Postnatal development in the cold render bird mitochondria more susceptible to heat stress.

Research on birds suggests that extreme weather events during development may have long-lasting consequences on form and function. The underlying cellular mechanisms mediating such phenotypic effects are poorly studied. We raised Japanese quail in warm (30°C) or cold (10°C) temperatures from hatching until adulthood and then measured mitochondrial metabolism in intact blood cells at representative normothermic body temperature (41°C) and a hyperthermic temperature (45°C), that quail commonly attain when heat stressed. To investigate whether any postnatal developmental effects were reversible, half of the cold- and warm-acclimated birds were assigned to a common garden (20°C) three weeks before the measurements. Across groups, hyperthermia was associated with increased proton leak but decreased phosphorylating respiration (where ATP is produced) and maximal working capacity of the mitochondria. Cold-reared birds were more strongly affected by heat stress: the increase in proton leak was 1.6-fold higher compared with warm-acclimated birds. This did not reflect developmental programming, as the difference did not remain in the common-garden birds. Our study describes the cellular consequences of overheating and suggests that cold acclimation during postnatal development is traded off against heat tolerance at the level of cellular metabolism. These findings have potential implications for understanding avian responses to climate change.