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Abstract Parents must decide how to allocate energy gained from foraging between self and offspring. Storm-petrels (Procellariiformes: Hydrobatidae) are pelagic seabirds that travel hundreds of kilometers across multiple days before returning to the nesting burrow to feed a dependent chick. Parents return to the nest with food stored in the proventriculus, a portion of which is regurgitated to their offspring. As the chick grows, provisioning demands increase. However, it is unknown whether parents meet this increasing demand by (1) altering their foraging strategies to acquire more food or (2) allocating a greater proportion of their intake to the chick. We designed, validated, and implemented a new technology—the Burrow Scale Monitor—to measure Leach's storm-petrels (Hydrobates leucorhous) as they entered and exited the nesting burrow. We monitored breeding adults over the first 30 d of chick rearing to determine whether storm-petrel parents adjust their foraging intake to the age of the chick or simply adjust energy allocation at the nest. Food delivery increased with chick age, but this increase was driven to a much greater extent by parents delivering a greater proportion of their body mass as food (ie, a shift in parental allocation) rather than by adults adjusting their foraging strategy to match chick age. Only by measuring adult body mass on arrival and exit at the nesting burrow could we understand how parents adapt their provisioning strategy to the increasing demands of the growing chick. 

ABSTRACT The ability of organisms to effectively respond to challenges is critical for survival. We investigated how an acute stressor affected corticosterone, mitochondrial function, and DNA oxidative damage in a wild population of Leach's storm‐petrels (Hydrobates leucorhous). We conducted a standardized 20‐min handling procedure on storm‐petrel chicks and collected baseline and post‐handling blood samples. We measured plasma corticosterone and red blood cell DNA oxidative damage levels through the detection of a mutated DNA base 8‐Hydroxy‐2'‐deoxyguanosine (8‐OHdG). In addition, we quantified six measures of mitochondrial aerobic metabolism from red blood cells. Overall, the handling stressor increased plasma corticosterone levels and decreased mitochondrial efficiency to produce ATP. Although the increase in corticosterone was inversely related to the change in DNA oxidative damage, the decrease in mitochondrial efficiency was positively correlated with the change in DNA oxidative damage. Thus, over an acute stress response, individuals who had the largest increase in corticosterone also had the least amount of oxidative damage. In addition, individuals who prioritized ATP production during the acute stress also showed higher levels of oxidative damage. This work highlights the complex pathways by which corticosterone and mitochondrial efficiency affect oxidative damage during acute stress, providing new insights into the trade‐offs underlying physiological responses in wild animals.