Exercise, cognition, arousal, catecholamines, central executive, BDNF, age
Abstract
Early research into the effects of acute exercise on cognition were atheoretical and of poor design. In the 1990s and 2000s, cognitive-energetical theories and the catecholamines hypothesis have been developed as rationales for effects of acute exercise on cognition. It was claimed that acute exercise was a stressor and as such would affect cognition in an inverted-U manner, the same as other stressors. However, the inverted-U effect was rarely supported. Later research has somewhat consistently shown that moderate intensity, short to moderate duration exercise induces improved cognitive performance. However, the effects of heavy exercise and long-duration, moderate intensity exercise treatments remain somewhat equivocal, except for autonomous tasks which are facilitated. Recent research suggests that undertaking exercise, while simultaneously carrying out a motor task, is more beneficial than simply exercising before undertaking the cognitive tasks. Research examining the effect of chronic exercise on cognition was also originally atheoretical and poorly designed. Improved research designs have led to some consistency in findings and the evidence for chronic exercise having a facilitative effect on cognition is fairly consistent but only a small to moderate improvement has been demonstrated. Human studies provide a prima facie case for brain derived neurotrophic factor being a mediator in the chronic exercise-cognition interaction and evidence from animal studies strongly supports this. Recent work provides support for claims that exercise, while simultaneously undertaking a motor task, is more beneficial than simply exercising.
