)