Physiological mechanisms determining thermal limits in fishes are debated but remain elusive. It has been hypothesised that motor function loss, observed as loss of equilibrium during acute warming, is due to direct thermal effects on brain neuronal function. To test this, we mounted cooling plates on the heads of Atlantic cod (Gadus morhua) and quantified whether local brain cooling increased wholeorganism acute upper thermal tolerance. Brain cooling reduced brain temperature by 2-6°C below ambient water temperature and increased thermal tolerance by 0.5 and 0.6°C on average relative to instrumented and uninstrumented controls, respectively, suggesting that direct thermal effects on brain neurons may contribute to setting upper thermal limits in fish. However, the improvement in thermal tolerance with brain cooling was small relative to the difference in brain temperature, demonstrating that other mechanisms (e.g. failure of spinal and peripheral neurons, or muscle) may also contribute to controlling acute thermal tolerance.

Significance Plastic individuals can buffer environmental changes, maintaining a stable performance across gradients. Plasticity is therefore thought to be particularly beneficial for the survival of wild populations that experience large environmental fluctuations, such as diel and seasonal temperature changes. Maintaining plasticity is widely assumed to be costly; however, empirical evidence demonstrating this cost is scarce. Here, we predict that if plasticity is costly, it would be readily lost in a stable environment, such as a laboratory. To test this, we measured a diverse range of phenotypic traits, spanning gene expression, physiology, and behavior, in wild and laboratory zebrafish acclimated to 15 temperatures. We show that laboratory fish have lost plasticity in many traits, demonstrating that maintaining plasticity carries a cost.

Temperature has a dramatic effect on the physiology of ectothermic animals, impacting most of their biology. When temperatures increase above optimal for an animal, their growth gradually decreases. The main mechanism behind this growth rate reduction is unknown. Here, we suggest the 'aerobic scope protection' hypothesis as a mechanistic explanation for the reduction in growth. After a meal, metabolic rate, and hence oxygen consumption rate, transiently increases in a process called specific dynamic action (SDA). At warmer temperatures, the SDA response usually becomes temporally compressed, leading to a higher peak oxygen consumption rate. This peak in oxygen consumption rate takes up much of the animal's aerobic scope (the difference between resting and maximum rates of oxygen consumption), leaving little residual aerobic scope for other functions (e.g. foraging, predator avoidance, immune function). We propose that water-breathing ectothermic animals will protect their postprandial residual aerobic scope by reducing meal sizes in order to regulate the peak SDA response during times of warming, leading to reductions in growth. This hypothesis is consistent with the published literature on fishes, and we suggest predictions to test it.

Temperature has a dramatic effect on the physiology of ectothermic animals, impacting most of their biology. When temperatures increase above optimal for an animal, their growth rate tends to decrease. The mechanism behind this growth rate reduction is unknown. Here, we suggest the aerobic scope protection hypothesis as a mechanistic explanation for the reduction in growth. After a meal, metabolic rate, and hence oxygen consumption rate, transiently increases in a process called specific dynamic action (SDA). At warmer temperatures, the SDA response becomes temporally compressed, leading to a higher peak oxygen consumption rate. This peak in oxygen consumption rate takes up much of the animal’s aerobic scope (the difference between maximum and resting rates of oxygen consumption), leaving little residual aerobic scope for other functions. We propose that animals will actively protect their postprandial residual aerobic scope by reducing meal sizes in order to regulate the peak SDA response. This hypothesis is consistent with the published literature and we suggest further predictions to test it.

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