Date of Award
Master of Science
Climate change is predicted to cause shifts in average temperature and increase extreme heat events. The common paradigm is species will shift their range in order to deal with the changing climate, but endotherms may have the ability to physiologically acclimate to these changes. To test this I measured body temperatures (Tb), metabolic rate, corticosterone expression, heat shock protein accumulation, and immune function to determine the integrative systems responses to heat stressors in mice. I tested mice with chronic heat stress and acute heat stressors to simulate predicted changes in future climates. Overall I found that chronic heat stress, but not acute heat stressors caused an increase in Tb. Metabolic rate was not changed by any temperature treatment. Corticosterone was suppressed in acute, but not chronic, heat stress treatments. This suppression of corticosterone response in the acute heat groups is likely because prolonged corticosterone responses are costly to other physiological systems. All heat treatments caused accumulation of HSPs, with the acute stressors having a higher accumulation. This indicates acute heat stressors are more stressful than chronic heat stress, and suggests a shift from endocrine system to cellular level stress protection. Finally I found that no heat treatment had a detrimental effect on immune function. All of my results lead to the conclusion that endotherms do have the ability to physiologically acclimate to potential changing climates. Integrating this knowledge allows us to better forecast endothermic responses to climate change, and will lead to more realistic and robust climate change models for endotherm species.
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