Elevated CO2increases energetic cost and ion movement in the marine fish intestine.
Energetic costs associated with ion and acid-base regulation in response to ocean acidification have been predicted to decrease the energy available to fish for basic life processes. However, the low cost of ion regulation (6-15% of standard metabolic rate) and inherent variation associated with whole-animal metabolic rate measurements have made it difficult to consistently demonstrate such a cost. Here we aimed to gain resolution in assessing the energetic demand associated with acid-base regulation by examining ion movement and O2consumption rates of isolated intestinal tissue from Gulf toadfish acclimated to control or 1900 μatm CO2(projected for year 2300). The active marine fish intestine absorbs ions from ingested seawater in exchange for HCO3-to maintain water balance. We demonstrate that CO2exposure causes a 13% increase of intestinal HCO3-secretion that the animal does not appear to regulate. Isolated tissue from CO2-exposed toadfish also exhibited an 8% higher O2consumption rate than tissue from controls. These findings show that compensation for CO2leads to a seemingly maladaptive persistent base (HCO3-) loss that incurs an energetic expense at the tissue level. Sustained increases to baseline metabolic rate could lead to energetic reallocations away from other life processes at the whole-animal level.
University of Miami- Rosenstiel School of Marine and Atmospheric Science, 4600 Rickenbacker Causeway, Miami, FL 33149, USA.
Rachael M
RM
Heuer
University of Miami- Rosenstiel School of Marine and Atmospheric Science, 4600 Rickenbacker Causeway, Miami, FL 33149, USA.
Martin
M
Grosell
Comp Biochem Physiol B Biochem Mol Biol. 2013 Sep;166(1):48-57
23827663
Proc Natl Acad Sci U S A. 2012 Oct 30;109(44):18192-7
23077257
Comp Biochem Physiol A Mol Integr Physiol. 2015 Sep;187:160-7
26005104
Physiol Zool. 1998 Sep-Oct;71(5):492-505
9754526
Aquat Toxicol. 2015 Jan;158:171-80
25438123
J Exp Biol. 2009 Dec;212(Pt 23):3873-81
19915130
J Comp Physiol B. 2010 Nov;180(8):1213-25
20571812
Acta Physiol (Oxf). 2011 Jul;202(3):421-34
21362153
J Exp Biol. 2008 Jul;211(Pt 14):2327-35
18587127
Science. 2008 Jun 13;320(5882):1490-2
18497259
Comp Biochem Physiol A Mol Integr Physiol. 2015 Apr;182:102-12
25535111
Physiol Biochem Zool. 2012 Sep-Oct;85(5):450-9
22902373
Proc Natl Acad Sci U S A. 2015 Apr 14;112(15):4696-701
25825763
J Fish Biol. 2014 Apr;84(4):1210-20
24665828
J Exp Biol. 2013 Aug 1;216(Pt 15):2771-82
23842625
Comp Biochem Physiol A Mol Integr Physiol. 2013 Nov;166(3):482-9
23916817
Am J Physiol Regul Integr Comp Physiol. 2006 Oct;291(4):R1145-56
16709644
Am J Physiol Regul Integr Comp Physiol. 2014 Nov 1;307(9):R1061-84
25163920
Conserv Physiol. 2013 Sep 21;1(1):cot023
27293607
Sci Rep. 2016 Sep 13;6:33216
27620837
Proc Natl Acad Sci U S A. 2010 Jul 20;107(29):12930-4
20615968
J Comp Physiol B. 2012 Oct;182(7):921-34
22581071
J Exp Biol. 2010 Feb 1;213(3):459-68
20086131
Front Zool. 2012 Oct 18;9(1):28
23075125
Am J Physiol. 1999 Sep;277(3 Pt 2):R631-9
10484478
J Exp Zool. 2002 Aug 1;293(3):302-19
12115903
J Comp Physiol B. 2016 May;186(4):447-60
26922790
J Exp Biol. 2013 Jun 1;216(Pt 11):2103-10
23470659
Science. 2009 Jun 26;324(5935):1683
19556502
Comp Biochem Physiol A Mol Integr Physiol. 2013 Jan;164(1):154-61
22884997
Science. 2009 Jan 16;323(5912):359-62
19150840
Science. 2015 Jun 5;348(6239):1132-5
26045435
Front Physiol. 2016 Jun 02;7:198
27313538
J Exp Biol. 1983 Nov;107:9-20
6668465
Comp Biochem Physiol A Mol Integr Physiol. 2013 Jun;165(2):119-30
23416137
Respir Physiol Neurobiol. 2006 Nov;154(1-2):199-215
16777496
J Comp Physiol B. 2016 Jan;186(1):97-109
26487347
Physiol Biochem Zool. 2016 Sep-Oct;89(5):402-16
27617361
J Exp Biol. 2012 Nov 15;215(Pt 22):3865-73
23100485
Nature. 2003 Sep 25;425(6956):365
14508477