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 (medelaldern 22,8 år) genomförde en randomiserad placebokontrollerad studie. 1 200 mg NMN/dag minskade vissa inflammatoriska markörer efter träning. 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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