Diel cycling hypoxia enhances hypoxia tolerance in rainbow trout ( Oncorhynchus mykiss ): evidence of physiological and metabolic plasticity

Many fish naturally encounter a daily cycle of hypoxia, but it is unclear whether this exposure hardens hypoxia-intolerant fish to future hypoxia or leads to accumulated stress and death. The rainbow trout ( ) is a putatively hypoxia-sensitive species found in rivers and estuaries that may routinely...

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Published inJournal of experimental biology Vol. 222; no. Pt 14
Main Authors Williams, Kenneth J, Cassidy, Alicia A, Verhille, Christine E, Lamarre, Simon G, MacCormack, Tyson J
Format Journal Article
LanguageEnglish
Published England 23.07.2019
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Summary:Many fish naturally encounter a daily cycle of hypoxia, but it is unclear whether this exposure hardens hypoxia-intolerant fish to future hypoxia or leads to accumulated stress and death. The rainbow trout ( ) is a putatively hypoxia-sensitive species found in rivers and estuaries that may routinely experience hypoxic events. Trout were exposed to one of four 135 h treatments in a swim-tunnel respirometer: (1) air-saturated control (20.7 kPa ); (2) diel cycling O (20.7-4.2 kPa  over 24 h); (3) acute hypoxia (130 h at 20.7 kPa  followed by 5 h at 4.2 kPa ); and (4) the mean oxygen tension (12.4 kPa ) experienced by the diel cycled fish. Some responses were similar in diel O cycled and mean -treated fish, but overall, exposure to ecologically representative diel hypoxia cycles improved hypoxia tolerance. Diel hypoxia-induced protective responses included increased inducible HSP70 concentration and mean corpuscular hemoglobin concentration, as well as reduced plasma cortisol. Acclimation to diel hypoxia allowed metabolic rates to decline during hypoxia, reduced oxygen debt following subsequent exposures, and allowed fish to return to an anabolic phenotype. The data demonstrate that acute diel cycling hypoxia improves hypoxia tolerance in previously intolerant fish through the activation of cellular protective mechanisms and a reduction in metabolic O requirements.
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ISSN:0022-0949
1477-9145
DOI:10.1242/jeb.206045