Flying animals generate large amounts of heat, which must be dissipated to avoid overheating. In birds, heat dissipation is complicated by feathers, which cover most body surfaces and retard heat loss. To understand how birds manage heat budgets during flight, it is critical to know how heat moves from the skin to the external environment. Hummingbirds are instructive because they fly at speeds from 0 to more than 12 m s−1, during which they transit from radiative to convective heat loss. We used infrared thermography and particle image velocimetry to test the effects of flight speed on heat loss from specific body regions in flying calliope hummingbirds (Selasphorus calliope). We measured heat flux in a carcass with and without plumage to test the effectiveness of the insulation layer. In flying hummingbirds, the highest thermal gradients occurred in key heat dissipation areas (HDAs) around the eyes, axial region and feet. Eye and axial surface temperatures were 8°C or more above air temperature, and remained relatively constant across speeds suggesting physiological regulation of skin surface temperature. During hovering, birds dangled their feet, which enhanced radiative heat loss. In addition, during hovering, near-body induced airflows from the wings were low except around the feet (approx. 2.5 m s−1), which probably enhanced convective heat loss. Axial HDA and maximum surface temperature exhibited a shallow U-shaped pattern across speeds, revealing a localized relationship with power production in flight in the HDA closest to the primary flight muscles. We conclude that hummingbirds actively alter routes of heat dissipation as a function of flight speed.

The annual cycle of a migrating bird involves metabolically distinct stages of substantial fatty acid storage and periods of increased fatty acid mobilization and utilization, and thus requires a great deal of phenotypic flexibility. Specific mechanisms directing stage transitions of lipid metabolism in migrants are largely unknown. This study characterized the role of the PPARs ( peroxisome proliferatoractivated receptors) in regulating migratory adiposity of the gray catbird (Dumetella carolinensis). Catbirds increased adipose storage during spring and autumn migration and showed increased rates of basal lipolysis during migration and tropical overwintering. Expression of the PPAR target genes involved in fat uptake and storage, FABPpm and PLIN3, increased during pre-migratory fattening. We found significant correlation between PPARγ and target gene expression in adipose but little evidence that PPARα expression levels drive metabolic regulation in liver during the migratory cycle.

Phenotypic flexibility across the annual cycle allows birds to adjust to fluctuating ecological demands. Varying energetic demands associated with time of year have been demonstrated to drive metabolic and muscle plasticity in birds, but it remains unclear what molecular mechanisms control this flexibility. We sampled gray catbirds at five stages across their annual cycle: tropical overwintering (January), northward spring (late) migration (early May), breeding (mid June), the fall pre-migratory period (early August) and southward fall (early) migration (end September). Across the catbird's annual cycle, cold-induced metabolic rate (V O2summit) was highest during migration and lowest during tropical wintering. Flight muscles exhibited significant hypertrophy and/or hyperplasia during fall migratory periods compared with breeding and the fall pre-migratory period. Changes in heart mass were driven by the tropical wintering stage, when heart mass was lowest. Mitochondrial content of the heart and pectoralis remained constant across the annual cycle as quantified by aerobic enzyme activities (CS, CCO), as did lipid catabolic capacity (HOAD). In the pectoralis, transcription factors PPARα, PPARδ and ERRβ, coactivators PGC-1α and β, and genes encoding proteins associated with fat uptake (FABPpm, Plin3) were unexpectedly upregulated in the tropical wintering stage, whereas those involved in fatty acid oxidation (ATGL, LPL, MCAD) were downregulated, suggesting a preference for fat storage over utilization. Transcription factors and coactivators were synchronously upregulated during pre-migration and fall migration periods in the pectoralis but not the heart, suggesting that these pathways are important in preparation for and during early migration to initiate changes to phenotypes that facilitate long-distance migration.

Physiology-life history interactions suggest that birds living with a fast 'pace-of-life' should have higher metabolic capacity to provision higher reproductive activity. Previous work supports this, but does not consider migration. We measured summit metabolism ( _ VO 2 summit ) in Northern Waterthrush (Parkesia noveboracensis) while wintering in the Republic of Panama, migrating northwards through eastern North America, and while breeding in northeastern North America. _ VO 2 summit is similar between breeding and overwintering (non-migratory) and is significantly elevated in migration. These data suggest that migration is a driver of phenotypic flexibility in these birds and that migration, like winter survival, may be an important determinant of connections between life history and physiology.

Prenatal exposure to excess androgen may result in impaired adult fertility in a variety of mammalian species. However, little is known about what feedback mechanisms regulate gonadotropin secretion during early gestation and how they respond to excess T exposure. The objective of this study was to determine the effect of exogenous exposure to T on key genes that regulate gonadotropin and GnRH secretion in fetal male lambs as compared with female cohorts. We found that biweekly maternal testosterone propionate (100 mg) treatment administered from day 30 to day 58 of gestation acutely decreased (P < .05) serum LH concentrations and reduced the expression of gonadotropin subunit mRNA in both sexes and the levels of GnRH receptor mRNA in males. These results are consistent with enhanced negative feedback at the level of the pituitary and were accompanied by reduced mRNA levels for testicular steroidogenic enzymes, suggesting that Leydig cell function was also suppressed. The expression of kisspeptin 1 mRNA, a key regulator of GnRH neurons, was significantly greater (P < .01) in control females than in males and reduced (P < .001) in females by T exposure, indicating that hypothalamic regulation of gonadotropin secretion was also affected by androgen exposure. Although endocrine homeostasis was reestablished 2 weeks after maternal testosterone propionate treatment ceased, additional differences in the gene expression of GnRH, estrogen receptor-β, and kisspeptin receptor (G protein coupled receptor 54) emerged between the treatment cohorts. These changes suggest the normal trajectory of hypothalamic-pituitary axis development was disrupted, which may, in turn, contribute to negative effects on fertility later in life.

Evidence suggests that the hypothalamic–pituitary–gonadal (HPG) axis is active during the critical period for sexual differentiation of the ovine sexually dimorphic nucleus, which occurs between gestational day (GD) 60 and 90. Two possible neuropeptides that could activate the fetal HPG axis are kisspeptin and neurokinin B (NKB). We used GD85 fetal lambs to determine whether intravenous administration of kisspeptin-10 (KP-10) or senktide (NKB agonist) could elicit luteinizing hormone (LH) release. Immunohistochemistry and fluorescent in situ hybridization (FISH) were employed to localize these peptides in brains of GD60 and GD85 lamb fetuses. In anesthetized fetuses, KP-10 elicited robust release of LH that was accompanied by a delayed rise in serum testosterone in males. Pretreatment with the GnRH receptor antagonist (acyline) abolished the LH response to KP-10, confirming a hypothalamic site of action. In unanesthetized fetuses, senktide, as well as KP-10, elicited LH release. The senktide response of females was greater than that of males, indicating a difference in NKB sensitivity between sexes. Gonadotropin-releasing hormone also induced a greater LH discharge in females than in males, indicating that testosterone negative feedback is mediated through pituitary gonadotrophs. Kisspeptin and NKB immunoreactive cells in the arcuate nucleus were more abundant in females than in males. Greater than 85% of arcuate kisspeptin cells costained for NKB. FISH revealed that the majority of these were kisspeptin/NKB/dynorphin (KNDy) neurons. These results support the hypothesis that kisspeptin–GnRH signaling regulates the reproductive axis of the ovine fetus during the prenatal critical period acting to maintain a stable androgen milieu necessary for brain masculinization.

Background: Northern Cardinals (Cardinalis cardinalis) are able to endure drastic seasonal variations in ambient temperature. Many endotherms in these conditions utilize heterothermy (e.g., torpor) to conserve energy by adjusting their body temperatures according to changing environmental conditions. Previous research shows that cardinals reduce energy expenditure during winter nights. By examining whole-animal function, we asked whether this reduced metabolism was a result of decreased activity or an induced state of torpor. We measured body mass, percent fat content, metabolic rate (V O 2 ) across a range of ambient temperatures and body temperature (T b ) using data loggers during both summer (August to early September) and winter (December to January) conditions. We hypothesized that: (a) daily winter T b fluctuations would reveal an induced torpor, and (b) alterations of insulation would play a significant role in thermoregulation.Results: Although insulation in the form of fat stores was higher in the winter, there was no seasonal difference in whole body conductance. We found no evidence for torpor, but found a slight depression in overall circadian temperature rhythms for the winter animals compared to summer animals, resulting in a predicted 10-16 % savings in daily energy expenditure. Conclusions:Our findings support recent work showing that thermoregulatory mechanisms are not as fixed as previously thought and, while fat deposits may function to increase insulation, they are more likely important for fuel storage. These data identify subtle changes in the homeostatic set point for body temperature and show that these slight alterations can have significant impacts on daily energy expenditure in wild birds.

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