Evidence map›Paper›PMID 41705654›Full record

Trial reportJournal of the International Society of Sports Nutrition2026

Anti-inflammatory effects of nicotinamide mononucleotide (NMN) in human skeletal muscle after BFR-exercise.

Dai-Lin Yang, Kuo-Ching Chao, Hui-Tai Yang, Kuei-Hung Chen, Luthfia Dewi, Giancarlo Condello, Mengxin Ye, Andrew Nicholls, Yu-Chieh Liao, Chih-Yang Huang and 1 more

Abstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Journal of the International Society of Sports Nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Dai-Lin YangLaboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Kuo-Ching ChaoDepartment of Internal Medicine, China Medical University Hospital, Taipei, Taiwan.
Hui-Tai YangLaboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Kuei-Hung ChenLaboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Luthfia DewiDepartment of Nutrition, Universitas Muhammadiyah Semarang, Semarang, Indonesia.
Giancarlo CondelloDepartment of Medicine and Surgery, University of Parma, Parma, Italy.
Mengxin YeCollege of Physical Education and Health Science, Zhejiang Normal University, Jinhua, China.
Andrew NichollsLaboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Yu-Chieh LiaoLaboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Chih-Yang HuangDepartment of Biotechnology, Asia University, Taichung, Taiwan.
Chia-Hua KuoDepartment of Health and Physical Education, Laboratory of Exercise Biochemistry, The Education University of Hong Kong, New Territories, Hong Kong SAR.ORCID 0000-0002-1731-4984

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundβ-Nicotinamide mononucleotide (NMN) inhibits acute inflammation in injured animal tissues.

aimWe examined whether NMN supplementation attenuates inflammation induced by blood flow restriction-resistance exercise (BFR-exercise) in human skeletal muscle.

methodsEleven untrained men (22.8 ± 1.5 y) completed a randomized, placebo-controlled, counterbalanced crossover trial, receiving either Placebo or NMN (1200 mg/d) for 7 d, with a 3-week washout between conditions. Multiple muscle biopsies were obtained before and after BFR-exercise.

resultsBFR-exercise-induced significant muscle necrosis at 0 h, which resolved within 24 h in both conditions. NMN supplementation suppressed exercise-induced increases in TNF-α and IL-10 mRNA but delayed the rise in p21 mRNA, suggesting attenuated inflammatory signaling and delayed myogenic differentiation. The resolution of infiltrating cells from necrotic regions was moderately delayed by NMN. BFR-exercise increased the mitochondrial content in exercised muscle by 171% after 24 h of recovery. However, this adaptation was abolished with NMN. Immunofluorescence staining with TOM20 and myeloperoxidase (MPO) revealed that infiltrating phagocytes carried substantially more mitochondria than myofiber cytoplasm, forming a diffusion gradient toward damaged regions of myofibers. This concentration difference between phagocytes and myofibers was further confirmed using COX4 immunostaining in biopsied muscle from an additional participant.

conclusionsNMN supplementation, while inhibiting inflammatory signaling in exercised human skeletal muscle, may also suppress mitochondrial replenishment from phagocytes to repairing myofibers.

Indexed as

Anti-Inflammatory AgentsInflammationMuscle, SkeletalNicotinamide MononucleotideResistance TrainingAdultCross-Over StudiesDietary SupplementsHumansInterleukin-10MaleNecrosisPost-Exercise RecoveryPost-Exercise Recovery TechniquesTumor Necrosis Factor-alphaYoung AdultAnti-Inflammatory AgentsInterleukin-10Nicotinamide MononucleotideTumor Necrosis Factor-alphainflammationIschemic reperfusionmitochondrial transferNETosisp16INK4Ap21

Identifiers

PMID41705654
PMCPMC12918316

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.