Commentaries on Viewpoint: Reappraisal of the acute, moderate intensity exercise-catecholamines interaction effect on speed of cognition: Role of the vagal/NTS afferent pathway.

TO THE EDITOR: The authors present an interesting analysis of the effect of moderate-intensity exercise-induced catecholamines on cognition speed (4). They summarize that moderate and catecholamine threshold (CT) exercise facilitates the speed of cognition and attribute it to activation of adrenergic neurons in the vagal/ NTS/LC pathway (4). Catecholamine release is also regulated by stress (1), in addition to other factors. Stress, and subsequent stress hormone release, may affect this pathway and the resulting speed of cognition. Even moderate-intensity exercise is a stressor, which requires adaptive responses of many body systems (3), including the vagal/NTS afferent pathway. Corticotropin-releasing hormone (CRH) neurons release CRH to the pituitary gland for subsequent release of ACTH, but they also possess axons that terminate in the LC/NE-sympathetic system neurons in the NTS (3). Physiological stressors have been shown to activate neurons in the NTS and induce ACTH release (5). Cortisol released by the adrenal cortex in response to ACTH can result in negative feedback effects on ACTH secretion, the hypothalamic CRH neurons, and the LC/ NE-sympathetic system (5). In this way, cortisol may cause disruptions in dopamine neurochemistry or alter regulation of dopamine release. Alterations in dopamine neurotransmission (excessive or insufficient) by cortisol can affect cognitive function (2), and individual responses to the stress of exercise may explain the lack of mean effect size differences for moderate vs. CT exercise. Conversely, moderate-intensity exercise-induced cortisol release may parallel the CT and positively affect dopaminecontaining neurons excitability and speed of cognition.