Date of Award


Document Type


Degree Name

Doctor of Philosophy (PhD)


Biomedical and Veterinary Medical Sciences - Comparative Biomedical Sciences

First Advisor

David W. Horohov


The physiologic demands of exercise constitute a form of stress which is accompanied by modulation of immune responses. However, numerous studies in many different model systems have failed to clearly define the effects of exercise on immunity. Furthermore, the role of the neuroendocrine system in exercise-induced immunomodulation has been largely unexplored. To address these issues, we evaluated the effect of acute exercise stress on 3 indices of immune function in horses, before and after completion of a 12 week treadmill-based physical conditioning program. In addition, we determined the effects of corticosteroids, catecholamines, beta endorphin, and adrenocorticotropic hormone on these same immune parameters. In this work, we found that an acute severe exercise challenge of unconditioned horses induced immediate and significant post-exercise decreases in pokeweed mitogen (PWM) and equine influenza virus type 2 lymphoproliferative responses. Lymphokine activated killer (LAK) cell activity was also significantly elevated. After training, basal immune responses of resting horses were unchanged compared to those of untrained animals. Further, acute exercise stress no longer produced significant elevations of equine LAK activity, and depressions in PWM responses were delayed and enhanced. Of the neuroendocrine compounds tested for their effects on immune responses, most were capable, at one or more of their tested concentrations, of causing changes in PWM, influenza, or LAK responses similar to those observed after exercise. Physical conditioning attenuated their effects. Surprisingly, in vitro corticosteroids augmented influenza, LAK, and PWM responses depending upon concentration. However, intravenous cortisol injection did not mimic immediate post-exercise changes in the hemogram or immune responses. We conclude that acute exercise stress of horses may be temporarily immunosuppressive, but the observed decrease in lymphoproliferative responses is partially offset by increases in LAK cell-mediated cytotoxicity. While providing no enhancement of basal immune responses, physical conditioning may serve to increase the severity of immune suppression following exercise, possibly contributing to increased morbidity of equine athletes experiencing repeated episodes of exercise stress. Finally, direct effects of corticosteroids, catecholamines and neuropeptides on immune cell function may contribute to exercise effects on immunity in unfit horses and to a lesser extent in fit horses.