TO THE EDITOR: Leischik et al. (see Ref. 1) provide an overview of the problems facing those researching the effects of exercise, both acute and chronic, on cognitive function. I agree with their comments, but the viewpoint (2) was only concerned with a specific anomaly in the ability of the catecholamine hypothesis to explain the effects of acute exercise on cognitive performance. This is only part of the process by which acute exercise affects immediate cognitive functioning and is not meant to be a comprehensive explanation of even the effects of acute exercise, let alone the comprehensive exercise-cognition interaction.Jones (see Ref. 1) points to the fact that even moderate intensity exercise is a stressor and, as such, may initiate activation of the hypothalamic-pituitary-adrenal (HPA) axis hormones, resulting in release of norepinephrine by the locus ceruleus. This is in line with the argument put forward by my colleagues and me (3) that perceptions of stress lead to feedforward from the higher centers of the brain to the hypothalamus, which projects to the locus ceruleus and induces the release of norepinephrine. However, this will only occur if the individual perceives the exercise as being stressful. Judging by the fact that moderate intensity exercise is generally thought to need to be of Ͼ45 min duration before plasma cortisol concentrations show an increase, one might claim that subcatecholamines threshold exercise is not perceived as being stressful enough to initiate HPA axis activation. However, this does not exclude the possibility of release of corticotrophin releasing hormone in the brain and this can initiate the synthesis and release of norepinephrine from the locus ceruleus (see Ref. 3 for a discussion). Although perceptions of stress vary from individual to individual, in all exercisers heart rate, tidal volume, and blood pressure begin to increase immediately after that exercise begins. Afferent feedback will activate mechanoreceptors, or more accurately stretch receptors, and baroreceptors on the vagus nerve and, via the nucleus tractus solitarii, stimulate the release of norepinephrine by the locus ceruleus.Budde et al. (see Ref. 1) question how increased concentrations of norepinephrine affect cognition.