In fish, maximum O-2 consumption rate ((M) over dot(O2,max)) 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 (M) over dot(O2,max), aerobic scope, cardiac function and blood parameters to address this knowledge gap. Relative to normoxia, (M) over dot(O2,max) was 33% higher under hyperoxia, and this drove a similar increase in aerobic scope. Cardiac output was significantly elevated under hyperoxia at (M) over dot(O2,max) because of increased stroke volume, indicating that hyperoxia released a constraint on cardiac contractility apparent with normoxia. Thus, hyperoxia improved maximal cardiac performance, thereby enhancing tissue O-2 delivery and allowing a higher (M) over dot(O2,max) Venous blood O-2 partial pressure (PvO(2)) was elevated in hyperoxia at (M) over dot(O2,max), suggesting a contribution of improved luminal O-2 supply in enhanced cardiac contractility. Additionally, despite reduced haemoglobin and higher PvO(2), hyperoxia treated fish retained a higher arterio-venous O-2 content difference at (M) over dot(O2,max). This may have been possible because of hyperoxia offsetting declines in arterial oxygenation that are known to occur following exhaustive exercise in normoxia. If this occurs, increased contractility at (M) over dot(O2,max) with hyperoxia may also relate to an improved O-2 supply to the compact myocardium via the coronary artery. Our findings show (M) over dot(O2,max) and aerobic scope may be limited in normoxia following exhaustive exercise as a result of constrained maximal cardiac performance and highlight the need to further examine whether or not exhaustive exercise protocols are suitable for eliciting (M) over dot(O2,max) and estimating aerobic scope in rainbow trout.