Anti-inflammatory effects of nicotinamide mononucleotide (NMN) in human skeletal muscle after BFR-exercise.
Dai-Lin Yang, Kuo-Ching Chao, Hui-Tai Yang et al.
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In 30 seconds
This randomized, placebo-controlled, counterbalanced crossover trial examined whether nicotinamide mononucleotide (NMN) alters inflammation after blood flow restriction-resistance exercise in 11 untrained men. Participants received NMN (1200 mg/d) or placebo for 7 d, with a 3-week washout between conditions. Exercise-induced muscle necrosis resolved within 24 h in both conditions. NMN suppressed increases in TNF-α and IL-10 mRNA, but delayed p21 mRNA elevation and the resolution of infiltrating cells. Exercise increased muscle mitochondrial content by 171% after 24 h; this adaptation was abolished with NMN.
Key findings
- NMN suppressed exercise-induced increases in TNF-α and IL-10 mRNA, while delaying the rise in p21 mRNA.
- Resolution of infiltrating cells from necrotic muscle regions was moderately delayed with NMN.
- Exercise increased mitochondrial content in muscle by 171% after 24 h; NMN abolished this increase.
Why it matters
The findings suggest that dampening inflammatory signaling after exercise may coincide with slower cellular repair processes and loss of a short-term mitochondrial adaptation. Inflammation and immune-cell activity may contribute to muscle recovery, not simply represent processes to suppress. The proposed transfer of mitochondria from phagocytes to repairing myofibers is an intriguing interpretation, but the study does not establish its clinical significance.
What to keep in mind
The trial included only 11 untrained men, and the reported outcomes concern short-term responses to one exercise model.