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Cardiac oxygen limitation during an acute thermal challenge in the European perch: Effects of chronic environmental warming and experimental hyperoxia

Journal article
Authors Andreas Ekström
Jeroen Brijs
T. D. Clark
A. Gräns
Fredrik Jutfelt
Erik Sandblom
Published in American Journal of Physiology. Regulatory Integrative and Comparative Physiology
Volume 311
Issue 2
Pages R440-R449
ISSN 0363-6119
Publication year 2016
Published at Department of Biological and Environmental Sciences
Pages R440-R449
Language en
Keywords Cardiac performance, Myocardial oxygenation, PvO2 threshold, Teleost, Thermal acclimation
Subject categories Construction Management, Energy Systems


Oxygen supply to the heart has been hypothesized to limit cardiac performance and whole animal acute thermal tolerance (CTmax) in fish. We tested these hypotheses by continuously measuring venous oxygen tension (PvO2) and cardiovascular variables in vivo during acute warming in European perch (Perca fluviatilis) from a reference area during summer (18°C) and a chronically heated area (Biotest enclosure) that receives warm effluent water from a nuclear power plant and is normally 5–10°C above ambient (24°C at the time of experiments). While CTmax was 2.2°C higher in Biotest compared with reference perch, the peaks in cardiac output and heart rate prior to CTmax occurred at statistically similar PvO2 values (2.3– 4.0 kPa), suggesting that cardiac failure occurred at a common critical PvO2 threshold. Environmental hyperoxia (200% air saturation) increased PvO2 across temperatures in reference fish, but heart rate still declined at a similar temperature. CTmax of reference fish increased slightly (by 0.9°C) in hyperoxia, but remained significantly lower than in Biotest fish despite an improved cardiac output due to an elevated stroke volume. Thus, while cardiac oxygen supply appears critical to elevate stroke volume at high temperatures, oxygen limitation may not explain the bradycardia and arrhythmia that occur prior to CTmax. Acute thermal tolerance and its thermal plasticity can, therefore, only be partially attributed to cardiac failure from myocardial oxygen limitations, and likely involves limiting factors on multiple organizational levels. © 2016 the American Physiological Society.

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