Meeting Abstract
Currently, the primary mechanism establishing upper thermal limits is unknown. The classic protein denaturation hypothesis remains unlikely as most proteins denature at temperatures higher than the critical thermal limits for organisms. Alternatively, the oxygen and capacity-limited thermal tolerance (OCLTT) hypothesis predicts that increasing temperatures cause a mismatch between oxygen supply and demand, forcing the animal to transition to anaerobic metabolism, which fails to meet energetic demand leading to organismal death. Most support for the OCLTT hypothesis has come from aquatic animals with relatively little support in terrestrial animals. Yet in the embryonic stage, terrestrial animals may be more susceptible to oxygen limitation due to underdeveloped cardio-respiratory systems and living in an aquatic medium. We tested this hypothesis in Japanese quail (Coturnix coturnix) embryos by attempting to artificially increase basal metabolic rate with treatment of thyroid hormone (T3). Halfway through development, T3 dissolved in DMSO was injected into the yolk of half of the eggs, while the other half received vehicle only. Embryos were then exposed to 48.0°C for one hour to measure survivorship. If the OCLTT hypothesis were correct, the embryos injected with T3 should show reduced survivorship at high temperatures due to increased oxygen demand. In fact, survivorship in the T3 injected group was one quarter of that in the control group suggesting that oxygen availability may be limiting thermal tolerance. However, the relationship between metabolic rate and survivorship was weak indicating a possible secondary effect of T3 independent of metabolic rate. Therefore, further studies are necessary to elucidate the direct mechanisms behind this effect.
