Studie
Anti-inflammatory effects of nicotinamide mononucleotide (NMN) in human skeletal muscle after BFR-exercise.
In 11 young men, 1,200 mg/day NMN reduced some exercise-induced inflammatory signals but blocked a 171% rise in muscle mitochondrial content.
Elva otränade män, medelålder 22,8 år, genomförde en randomiserad placebokontrollerad balanserad överkorsningsstudie. De tog placebo eller NMN i 1 200 mg/dag i 7 dagar, åtskilda av en 3 veckor lång washoutperiod, och genomförde sedan styrketräning med begränsat blodflöde. Flera muskelbiopsier togs före och efter träningen. Exercise caused muscle necrosis immediately after the session, resolving within 24 hours in both conditions. NMN suppressed exercise-related increases in TNF-α and IL-10 messenger RNA, but it delayed the rise in p21 messenger RNA and moderately delayed clearance of infiltrating cells from necrotic regions. The more concerning result was mitochondrial content: exercise increased it by 171% after 24 hours of recovery, whereas NMN abolished that increase. Microscopy suggested that infiltrating phagocytes carried more mitochondria than myofibre cytoplasm and formed a gradient towards damaged muscle. This is an acute mechanistic experiment, not a test of strength, health, disease risk, or aging. Lower inflammatory signalling was accompanied by signals consistent with delayed repair and lost mitochondrial adaptation, so it does not provide a straightforward pro-longevity result.
NMN inhibited inflammatory signalling in exercised human skeletal muscle but may also suppress mitochondrial replenishment during repair.
Only 11 young, untrained men were studied for 7 days per condition. The endpoints were biopsy-based molecular measures after deliberately damaging exercise; there were no long-term functional or clinical outcomes.
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