Beyond the catecholamines hypothesis for an acute exercise–cognition interaction: A neurochemical perspective

Research shows that moderate duration, moderate intensity, acute exercise generates increases in plasma catecholamines concentrations, which stimulate the vagal/nucleus tractus solitarii pathway. This induces the synthesis and release of catecholamines in the brain. Moderate increases in catecholamines concentrations facilitate performance of most cognitive tasks. Long duration, moderate intensity, and heavy exercise generate excessive concentrations of catecholamines, as well as resulting in increased concentrations of cortisol, which interact with catecholamines to inhibit working memory. However, heavy exercise has a beneficial effect on long-term memory due to activation of β-adrenoreceptors in the hippocampus and increased exercise-induced brain-derived neurotrophic factor (BDNF) levels, which aid neurogenesis and neuroplasticity. Heavy exercise also facilitates performance of autonomous tasks, probably due to activation of α1- and β-adrenoreceptors. With attention/perception tasks results are somewhat equivocal, although theoretically activation of α1- and β-adrenoreceptors should also aid the performance of these tasks.