Developing the catecholamines hypothesis for the acute exercise-cognition interaction in humans: Lessons from animal studies.

The catecholamines hypothesis for the acute exercise-cognition interaction in humans fails to adequately explain the interaction between peripherally circulating catecholamines and brain concentrations; how different exercise intensities×durations affect different cognitive tasks; and how brain catecholamines, glucocorticoids, BDNF and 5-hydroxytryptamine interact. A review of the animal literature was able to clarify many of the issues. Rodent studies showed that facilitation of cognition during short to moderate duration (SMD), moderate exercise could be accounted for by activation of the locus coeruleus via feedback from stretch reflexes, baroreceptors and, post-catecholamines threshold, β-adrenoceptors on the vagus nerve. SMD, moderate exercise facilitates all types of task by stimulation of the reticular system by norepinephrine (NE) but central executive tasks are further facilitated by activation of α2A-adrenoceptors and D1-dopaminergic receptors in the prefrontal cortex, which increases the signal to 'noise' ratio. During long-duration, moderate exercise and heavy exercise, brain concentrations of glucocorticoids and 5-hydroxytryptamine, the latter in moderate exercise only, also increase. This further increases catecholamines release. This results in increased activation of D1-receptors and α1-adrenoceptors, in the prefrontal cortex, which dampens all neural activity, thus inhibiting central executive performance. However, activation of β- and α1-adrenoceptors can positively affect signal detection in the sensory cortices, hence performance of perception/attention and autonomous tasks can be facilitated. Animal studies also show that during long-duration, moderate exercise and heavy exercise, NE activation of β-adrenoceptors releases cAMP, which modulates the signaling and trafficking of the BDNF receptor Trk B, which facilitates long-term potentiation.