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ABSTRACT Vertebrates utilize various respiratory organs such as gills, lungs and skin in combination with diverse cardiovascular structures, including single-, three- and four-chambered hearts, to enable oxygen delivery and carbon dioxide removal. They also exhibit differences in aerobic and anaerobic metabolism during exertion, but the cardiorespiratory gas transport of all vertebrates is a four-step process governed by Fick's Principle and Fick's Law of Diffusion over the entire range of metabolic rates. Hillman et al. (2013) suggested that previous exercise studies have focused too narrowly on mammals and proposed that the cardiorespiratory system's excess capacity serves an evolutionary role in enhancing CO2 excretion in non-mammalian vertebrates. In contrast, an analysis by Hicks and Wang (2021) concluded that vertebrates maintain effective gas exchange even at peak activity, finding no evidence of arterial hypercapnia at maximal oxygen consumption and thus challenging the proposal of significant limitations to pulmonary or branchial CO2 efflux. In the present study, we investigated the limits for CO2 exchange in exercising American alligators (Alligator mississippiensis) and provide evidence that the cardiorespiratory system is adequately built to sustain CO2 excretion during strenuous exercise and maintain arterial PCO2, with no evidence of diffusion limitation for pulmonary CO2 excretion. 

Developmental oxygen is a powerful stressor that can induce morphological and functional changes in the cardiovascular systems of embryonic and juvenile vertebrates. This plasticity has been ascribed, at least in part, to the unique status of the developing cardiovascular system, which undergoes organogenesis while meeting the tissue oxygen demands of the embryo. We have previously reported an array of functional and morphological changes in embryonic American alligators that persist into juvenile life. Most notably, cardiac enlargement as well as functional parameters of anesthetized juvenile alligators remains after embryonic hypoxic exposure. Because the effects of developmental oxygen in crocodilians have only been investigated in anesthetized animals, we explored the pressure dynamics of both ventricles as well as systemic pressure in response to stressors of acute hypoxia and swimming. Our current findings demonstrate that developmental programming of cardiac function (intraventricular pressure and heart rate) does persist into juvenile life, but it is chamber-specific and depends on the experimental manipulation. Acute hypoxic exposure revealed that juvenile alligators that had experienced 10% O 2 as embryos maintain right ventricle function and increase left ventricle function during exposure. Finally, the data indicate blood flow in the left aorta must originate from the left ventricle during acute hypoxia and swimming.