Juvenile Antarctic rockcod (Trematomus bernacchii) are physiologically robust to CO 2 -acidified seawater

• Published in: Journal of Experimental Biology
• Main Authors: Davis, BE, Miller, NA, Flynn, EE, Todgham, AE
• Format: Article in Journal/Newspaper
• Language: English
• Published: eScholarship, University of California 2016
• Subjects: Antarctica; Cardiorespiratory physiology; Early life stages; Notothenioid; Ocean acidification; Antarctic; Ross Sea; Antarc*
• Online Access: http://www.escholarship.org/uc/item/1z94h6p7

© 2016, Company of Biologists Ltd. All rights reserved. To date, numerous studies have shown negative impacts of CO2-acidified seawater (i.e. ocean acidification, OA) on marine organisms, including calcifying invertebrates and fishes; however, limited research has been conducted on the physiological effects of OA on polar fishes and even less on the impact of OA on early developmental stages of polar fishes. We evaluated aspects of aerobic metabolism and cardiorespiratory physiology of juvenile emerald rockcod, Trematomus bernacchii, an abundant fish in the Ross Sea, Antarctica, to elevated partial pressure of carbon dioxide (PCO2) [420 (ambient), 650 (moderate) and 1050 (high) μatm PCO2] over a 1 month period. We examined cardiorespiratory physiology, including heart rate, stroke volume, cardiac output and ventilation rate, whole organism metabolism via oxygen consumption rate and sub-organismal aerobic capacity by citrate synthase enzyme activity. Juvenile fish showed an increase in ventilation rate under high PCO2compared with ambient PCO2, whereas cardiac performance, oxygen consumption and citrate synthase activity were not significantly affected by elevated PCO2. Acclimation time had a significant effect on ventilation rate, stroke volume, cardiac output and citrate synthase activity, such that all metrics increased over the 4 week exposure period. These results suggest that juvenile emerald rockcod are robust to near-future increases in OA and may have the capacity to adjust for future increases in PCO2by increasing acid-base compensation through increased ventilation.