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Updated: Dec 18, 2025

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Published on: September 5, 2018
Mitochondrial performance of a continually growing marine bivalve, Mytilus edulis, depends on body size
Alexey Sukhotin1, Anton Kovalev2,3, Eugene Sokolov4
1White Sea Biological Station, Zoological Institute of Russian Academy of Sciences, Saint-Petersburg 199034, Russia alexey.sukhotin@zin.ru.
Abstract:
Allometric decline of mass-specific metabolic rate with increasing body size in organisms is a well-documented phenomenon. Despite a long history of research, the mechanistic causes of metabolic scaling with body size remain under debate. Some hypotheses suggest that intrinsic factors such as allometry of cellular and mitochondrial metabolism may contribute to the organismal-level metabolic scaling. The aim of our present study was to determine the metabolic allometry at the mitochondrial level using a continually growing marine ectotherm, the mussel Mytilus edulis, as a model. Mussels from a single cohort that considerably differed in body size were selected, implying faster growth in the larger specimens. We determined the body mass-dependent scaling of the mitochondrial proton leak respiration, respiration in the presence of ADP indicative of the oxidative phosphorylation (OXPHOS), and maximum activity of the mitochondrial electron transport system (ETS) and cytochrome c oxidase (COX). Respiration was measured at normal (15°C), and elevated (27°C) temperatures. The results demonstrated a pronounced allometric increase in both proton leak respiration and OXPHOS activity of mussel mitochondria. Mussels with faster growth (larger body size) showed an increase in OXPHOS rate, proton leak respiration rate, and ETS and COX activity (indicating an overall improved mitochondrial performance) and higher respiratory control ratio (indicating better mitochondrial coupling and potentially lower costs of mitochondrial maintenance at the same OXPHOS capacity) compared with slower growing (smaller) individuals. Our data show that the metabolic allometry at the organismal level cannot be directly explained by mitochondrial functioning.
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