Experimental increase in predation risk causes a cascading stress response in free-ranging snowshoe hares.

Abstract

Extensive research confirms that environmental stressors like predation risk can profoundly affect animal condition and physiology. However, there is a lack of experimental research assessing the suite of physiological responses to risk that may arise under realistic field conditions, leaving a fragmented picture of risk-related physiological change and potential downstream consequences on individuals. We increased predation risk in free-ranging snowshoe hares (Lepus americanus) during two consecutive summers by simulating natural chases using a model predator and monitored hares intensively via radio-telemetry and physiological assays, including measures designed to assess changes in stress physiology and overall condition. Compared to controls, risk-augmented hares had 25.8% higher free plasma cortisol, 15.9% lower cortisol-binding capacity, a greater neutrophil:lymphocyte skew, and a 10.4% increase in glucose. Despite these changes, intra-annual changes in two distinct condition indices, were unaffected by risk exposure. We infer risk-augmented hares compensated for changes in their stress physiology through either compensatory foraging and/or metabolic changes, which allowed them to have comparable condition to controls. Although differences between controls and risk-augmented hares were consistent each year, both groups had heightened stress measures during the second summer, likely reflecting an increase in natural stressors (i.e., predators) in the environment. We show that increased predation risk in free-ranging animals can profoundly alter stress physiology and that compensatory responses may contribute to limiting effects of such changes on condition. Ultimately, our results also highlight the importance of biologically relevant experimental risk manipulations in the wild as a means of assessing physiological responses to natural stressors.