Summary
1Regular physical exercise enhances memory functions and neurogenesis in the 2 hippocampus, an effect partially mediated by BDNF (Brain Derived Neurotrophic 3 Factor). Acute exercise promotes the release of endocannabinoids (especially 4 anandamide, AEA), which are small lipophilic molecules that enhance BDNF release 5 and have been shown to improve hippocampal plasticity in rodents. How a single 6 session of exercise affects BDNF and AEA levels, and how these biomarkers 7 influence memory performance remains to date unknown. Here we combined blood 8 biomarkers, behavioral and fMRI measurements to assess the impact of moderate 9 and high intensity acute physical exercise on memory and underlying 10 neurophysiological mechanisms in humans. We hypothesized that moderate intensity 11 exercise would optimize memory consolidation and enhance hippocampal activity via 12 BDNF and/or endocannabinoid signaling. We tested associative memory 13 performance in nineteen healthy participants across three visits: each visit consisted 14 of a learning and a test part performed in fMRI separated by a period of exercise 15 (moderate or high intensity) or rest. A long-term memory retest took place 3 months 16 later. We report a selective increase in memory performance after moderate but not 17 after high intensity exercise or rest at test and at long-term retest. Acute exercise 18 boosted both BDNF and AEA levels: AEA increase after moderate intensity exercise 19 correlated with hippocampal activity during retrieval suggesting that AEA may have 20 an acute effect on synaptic plasticity in human. Whereas exercise-induced BDNF 21 correlated with enhanced hippocampal memory representations measured using a 22 decoding approach after moderate intensity exercise and with long-term, memory 23 effects.