Acute rises in glucocorticoid hormones allow individuals to adaptively respond to environmental challenges but may also have negative consequences, including oxidative stress. While the effects of chronic glucocorticoid exposure on oxidative stress have been well characterized, those of acute stress or glucocorticoid exposure have mostly been overlooked. We examined the relationship between acute stress exposure, glucocorticoids and oxidative stress in Japanese quail (Coturnix japonica). We (i) characterized the pattern of oxidative stress during an acute stressor in two phenotypically distinct breeds; (ii) determined whether corticosterone ingestion, in the absence of acute stress, increased oxidative stress, which we call glucocorticoid-induced oxidative stress (GiOS); and (iii) explored how prior experience to stressful events affected GiOS. Both breeds exhibited an increase in oxidative stress in response to an acute stressor. Importantly, in the absence of acute stress, ingesting corticosterone caused an acute rise in plasma corticosterone and oxidative stress. Lastly, birds exposed to no previous acute stress or numerous stressful events had high levels of GiOS in response to acute stress, while birds with moderate prior exposure did not. Together, these findings suggest that an acute stress response results in GiOS, but prior experience to stressors may modulate that oxidative cost.

Elevations in glucocorticoid levels (GCs) in breeding females may induce adaptive shifts in offspring life histories. Offspring produced by mothers with elevated GCs may be better prepared to face harsh environments where a faster pace of life is beneficial. We examined how experimentally elevated GCs in pregnant or lactating North American red squirrels (Tamiasciurus hudsonicus) affected offspring postnatal growth, structural size, oxidative stress levels (two antioxidants and oxidative protein damage) in three different tissues (blood, heart, liver), and liver telomere lengths. We predicted that offspring from mothers treated with GCs would grow faster but would also have higher levels of oxidative stress and shorter telomeres, which may predict reduced longevity. Offspring from mothers treated with GCs during pregnancy were 8.3% lighter around birth but grew (in body mass) 17.0% faster than those from controls, whereas offspring from mothers treated with GCs during lactation grew 34.8% slower than those from controls and did not differ in body mass around birth. Treating mothers with GCs during pregnancy or lactation did not alter the oxidative stress levels or telomere lengths of their offspring. Fast-growing offspring from any of the treatment groups did not have higher oxidative stress levels or shorter telomere lengths, indicating that offspring that grew faster early in life did not exhibit oxidative costs after this period of growth. Our results indicate that elevations in maternal GCs may induce plasticity in offspring growth without long-term oxidative costs to the offspring that might result in a shortened lifespan.

Building on the predictions of state‐dependent life‐history theory, telomeres are hypothesized to either correlate with or function as an adaptive, proximate mediator of an individual's behaviour and life‐history strategy. To further understand the relationship between telomeres, behaviour and life‐history strategies, we measured male behaviour, telomere lengths and telomere dynamics in a free‐living population of known‐age, male wire‐tailed manakins Pipra filicauda. Male wire‐tailed manakins perform coordinated displays with other males at leks and these displays form the basis of long‐term coalition partnerships. Males exhibit consistent individual differences in the number of social partners within their social network and the frequency of social interactions. Male sociality is also positively correlated with both social rise and reproductive success. We measured male behaviour using a telemetry‐based, proximity datalogging system and blood telomere lengths were quantified using qPCR. We examined the relationships between telomere length, telomere dynamics, social status, and male behaviour. We also quantified the repeatability of telomere lengths, examined age‐related changes in telomere length, and tested for instances of telomere elongation that exceed residual error in telomere length. Telomere length was found to be highly repeatable. More social males exhibited shorter telomeres and higher rates of telomere attrition. Telomeres did not significantly vary with age within or between individuals in either of the male social classes. Two out of 25 individuals exhibited patterns telomere elongation that exceeded residual error in telomere measurements. Here we show that telomeres consistently vary between male wire‐tailed manakins and these differences are related to variation in male social behaviour. In this relatively long‐lived species, telomeres appear to be flexible traits that can increase or decrease in length. Overall, this study provides observational support for the hypothesis that telomeres act as a molecular marker that relates to behaviour in a state‐dependent manner. We also provide insight into the molecular consequences of individual variation in male social behaviour. A free Plain Language Summary can be found within the Supporting Information of this article.

19Elevations in glucocorticoid levels (GCs) in breeding females may induce adaptive shifts in 20 offspring life histories. Offspring produced by mothers with elevated GCs may be better 21 prepared to face harsh environments where a faster pace of life is beneficial. We examined how 22 experimentally elevated GCs in pregnant or lactating North American red squirrels 23 (Tamiasciurus hudsonicus) affected offspring growth in body mass, structural (skeletal) size, 24 oxidative stress levels (balance of two antioxidants and one measure of oxidative protein 25 damage) in three different tissues (blood, heart, liver), and liver telomere lengths. We predicted 26 that offspring from mothers treated with GCs would grow faster but would also have higher 27 levels of oxidative stress and shorter telomeres, which may predict reduced longevity. Offspring 28 from mothers treated with GCs during pregnancy grew (in body mass) 17.0% faster than those 29 from controls, whereas offspring from mothers treated with GCs during lactation grew 34.8% 30 slower than those from controls. Treating mothers with GCs during pregnancy or lactation did 31 not alter the oxidative stress levels or telomere lengths of their offspring. Fast-growing offspring 32 from any of the treatment groups did not have higher oxidative stress levels or shorter telomere 33 lengths, indicating that offspring that grew faster early in life (~1 to 25 d of age) did not exhibit 34 oxidative costs after this period of growth, when these measures of oxidative stress and telomere 35 lengths were obtained (~70 d of age). Our results indicate that elevations in maternal GCs may 36 induce plasticity in offspring growth without long-term oxidative costs to the offspring that 37 might result in a shortened lifespan. 38 39

Maternal stress during reproduction can influence how offspring respond to stress later in life. Greater lifetime exposure to glucocorticoid hormones released during stress is linked to greater risks of behavioral disorders, disease susceptibility, and mortality. The immense variation in individual’s stress responses is explained, in part, by prenatal glucocorticoid exposure. To explore the long-term effects of embryonic glucocorticoid exposure, we injected Japanese quail (Coturnix japonica) eggs with corticosterone. We characterized the endocrine stress response in offspring and measured experienced aggression at three different ages. We found that prenatal glucocorticoid exposure affected (1) the speed at which the stress response was terminated suggesting dysregulated negative feedback, (2) baseline corticosterone levels in a manner dependent on current environmental conditions with higher levels of experienced aggression associated with higher levels of baseline corticosterone, (3) the magnitude of an acute stress response based on baseline concentrations. We finish by proposing a framework that can be used to test these findings in future work. Overall, our findings suggest that the potential adaptive nature of prenatal glucocorticoid exposure is likely dependent on environmental context and may also be tempered by the negative effects of longer exposure to glucocorticoids each time an animal faces a stressor.