UVM Theses and Dissertations
Format:
Print
Author:
Hare, Brendan D.
Dept./Program:
Psychology
Year:
2013
Degree:
M.A.
Abstract:
Affective disorders, including anxiety and depression, affect millions of Americans each year. Exercise has been demonstrated to reduce symptoms of depression and anxiety in humans. Importantly, exercise has similar effects in animal models, as evidenced by reductions in anxiety like responding across a number of measures including the response to startle eliciting noise-bursts. There is accumulating, though often mixed, evidence that exercise alters the function of the hypothalamic adrenal pituitary (HPA) axis resulting in enhanced regulation of the stress response. As dysfunction within the HPA-axis, and subsequently response to stressors, is a hallmark of many affective disorders, examination of the HPA-axis during the acquisition of exercise, and the stress response following exercise acquisition, may provide insight into the mechanisms underlying enhanced regulation of the HPA-axis in exercising animals.
The present set of experiments aims to observe changes in HPA-axis function during the acquisition of exercise, characterize the time-course of the restraint stress response in exercising C57BL/6J mice, and directly test the sensitivity of the adrenal cortex and HPA-axis negative feedback mechanisms in exercising animals. It was hypothesized that changes in HPA-axis function occur in response to exercise rendering the HPA-axis both more sensitive to high intensity stress induced inputs, and more sensitive to corticosterone induced negative feedback. Contrary to our hypothesis, there was no change in the diurnal rhythm of HPA-axis mediated corticosterone release during the acquisition or maintenance of exercise. Exercise was observed to alter the time-course of the HPA-axis response to restraint stress resulting in a shorter time to peak corticosterone and a more rapid decay of corticosterone release following stressor termination.
These changes were concurrent with an exercise induced decrease in startle amplitude, as well as increased adrenal size in exercising animals. Exercising animals demonstrated an augmented response to low dose (5ug/kg) adrenocorticotropic hormone suggesting increased adrenal sensitivity induced by exercise. However, exercising and sedentary mice demonstrated equivalent suppression of HPA-axis activity in an intra-peritoneal as well as intracerebroventricular dexamethasone suppression tests designed to test peripheral and central glucocorticoid agonist induced negative feedback respectively. Thus, it appears that exercise is not associated with a change in diurnal rhythm of corticosterone release, but is associated with a more rapid response following stress. The increased time to peak and faster decay of corticosterone is not due to increased corticosterone-mediated feedback centrally or peripherally. However, it may be mediated in part by increased adrenal sensitivity.
The present set of experiments aims to observe changes in HPA-axis function during the acquisition of exercise, characterize the time-course of the restraint stress response in exercising C57BL/6J mice, and directly test the sensitivity of the adrenal cortex and HPA-axis negative feedback mechanisms in exercising animals. It was hypothesized that changes in HPA-axis function occur in response to exercise rendering the HPA-axis both more sensitive to high intensity stress induced inputs, and more sensitive to corticosterone induced negative feedback. Contrary to our hypothesis, there was no change in the diurnal rhythm of HPA-axis mediated corticosterone release during the acquisition or maintenance of exercise. Exercise was observed to alter the time-course of the HPA-axis response to restraint stress resulting in a shorter time to peak corticosterone and a more rapid decay of corticosterone release following stressor termination.
These changes were concurrent with an exercise induced decrease in startle amplitude, as well as increased adrenal size in exercising animals. Exercising animals demonstrated an augmented response to low dose (5ug/kg) adrenocorticotropic hormone suggesting increased adrenal sensitivity induced by exercise. However, exercising and sedentary mice demonstrated equivalent suppression of HPA-axis activity in an intra-peritoneal as well as intracerebroventricular dexamethasone suppression tests designed to test peripheral and central glucocorticoid agonist induced negative feedback respectively. Thus, it appears that exercise is not associated with a change in diurnal rhythm of corticosterone release, but is associated with a more rapid response following stress. The increased time to peak and faster decay of corticosterone is not due to increased corticosterone-mediated feedback centrally or peripherally. However, it may be mediated in part by increased adrenal sensitivity.