Emerging research demonstrates that exercise is favorably associated with several cognitive outcomes, including episodic memory function. The majority of the mechanistic work describing the underlying mechanisms of this effect has focused on chronic exercise engagement. Such mechanisms include, e.g., chronic exercise-induced neurogenesis, gliogenesis, angiogenesis, cerebral circulation, and growth factor production. Less research has examined the mechanisms through which acute (vs. chronic) exercise subserves episodic memory function. The purpose of this review is to discuss these potential underlying mechanisms, which include, e.g., acute exercise-induced (via several pathways, such as vagus nerve and muscle spindle stimulation) alterations in neurotransmitters, synaptic tagging/capturing, associativity, and psychological attention.
No previous studies have evaluated the potential combined effects of acute exercise and acute hypoxia exposure on memory function, which was the purpose of this study. Twenty-five participants (Mage = 21.2 years) completed two laboratory visits in a counterbalanced order, involving 1) acute exercise (a 20-min bout of moderate-intensity exercise) and then 30 min of exposure to hypoxia (FIO2 = 0.12), and 2) exposure to hypoxia alone (FIO2 = 0.12) for 30 min. Following this, participants completed a cued-recall and memory interference task (AB/AC paradigm), assessing cued-recall memory (recall 1 and recall 2) and memory interference (proactive and retroactive interference). For cued-recall memory, we observed a significant main effect for condition, with Exercise + Hypoxia condition having significantly greater cued-recall performance than Hypoxia alone. Memory interference did not differ as a function of the experimental condition. This experiment demonstrates that engaging in an acute bout of exercise prior to acute hypoxia exposure had an additive effect in enhancing cued-recall memory performance.