Journal
PHYSIOLOGY
Volume 38, Issue 3, Pages 141-158Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiol.00027.2022
Keywords
climate change; fish physiology; temperature; thermal biology
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This review investigates the reasons behind fish heat failure at thermal extremes and the physiological mechanisms that determine acute upper thermal tolerance. The study proposes that rapid direct thermal impacts on fish are influenced by molecular mechanisms such as reaction rates, protein structure, and membrane fluidity. These molecular effects during acute warming lead to loss of equilibrium and death through different cellular, organ, and physiological pathways, including mitochondrial dysfunction, oxygen limitation, and impacted excitability of excitable cells. The study concludes that a single mechanism for acute upper thermal tolerance is not found across species and contexts, suggesting that the limiting mechanisms during acute warming differ between species, life stages, and recent thermal history. Future research is proposed to elucidate major patterns of physiological thermal limitations in fish.
This review is focused on the questions of why fish exhibit heat failure at thermal extremes and which physiological mechanisms determine the acute upper thermal tolerance. We propose that rapid direct thermal impacts on fish act through three fundamental molecular mechanisms reaction rates, protein structure, and membrane fluidity. During acute warming, these molecular effects then lead to loss of equilibrium and death through various cellular, organ, and physiological pathways. These pathways include mitochondrial dysfunction, oxygen limitation, and impacted excitability of excitable cells and eventually lead to neural and/or muscular failure. The pathways may also lead to loss of homeostasis and subsequent heat failure. There is strong evidence in some species for oxygen limitation in these processes and strong evidence against it in other species and contexts. The limiting mechanisms during acute warming therefore appear to differ between species, life stages, and recent thermal history. We conclude that a single mechanism underpinning the acute upper thermal tolerance across species and contexts will not be found. Therefore, we propose future avenues of research that can elucidate major patterns of physiological thermal limitations in fish
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