The Stress response Long term stress response; This response is also regulated by the hypothalamus but in this case it is via the endocrine system. The hypothalamus, in response to stressors, secretes CRH ( corticotropin releasing hormone) which, in turn, stimulates the anterior pituitary to secrete ACTH ( adrenocorticotropic hormone) which then stimulates the adrenal cortex to secrete glucocorticoids ( cortisol). This is all regulated via a negative feedback mechanism. Glucocorticoids have several positive effects that help to cope with stressors including; - Increasing blood [glucose]. This makes glucose more available to provide energy for brain and skeletal muscle function. - Inhibiting protein synthesis so that instead the amino acids can be available for gluconeogenesis so that blood glucose levels can be maintained a high levels of availability - Limiting the inflammatory and the immune response during the stress period so that it can’t interfere with function. Unfortunately while the above changes can be useful they are also the basis for the downsides of long term stress. The negative effects can include; - Lowered level of immune response can lead to increased risks of infection - decreased protein synthesis can lead to reduced growth ( in children) and decreased rates of healing. - elevated blood glucose effects can act to exacerbate diabetes in those with that disease. Similarly if corticosteroid drugs are used for a long term you can have similar effects but also high levels of the drug will inhibit the longterm stress response via the negative feedback mechanism leading to an inadequate stress response Short term stress response; This response is also mediated by the hypothalamus which regulates the autonomic nervous system. The hypothalamus responds to stress by initiating an SNS response. The SNS response tends to be an all or nothing response because SNS nerves arise from the CNS at the thoracic and lumbar spinal nerves. These nerves are then interconnected via the chain ganglia so that if there is any SNS input it goes to all the effectors via all the SNS nerves. SNS effects include; - pupil dilation which can improve peripheral vision and dim light vision - increased heart rate which will increase the BP and potentially increase blood flow to critical tissues - peripheral vasoconstriction which will increase PVR and therefore increase BP and allow increased blood flow to critical tissues such as the skeletal muscles, brain and heart muscles. - increased sweat gland activity which allows for more efficient cooling - increased secretion of epinephrine and norepinephrine from the adrenal medulla. The norepinephrine from the adrenal medulla will have the same effects as the SNS since it is the same chemical as the SNS post-ganglion neuron to the effectors. As a hormone though its effects will last longer than as an SNS neurotransmitter. Epinephrine effects are different in that though epinephrine will stimulate many tissues the same way as norepinephrine it also has some of its own specific effects including; -bronchodilation which will increase airflow in ventilation and make more O2 available -increased metabolic rate for most tissues. This will generally improve function for most tissues to respond to the stress and it will also lead to more heat production -vasodilation for the blood vessels of the skeletal muscles and heart thus improving their blood flow - these are the critical tissues for dealing with stress. - increased blood glucose concentration which improves the supply to critical tissues. All of the above changes help to marshall resources for the critical tissues so that you can cope with stress more effectively but it should also be noted that this comes at a metabolic cost which must eventually be accounted and corrected for. An example of this is that the peripheral vasoconstriction leads to a great decrease in blood flow to the GI which can lead to decrease digestive system function and potentially peptic ulcers.
