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.

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.

A better understanding of the genetic and phenotypic architecture underlying life-history variation is a longstanding aim in biology. Theories suggest energy metabolism determines life-history variation by modulating resource acquisition and allocation trade-offs, but the genetic underpinnings of the relationship and its dependence on ecological conditions have rarely been demonstrated. The strong genetic determination of age-at-maturity by two unlinked genomic regions ( vgll3 and six6 ) makes Atlantic salmon ( Salmo salar ) an ideal model to address these questions. Using more than 250 juveniles in common garden conditions, we quantified the covariation between metabolic phenotypes—standard and maximum metabolic rates (SMR and MMR), and aerobic scope (AS)—and the life-history genomic regions, and tested if food availability modulates the relationships. We found that the early maturation genotype in vgll3 was associated with higher MMR and consequently AS. Additionally, MMR exhibited physiological epistasis; it was decreased when late maturation genotypes co-occurred in both genomic regions. Contrary to our expectation, the life-history genotypes had no effects on SMR. Furthermore, food availability had no effect on the genetic covariation, suggesting a lack of genotype-by-environment interactions. Our results provide insights on the key organismal processes that link energy use at the juvenile stage to age-at-maturity, indicating potential mechanisms by which metabolism and life-history can coevolve.