Ocean acidification refers to the increased levels of carbon dioxide predicted in the marine environment in the near future, and is an impending environmental concern for all marine life. For marine fishes, ocean acidification causes distress by making it more difficult for fish to remove carbon dioxide from their bodies, which results in a cascade of downstream acid-base disturbances that can jeopardize ecological performance. The primary objective of this work was to explore the ability of an economically important sportfish, the red drum, to offset these effects through respiratory and acid-base plasticity, which refers to the ability of animals to alter their physiology as a consequence of environmental change. A secondary objective of this work was to explore the secondary consequences of any observed plasticity according to the premise that physiological adaptations may have significant trade-offs. We first explored respiratory plasticity following exposure to ocean acidification using a combination of gene expression, enzyme assays and morphological characterization in the gills and red blood cells. Our results suggest that while fish were not able to manipulate their red blood cells to offset ocean acidification, they did reduce the thickness of their gills which theoretically reduces the diffusion limitations of carbon dioxide across the gill epithelium. Despite this observation, we were not able to quantify any tangible benefit of acclimation on the carbon dioxide load within fish plasma, as compared to control fish. Nonetheless, several trade-offs of the change in branchial diffusion distance were observed, all of which related to osmoregulatory physiology. The thinner gills of acclimated fish are also more prone to water loss to the marine environment, and to compensate fish were found to increase the osmoregulatory enzymes in their gills and intestines. Importantly, these osmoregulatory trade-offs were likely exacerbated by an increased ventilation rate in fish exposed to ocean acidification. While our work estimated that the ventilatory response reduced the change in blood chemistry following exposure to ocean acidification by about 40%, this also would result in additional water loss owing to the osmorespiratory compromise. A final aspect of this work was then to quantify the metabolic costs associated with ocean acidification acclimation with the hypothesis that the baseline cost of living (i.e. standard metabolic rate) for acclimated fish would be higher than fish acclimated to normal conditions. Contrary to our expectation, no significant change in standard or metabolic rate was detected. A subsequent study determined that this finding likely stemmed from the fact that osmoregulation itself only accounts for a fraction of standard metabolic rate. The second series of studies explored the plasticity of acid-base physiological systems in both early and later life stage red drum. With respect to later life stages, we found that red drum did have the potential for plasticity; however, this was not activated until fish were exposed to much higher carbon dioxide levels than those related to ocean acidification. Similar findings were observed with respect to acid-base plasticity in early life, whereby no significant changes in acid-base pathway were noted in fish reared under elevated carbon dioxide. Importantly, ocean acidification was found to significantly reduce embryonic survival during these studies, yet a significant number of larvae were also found to be tolerant to carbon dioxide levels an order of magnitude higher than ocean acidification. The overall conclusion of this work suggests that red drum generally maintain sufficient acid-base machinery in their bodies to tolerate typical environmental stressors, including ocean acidification. Furthermore, while sensitive individuals were observed in early life stages, there were also significant numbers of tolerant individuals that may serve as the bedrock for adaption. Additionally, several novel aspects of acid-base compensation were observed during these studies, including the presence of an anion exchanger (slc26a5) previously only found in the inner ear of higher vertebrates. Our work suggests that this transporter is found within the specialized ion transporting cells of the gills with an apical localization that may contribute to bicarbonate absorption from seawater. With respect to the broader impacts of this work, a total of four graduate students, one post-doc and nine undergraduates were trained as a part of this work. Furthermore, four international visiting graduate students were incorporated into these studies. Our data was publically disseminated to local stakeholders in a variety of avenues, including public presentations at the University of Texas at Austin, Texas State Aquarium and Coastal Conservation Agency members meeting. Finally, members of our research group incorporated our work into a variety of K-12 education initiatives including the University of Texas Marine Science Institute?s summer science program and a scientist in residence program that places graduate students directly in K-12 classrooms in Port Aransas, Texas. Last Modified: 10/30/2018 Submitted by: Andrew Esbaugh