Abstract

SummaryYellowtail kingfish (Seriola lalandi) are a highly active marine species, with increasing value in commercial aquaculture. While practices which manipulate oxygen (O2) dynamics through metabolic demand and environmental O2 supply have been shown to impact juvenile growth rate in fish development, there has been no work exploring the effects of O2 at the subcellular level. In addition, manipulation of O2 supply or demand via changes in environmental factors such as O2 levels or salinity, may impact whole animal performance. Still, there has been little work exploring the physiological effects at a subcellular level. Mitochondria (mt) consume O2 and are pivotal in central metabolism, directly impacting growth, and dictating whole animal performance. Here we explore the effects of manipulating O2 demand and supply on mt in yellowtail kingfish ventricle and skeletal muscle by exposure to chronic hyperoxia (200% [O2], 35 ppt) and to hypoosmotic conditions (100% [O2], 17.5 ppt). Chronic exposure to hypoosmotic conditions resulted in greater overall biomass, while it lowered relative ventricular mass compared to control fish. Mitochondrial respiratory flux for most measures remained consistent with control fish, with the exception of cytochrome c oxidase (COX) respiration. Chronic hyperoxia had no impact on overall morphology, and no significant effect on ventricle mt respiration, yet increased COX activity in skeletal muscle. These data indicate that lowering routine mt O2 demands in S. lalandi with hypoosmotic conditions has more impact than increasing O2 availability, and that this may enhance biomass output while maintaining mt integrity.

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