Hyperoxia Does Not Extend Critical Thermal Maxima (CTmax) in White- or Red-Blooded Antarctic Notothenioid Fishes

• Published in: Physiological and biochemical zoology Vol. 89; no. 1; pp. 1 - 9
• Main Authors: Devor, Devin P., Kuhn, Donald E., O’Brien, Kristin M., Crockett, Elizabeth L.
• Format: Journal Article
• Language: English
• Published: United States The University of Chicago Press 01.01.2016; University of Chicago Press
• Subjects: Aerobiosis; Animals; Antarctic Regions; Blood Chemical Analysis; Hemoglobins - analysis; Oxygen - metabolism; Perciformes - physiology; Thermotolerance; Antarctic fishes; critical thermal maximum; thermal stress; hyperoxic treatment
• ISSN: 1522-2152; 1537-5293
• DOI: 10.1086/684812

Understanding what limits the capacity of organisms to tolerate increasing temperatures is a critical objective in comparative biology. Using an experimental system of Antarctic notothenioid fishes, we sought to determine whether a mismatch between oxygen demand and oxygen supply was responsible for setting thermal tolerance limits. Previous studies have shown that Antarctic icefishes (family Channichthyidae), which lack hemoglobin, have lower critical thermal maxima (CTmax) than red-blooded notothenioids collected from the same region of the Antarctic (Western Antarctic Peninsula). In addition, within the notothenioid fishes there exists a positive correlation between CTmax and hematocrit. We tested the hypothesis that the lower CTmax of icefishes is associated with reduced oxygen supply. We employed an experimental heat ramp (4°C h−1) to determine CTmax under both normoxic and hyperoxic conditions and quantified correlates of oxygen limitation (lactate levels and expression of hypoxia-inducible factor-1α) in white-blooded Chaenocephalus aceratus and red-blooded Notothenia coriiceps. Hyperoxia, corresponding to a three- to fourfold increase in seawater Po2, did not extend CTmax in either species despite an overall mitigation in the rise of plasma and muscle lactate compared with the normoxic treatment. Our results also indicate that cardiac HIF-1α mRNA levels were insensitive to changes in both temperature and oxygen treatments. The absence of a change in CTmax with hyperoxia is likely to represent the contribution of factors beyond oxygen supply to physiological failure at elevated temperatures.