In fish, maximum O2 consumption rate (MO2max) and aerobic scope can be expanded following exhaustive exercise in hyperoxia; however, the mechanisms explaining this are yet to be identified. Here, in exhaustively exercised rainbow trout (Oncorhynchus mykiss), we assessed the influence of hyperoxia on MO2max, aerobic scope, cardiac function and blood parameters to address this knowledge gap. Relative to normoxia, MO2max was 33% higher under hyperoxia, and this drove a similar increase in aerobic scope. Cardiac output, due to increased stroke volume, was significantly elevated under hyperoxia at MO2max indicating hyperoxia released a constraint on cardiac contractility apparent with normoxia. Thus, hyperoxia improved maximal cardiac performance, thereby enhancing tissue O2 delivery and allowing a higher MO2max. Venous blood O2 partial pressure (PvO2) was elevated in hyperoxia at MO2max, suggesting a contribution of improved luminal O2 supply in enhanced cardiac contractility. Additionally, despite reduced haemoglobin and higher PvO2, hyperoxia treated fish retained a higher arterio-venous O2 content difference at MO2max. This may have been possible due to hyperoxia offsetting declines in arterial oxygenation known to occur following exhaustive exercise in normoxia. If this occurs, increased contractility at MO2max with hyperoxia may also relate to an improved O2 supply to the compact myocardium via the coronary artery. Our findings show MO2max and aerobic scope may be limited in normoxia following exhaustive exercise due to constrained maximal cardiac performance and highlight the need to further examine whether or not exhaustive exercise protocols are suitable for eliciting MO2max and estimating aerobic scope in rainbow trout.

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