Influence of 96h sub-lethal copper exposure on aerobic scope and recovery from exhaustive exercise in killifish (Fundulus heteroclitus)
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Production of industrial effluents have led to increased copper (Cu) pollution of aquatic ecosystems, impacting the physiology of aquatic vertebrates. Past work has shown that Cu exerts its toxicity by disruption ion regulation and/ or increasing oxidative stress. However, it remains unclear how Cu may influence aerobic metabolism and hypoxia tolerance, two possible targets of its toxicity. To address this issue, we exposed freshwater acclimated killifish (F. heteroclitus) to a 96 h Cu exposure at a target concentration of 100 μg L-1. We determined resting oxygen consumption (ṀO2), ṀO2max after exhaustive exercise, and followed ṀO2 for 3 h in post-exercise recovery in water with either no Cu or 100 μg L-1 Cu. We assessed hypoxia tolerance by determining the critical oxygen tension (Pcrit). It was found that killifish exposed to combined 96 h Cu exposure and Cu present during metabolic measurements, showed a significant decrease in ṀO2max and in aerobic scope (ṀO2max - ṀO2rest), compared to control fish. However, changes in blood and muscle lactate and muscle glycogen were not consistent with an upregulation of anaerobic metabolism as compensation for reduced aerobic performance in Cu exposed fish. Hypoxia tolerance was not influenced by the 96 h Cu exposure or by presence or absence of Cu during the Pcrit test. This study suggests that Cu differentially influences responses to changes in oxygen demand and oxygen availability.
