Fig. 1
Stress hormones released during high intense exercise. Stress responses to intense exercise are mediated by largely overlapping circuits in the limbic forebrain, the hypothalamus and the brainstem, so that the respective contributions on the neuroendocrine and autonomic systems are tuned in accordance with stressor and intensity [6]. When brainstem receives inputs that signal major homeostatic perturbations, such as respiratory distress, energy imbalance, desydration, visceral or somatic pain, inflammation or exteroceptive factors respond through a coordinated modulation of the HPA axis and the sympathetic and parasympathetic branch of the autonomic nervous system (ANS). By contrast, forebrain limbic regions have no direct connections with the HPA axis or the ANS and thus require intervening synapses before they can access autonomic or neuroendocrine neurons (top-down regulation) [6]. Briefly, exercise-induced stress results in activation of preganglionic sympathetic neurons in the intermediolateral cell column of the thoracolumbar spinal cord (shown in purple and clear grey). This sympathetic activation represents the classic 'fight or flight' response and it generally increases circulating levels of catecholamines. Parasympathetic tone can also be modulated during stress (shown in dark grey color). Parasympathetic actions are generally opposite to those of the sympathetic system and alter the vagal tone to the heart and lungs. Within the HPA axis, stress activates hypophysiotropic neurons in the paraventricular nucleus of the hypothalamus (PVN) that secrete releasing hormones, such as corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP), into the portal circulation of the median eminence. These releasing hormones act on the anterior pituitary to promote the secretion of adrenocorticotropic hormone (ACTH), which in turn acts on the inner adrenal cortex to initiate the synthesis and release of glucocorticoid hormones. Moreover, the adrenal cortex is directly innervated by the sympathetic nervous system, which can also regulate corticosteroid release. Additionally, gastrointestinal tract responds to stress in an endocrine manner by releasing hormones such as Gamma-amino butyric acid (GABA), neuropeptide Y and dopamine that have been purported to be involved in the gastrointestinal disturbances, anxiety, depression, reduced food intake and less stress coping. Microorganisms that colonize the digestive tract can be involved in the regulation of the HPA axis through the regulation or production of short chain fatty acids and neurotransmitters such as GABA, dopamine and serotonin, as well as cytokines. The neuroendocrine stress response to exercise is determined not only by the emotional stress but the volume of physical exposure, where volume consists of the intensity and/or duration of the exercise session. As exercise intensity is increased, there are approximately proportional increases in circulating concentrations of ACTH and cortisol. There is a critical threshold of exercise intensity that must be reached (~50–60% of maximal oxygen uptake [VO2max]) before circulating levels increase in response to exercise [170, 171]