Nicotinamide mononucleotide supplementation enhances aerobic capacity in amateur runners: a randomized, double-blind study

This was a six-week randomized, double-blind, placebo-controlled trial run at Guangzhou Sport University in China. Forty-eight healthy amateur runners from the Guangzhou Pearl River running team — 40 men and 8 women, aged 27 to 50 — were randomly assigned to one of four groups: placebo, 300 mg/day NMN, 600 mg/day NMN, or 1,200 mg/day NMN. Each group contained ten men and two women. All participants trained together during the study, running or cycling five to six times a week for 40 to 60 minutes per session, at an intensity guided by heart-rate zones set from a baseline cardiopulmonary exercise test.

The researchers were interested in whether adding NMN to a standard endurance-training program produced measurable gains in aerobic capacity beyond training alone. They measured a range of cardiopulmonary parameters before and after the six-week program, with a focus on the ventilatory thresholds (VT1 and VT2) — the exercise intensities at which breathing patterns shift as the body moves from primarily aerobic to increasingly anaerobic metabolism. Ventilatory thresholds are widely used markers of endurance capacity in exercise physiology.

The medium-dose (600 mg) and high-dose (1,200 mg) NMN groups showed larger improvements at the first ventilatory threshold than the placebo group, with the effect being larger at the higher dose. Peak VO₂max — the classic "top-end" measure of cardiovascular fitness — did not change significantly in any group, and neither did O₂-pulse, peak power, or body composition. The authors interpret this pattern as an improvement in how efficiently skeletal muscle uses oxygen at submaximal intensities, rather than an increase in the cardiovascular system's peak delivery capacity. No adverse events were reported at any dose over the six-week period.

• VO₂ at first ventilatory threshold (VT1) increased in a dose-dependent pattern. Effect sizes (Cohen's d) versus placebo were 0.61 for the 300 mg group (not significant, p=0.16), 1.45 for the 600 mg group (p<0.01), and 2.62 for the 1,200 mg group (p<0.01).
• Power output at VT1 followed the same dose-dependent pattern. Cohen's d versus placebo was 0.56 at 300 mg (p=0.18), 1.15 at 600 mg (p=0.01), and 2.30 at 1,200 mg (p<0.01).
• Percentage of VO₂max reached at VT1 increased significantly at 600 mg and 1,200 mg (Cohen's d 0.89 and 1.56 respectively, both p<0.05), meaning participants could sustain a higher fraction of their maximal capacity before crossing the first ventilatory threshold.
• Power at the second ventilatory threshold (VT2) improved at all three NMN doses versus placebo (p=0.02 at 300 mg, p=0.07 at 600 mg, p=0.01 at 1,200 mg), though the dose-response pattern was less clean than at VT1.
• VO₂max did not change significantly in any group. Neither did O₂-pulse, ΔVO₂/ΔWR, peak workload, or peak power.
• Body composition did not change. No significant differences in body mass, BMI, fat-free mass, or body-fat percentage between any of the four groups after six weeks.
• No adverse events were reported at any of the three doses over the six-week supplementation period. Exercise ECGs were unremarkable.

Limitations acknowledged by the authors:

• Testing was done on a cycle ergometer, not a treadmill. The training modality was primarily running, but the cardiopulmonary exercise test used a stationary bike. Prior work has shown VO₂max and ventilatory thresholds can differ by roughly 10% between the two, which introduces uncertainty in how the measured gains translate to running performance specifically.
• Blood lactate was not measured during the cardiopulmonary exercise test. Lactate would have provided a second, independent window into the metabolic adaptations underlying the ventilatory-threshold improvements. Its absence limits how confidently the authors' proposed mechanism (improved skeletal-muscle oxygen utilization) can be tied to the measured outcomes.
• Gender was not analyzed separately. Only 8 of 48 participants were women (2 per arm), which is too few to draw conclusions about whether men and women respond similarly.

Additional considerations for interpreting this study:

• Small sample size. With 12 participants per arm, the trial is well-powered to detect large effects on its primary ventilatory-threshold endpoints, but under-powered for many of the secondary endpoints reported as null (VO₂max, O₂-pulse, peak power). "No significant change" in these measures should not be read as evidence of no effect.
• Single site, single training program, recreationally trained participants. Findings may not generalize to sedentary populations, elite athletes, older adults, or people training under different protocols.
• Six-week duration. The trial does not speak to what happens with longer supplementation, whether the ventilatory-threshold gains plateau, or whether they persist after supplementation stops.
• The NMN material was provided by GeneHarbor (Hong Kong) Biotechnologies Ltd. The company also supplied the matching placebo. Whether GeneHarbor had any role in study design, data analysis, or manuscript preparation beyond material supply is not stated in the paper's declarations, which report no competing interests.
• Ventilatory thresholds are surrogate endpoints for endurance performance, not race times or field performance. The trial does not measure whether participants ran faster or longer in actual training or competition.