Daytime low tides that lead to high-temperature events in stranded rock pools often co-occur with algae-mediated hyperoxia as a result of strong solar radiation. Recent evidence shows aerobic metabolic scope (MS) can be expanded under hyperoxia in fish but so far this possibility has not been examined in intertidal species despite being an ecologically relevant scenario. Furthermore, it is unknown whether hyperoxia increases the upper thermal tolerance limits of intertidal fish and, therefore, their ability to withstand extreme high-temperature events. Therefore, we measured the metabolic response (massspecific rate of oxygen consumption, Ṁ O2 ) to thermal ramping (21-29°C) and the upper thermal tolerance limit (U TL ) of two intertidal triplefin fishes (Bellapiscis medius and Forsterygion lapillum) under hyperoxia and normoxia. Hyperoxia increased maximal oxygen consumption (Ṁ O2,max ) and MS of each species at ambient temperature (21°C) but also after thermal ramping to elevated temperatures such as those observed in rock pools (29°C). While hyperoxia did not provide a biologically meaningful increase in upper thermal tolerance of either species (>31°C under all conditions), the observed expansion of MS at 29°C under hyperoxia could potentially benefit the aerobic performance, and hence the growth and feeding potential, etc., of intertidal fish at non-critical temperatures. That hyperoxia does not increase upper thermal tolerance in a meaningful way is cause for concern as climate change is expected to drive more extreme rock pool temperatures in the future and this could present a major challenge for these species.

Hyperoxia occurs when water oxygen (O2) levels exceed normal atmospheric pressure (i.e., >100% air saturation). Fish can experience hyperoxia in shallow environments due to photosynthesis or in aquaculture through O2 supplementation. This review provides a comprehensive synthesis of the effects of hyperoxia on fish, spanning influences on cardiorespiratory function, acid‐base balance, oxidative stress and whole animal performance (e.g., thermal tolerance and growth). Fish hypoventilate in hyperoxia, but arterial and venous blood oxygenation increases in spite of reduced convection. Persistently high levels of blood oxygenation in hyperoxia do not commonly result in reduced blood O2 carrying capacity, but assessments in undisturbed fish are required to clarify this. Hypoventilation also causes the retention of carbon dioxide, hence respiratory acidosis. Another consequence of hyperoxia is increased levels of oxidative stress and concomitant changes to antioxidant defence systems. Despite these changes, however, the bulk of evidence shows no effect of hyperoxia on growth. Hyperoxia does impact the aerobic metabolic rate of fish with either no effect or elevated resting metabolic rate and substantial increases in maximum metabolic rate. There is also evidence that hyperoxia increases aerobic capacity improves cardiac performance and mitigates anaerobic stress during acute warming. Along with improved upper thermal tolerance in some species, these findings collectively suggest that hyperoxia might provide fish a metabolic refuge during acute warming. Since hyperoxia occurs in shallow aquatic habitats, further research establishing the ecophysiological implications of concomitant heat stress and hyperoxia is pertinent, particularly with a changing climate.

Intertidal fish species face gradual chronic changes in temperature and greater extremes of acute thermal exposure through climate-induced warming. As sea temperatures rise, it has been proposed that whole-animal performance will be impaired through oxygen and capacity limited thermal tolerance [OCLTT; reduced aerobic metabolic scope (MS)] and, on acute exposure to high temperatures, thermal safety margins may be reduced because of constrained acclimation capacity of upper thermal limits. Using the New Zealand triplefin fish (), this study addressed how performance in terms of growth and metabolism (MS) and upper thermal tolerance limits would be affected by chronic exposure to elevated temperature. Growth was measured in fish acclimated (12 weeks) to present and predicted future temperatures and metabolic rates were then determined in fish at acclimation temperatures and with acute thermal ramping. In agreement with the OCLTT hypothesis, chronic exposure to elevated temperature significantly reduced growth performance and MS. However, despite the prospect of impaired growth performance under warmer future summertime conditions, an annual growth model revealed that elevated temperatures may only shift the timing of high growth potential and not the overall annual growth rate. While the upper thermal tolerance (i.e. critical thermal maxima) increased with exposure to warmer temperatures and was associated with depressed metabolic rates during acute thermal ramping, upper thermal tolerance did not differ between present and predicted future summertime temperatures. This suggests that warming may progressively decrease thermal safety margins for hardy generalist species and could limit the available habitat range of intertidal populations.

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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