Effects of Malaria Infection on Post-Exercise Thermoregulation and Metabolism in the Western Fence Lizard, Sceloporus occidentalis


Meeting Abstract

P2.141  Tuesday, Jan. 5  Effects of Malaria Infection on Post-Exercise Thermoregulation and Metabolism in the Western Fence Lizard, Sceloporus occidentalis SCHOLNICK, David A.*; MANIVANH, Richard V.; NELSON, Whitney N.; Pacific University; Pacific University; Pacific University david.scholnick@pacificu.edu

Western fence lizards (Sceloporus occidentalis) infected with the malarial parasite, Plasmodium mexicanum select higher recovery body temperatures and have elevated cost of recovery when compared to uninfected lizards. Malarial infections depress hemoglobin concentrations by as much as 25% and elevate post-exercise lactate levels by almost 30%. Western fence lizards collected from southern Oregon and central California were screened for P. mexicanum. Lizards were placed in a temperature controlled treadmill at preferred body temperature (34.5°C) and induced to walk at constant speed for 5 minutes (0.7 m min-1) or sprint maximally (2 min of activity). Blood lactate and glucose levels were measured before activity, immediately after activity, and at 15, 30, 60 and 90 min during recovery. Malarial infections decreased lizard resting blood glucose levels and induced hyperglycemia post-exercise. Blood glucose was 27% higher in malaria infected lizards than uninfected lizards after 60 min of recovery. Elevated body temperatures following activity decreased lactate removal rates in malaria infected lizards by 1.5 times but had no significant effect on uninfected lizards. In a separate set of experiments hemoglobin concentrations in uninfected lizards were lowered by 25% in order to determine the impact of anemia associated with malarial infection upon recovery metabolism. Uninfected-anemic lizards had increased post-exercise oxygen consumption and blood glucose concentrations similar to malaria infected lizards. These results suggest that anemia associated with malaria infection can partially explain the elevated cost of recovery and disruptions in glucose regulation following activity.

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