Acute physical exercise improves memory consolidation in humans via BDNF and endocannabinoid signaling
AbstractRegular physical exercise enhances memory functions and neurogenesis in the hippocampus, an effect partially mediated by BDNF (Brain Derived Neurotrophic Factor). Acute exercise promotes the release of endocannabinoids (especially anandamide, AEA), which enhance BDNF release and improve hippocampal plasticity in rodents. How acute exercise affects BDNF and AEA levels and influences memory performance in humans remains to date unknown. Here we combined blood biomarkers, behavioral and fMRI measurements to assess the impact of acute physical exercise on associative memory and underlying neurophysiological mechanisms. For each participant, memory was tested after three conditions: rest, moderate or high exercise intensity. A long-term memory retest took place 3 months later. At both test and retest, memory performance increased after moderate but not high intensity exercise or rest. We also show that memory benefited from exercise-related increases in both AEA and BNDF levels: AEA boosted hippocampal activity during memory recall, while BDNF enhanced hippocampal memory representations and long-term performance.