Thermal plasticity of the cardiorespiratory system provides cross-tolerance protection to fish exposed to elevated nitrate.

Exposure to nitrate is toxic to aquatic animals due to the formation of methaemoglobin and a subsequent loss of blood-oxygen carrying capacity. Yet, nitrate toxicity can be modulated by other stressors in the environment, such as elevated temperatures. Acclimation to elevated temperatures has been shown to offset the negative effects of nitrate on whole animal performance in fish, but the mechanisms underlying this cross-tolerance interaction remain unclear. In this study, juvenile silver perch (Bidyanus bidyanus) were exposed to a factorial combination of temperature (28 °C or 32 °C) and nitrate concentrations (0, 50 or 100 mg NO3- L-1) treatments to test the hypothesis that thermal acclimation offsets the effects of nitrate via compensatory changes to the cardiorespiratory system (gills, ventricle and blood oxygen carrying capacity). Following 21 weeks of thermal acclimation, we found that fish acclimated to 32 °C experienced an expansion of gill surface area and an increase in ventricular thickness regardless of nitrate exposure concentration. Exposure to nitrate (both 50 and 100 mg NO3- L-1) reduced the blood oxygen carrying capacity of silver perch due to increases in methaemoglobin concentration and a right shift in oxygen-haemoglobin binding curves in fish from both thermal acclimation treatments. These results indicate that plasticity of the gills and ventricle of warm acclimated fish are potential mechanisms which may provide cross-tolerance protection to elevated nitrate concentrations despite nitrate induced reductions to oxygen transport.