Meeting Abstract
Although temperature defines a major axis of the fundamental niche, the proximate mechanisms that set the limits of thermal tolerance remain uncertain. Classically, high temperatures were thought to become lethal by disrupting the folding of proteins or the integrity of cell membranes. However, animals frequently die at temperatures far below those predicted to cause these cellular structures to fail. More recently, an alternative hypothesis based on oxygen limitation has been proposed: lethal thermal limits occur when cardiac and respiratory systems cannot sufficiently supply oxygen to the body. Oxygen deficiency presumably induces positive feedbacks that rapidly lead to systemic failure and hence death. Currently, support for this hypothesis is equivocal; studies examining a diverse group of aquatic ectotherms support the hypothesis, but studies examining terrestrial insects do not. Here, we present the first test of the oxygen limitation hypothesis in a terrestrial vertebrate. We compared the upper lethal limits of temperature among developing lizard embryos (Sceloporus tristichus) across a range of oxygen concentrations, spanning hypoxia to hyperoxia (10% – 30%). Eggs were incubated under a naturalistic diel cycle in which the maximal temperature of the cycle increased by 1.0°C each day. Heart rates of embryos were monitored daily to determine the point of death. Consistent with the hypothesis that oxygen limitation sets the lethal temperature, embryos exposed to normoxia and hyperoxia survived to higher temperatures than did embryos exposed to hypoxia. Our results suggest that critical high temperatures become lethal in S. tristichus embryos because tissues require more oxygen at high temperatures than developing respiratory and cardiac systems can deliver.
