Metabolic rate and mitochondrial physiology adjustments in Arctic char (Salvelinus alpinus) during cyclic hypoxia.

Diel fluctuations of oxygen levels characterize cyclic hypoxia and poses a significant challenge to wild fish populations. Although recent research has been conducted on the effects of hypoxia and reoxygenation, mechanisms by which fish acclimatize to cyclic hypoxia remain unclear, especially in hypoxia-sensitive species. We hypothesized that acclimation to cyclic hypoxia requires a downregulation of their aerobic metabolic rate (MR) and an upregulation of mitochondrial respiratory capacities to mitigate constraints on aerobic metabolism and the elevated risk of oxidative stress upon reoxygenation. We exposed Arctic char (Salvelinus alpinus) to ten days of cyclic hypoxia and measured their MR and mitochondrial physiology to determine how they cope with fluctuating oxygen concentrations. We measured oxygen consumption as a proxy of MR and observed that Arctic char defend their standard metabolic rate but decrease their routine metabolic rate during hypoxic phases, presumably through the repression of spontaneous swimming activities. At the mitochondrial level, acute cyclic hypoxia increases oxygen consumption without ADP (CI-LEAK) in liver and heart. Respiration in the presence of ADP (OXPHOS) temporarily increases in the liver and decreases in the heart. Cytochrome c oxidase (COX) affinity with oxygen also increases at day 3 in the liver. However, no change occurs in the brain, which is likely primarily preserved through preferential perfusion (albeit not measured in this study). Finally, in vivo measurements of reactive oxygen species revealed the absence of an oxidative burst in mitochondria in the cyclic hypoxia group. Our study shows that Arctic char acclimatize to cyclic hypoxia through organ-specific mitochondrial adjustments.

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