Acute CO2 tolerance in fishes is associated with air breathing but not the Root effect, red cell βNHE, or habitat

R B Shartau; T S Harter; D W Baker; D L Aboagye; P J Allen; A L Val; D A Crossley 2nd; Z F Kohl; M S Hedrick; C Damsgaard; C J Brauner

doi:10.1016/j.cbpa.2022.111304

Acute CO₂ tolerance in fishes is associated with air breathing but not the Root effect, red cell βNHE, or habitat

Comp Biochem Physiol A Mol Integr Physiol. 2022 Dec:274:111304. doi: 10.1016/j.cbpa.2022.111304. Epub 2022 Aug 30.

Authors

R B Shartau¹, T S Harter², D W Baker³, D L Aboagye⁴, P J Allen⁵, A L Val⁶, D A Crossley 2nd⁷, Z F Kohl⁸, M S Hedrick⁹, C Damsgaard¹⁰, C J Brauner¹¹

Affiliations

¹ Department of Biology, The University of Texas at Tyler, Tyler, TX, USA; Department of Zoology, University of British Columbia, Vancouver, BC, Canada. Electronic address: rshartau@uttyler.edu.
² Department of Zoology, University of British Columbia, Vancouver, BC, Canada; Marine Biology Research Division, Scripps Institution of Oceanography, University of California, San Diego, CA, USA. Electronic address: tharter@ucsd.edu.
³ Department of Fisheries and Aquaculture, Vancouver Island University, Nanaimo, BC, Canada. Electronic address: dan.baker@viu.ca.
⁴ Department of Wildlife, Fisheries and Aquaculture, Mississippi State University, Starkville, MS, USA.
⁵ Department of Wildlife, Fisheries and Aquaculture, Mississippi State University, Starkville, MS, USA. Electronic address: peter.allen@msstate.edu.
⁶ Laboratory of Ecophysiology and Molecular Evolution, Brazilian National Institute for Research of the Amazon (INPA), Manaus, AM, Brazil.
⁷ Department of Biological Sciences, University of North Texas, Denton, TX, USA. Electronic address: dane.crossley@unt.edu.
⁸ Department of Biological Sciences, University of North Texas, Denton, TX, USA.
⁹ Department of Biological Sciences, California State University, East Bay, Hayward, CA, USA. Electronic address: michael.hedrick@csueastbay.edu.
¹⁰ Section for Zoophysiology, Department of Biology, Aarhus University, Aarhus, Denmark. Electronic address: christian.damsgaard@aias.au.dk.
¹¹ Department of Zoology, University of British Columbia, Vancouver, BC, Canada. Electronic address: brauner@zoology.ubc.ca.

PMID: 36049728
DOI: 10.1016/j.cbpa.2022.111304

Abstract

High CO₂ (hypercapnia) can impose significant physiological challenges associated with acid-base regulation in fishes, impairing whole animal performance and survival. Unlike other environmental conditions such as temperature and O₂, the acute CO₂ tolerance thresholds of fishes are not understood. While some fish species are highly tolerant, the extent of acute CO₂ tolerance and the associated physiological and ecological traits remain largely unknown. To investigate this, we used a recently developed ramping assay, termed the Carbon Dioxide maximum (CD_max), that increases CO₂ exposure until loss of equilibrium (LOE) is observed. We investigated if there was a relationship between CO₂ tolerance and the Root effect, β-adrenergic sodium proton exchanger (βNHE), air-breathing, and fish habitat in 17 species. We hypothesized that CO₂ tolerance would be higher in fishes that lack both a Root effect and βNHE, breathe air, and reside in tropical habitats. Our results showed that CD_max ranged from 2.7 to 26.7 kPa, while LOE was never reached in four species at the maximum PCO₂ we could measure (26.7 kPa); CO₂ tolerance was only associated with air-breathing, but not the presence of a Root effect or a red blood cell (RBC) βNHE, or fish habitat. This study demonstrates that the diverse group of fishes investigated here are incredibly tolerant of CO₂ and that although this tolerance is associated with air-breathing, further investigations are required to understand the basis for CO₂ tolerance.

Keywords: CO(2); Carbon dioxide; Fish; Hypercapnia; Loss of equilibrium; Respiratory acidosis; Vertebrates.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adrenergic Agents
Animals
Carbon Dioxide*
Ecosystem
Erythrocytes / physiology
Fishes / physiology
Protons*
Sodium

Substances

Adrenergic Agents
Protons
Carbon Dioxide
Sodium