In endotherms, growth, reproduction, and survival are highly depended on energy metabolism. Maintenance of constant body temperature can be challenging for endotherms under continuously changing environmental conditions, such as low or high ambient temperatures or limited food. Thus, many birds may drop body temperature below normothermic values during the night, known as rest-phase hypothermia, presumably to decrease energy metabolism. Under the assumption of the positive link between aerobic metabolism and reactive oxygen species, it is reasonable to suggest that low body temperature, a proxy of energy metabolism, will affect oxidative stress of the birds. Aging may considerably affect behavior, performance and physiology in birds and still requires further investigation to understand age-specific changes along the lifespan of the organism. Until today, age-specific rest-phase hypothermic responses and their effect on oxidant-antioxidant status have never been investigated. We exposed 25 zebra finches (Taeniopygia guttata) of three age classes, 12 young birds (1.1–1.3 years old), 8 middle-aged (2.4–2.8 years old), and 5 old birds (4.2–7.5 years old) to day-long food deprivation or provided them normal access to food under thermoneutral conditions. We compared night-time body temperature, measured through implanted data loggers, and quantified plasma oxidative status (uric acid, antioxidant capacity, and d-ROM assay) the following morning. We found age-related differences in night-time body temperature following a day-long food deprivation while all three age groups remained normothermic in the night following a day with access to food. The lowest minimum body temperature (LSM ± SE: 36.6 ± 0.2°C) was observed in old individuals during rest-phase hypothermia. Surprisingly, these old birds also revealed the highest levels of plasma oxidative damage, while young and middle-aged birds maintained higher night-time body temperature and showed lower values of oxidative damage. These results lead us to propose a novel hypothesis on how aging may lead to an accumulation of oxidative damage; the impaired physiological capacity to thermoregulate with advancing age does increase the risk of oxidative stress under challenging conditions. When energy is limited, the risk to encounter oxidative stress is increasing via a compensation to defend normothermic body temperatures.

Animal life requires hard work but the ability to endure such workload appears to be limited. Heat dissipation limit (HDL) hypothesis proposes that the capacity to dissipate the excess of body heat during hard work may limit sustained energy use. Experimental facilitations of heat loss rate via feather-clipping in free-living birds seem to support HDL hypothesis but testing of HDL through laboratory experiments under controlled conditions is not reported. We employed a two-factorial experimental design to test HDL hypothesis by manipulating the capacity to dissipate heat through exposure of captive zebra finches (Taeniopygia guttata) to a cold and warm ambient temperature (14°C and 25°C), and through manipulation of the insulating layer of feathers around the brood patch in females (clipped and unclipped). To simulate foraging costs encountered in the wild we induced foraging effort by employing a feeding system that necessitated hovering to access food, which increased energetic costs of reproduction despite ad libitum conditions in captivity. We quantified the outcome of reproductive performance at the level of both parents, females, and offspring. Thermal limitations due to warm temperature appeared at the beginning of reproduction for both parents with lower egg-laying success, smaller clutch size and lower egg mass, compared to the cold. After hatching, females with an enhanced ability to dissipate heat through feather-clipping revealed higher body mass compared to unclipped females, and these clipped females also raised heavier and bigger nestlings. Higher levels for oxidative stress in plasma of females were detected prior to reproduction in warm conditions than in the cold. However, oxidative stress biomarkers of mothers were neither affected by temperature nor by feather-clipping during the reproductive activities. We document upregulation of antioxidant capacity during reproduction that seems to prevent increased levels of oxidative stress possibly due to the cost of female body condition and offspring growth. Our study on reproduction under laboratory-controlled conditions corroborates evidence in line with the HDL hypothesis. The link between temperature-constrained sustained performance and reproductive output in terms of quality and quantity is of particular interest in light of the current climate change, and illustrates the emerging risks to avian populations.

Eco-immunology considers resistance to antigens a costly trait for an organism, but actual quantification of such costs appears not straight forward. Costs of the immune response (IR) are e.g., visible in impaired coloration, reduced growth or reproductive success. Activation of the humoral IR is a slow, complex, and long-lasting process, which makes the quantification of its energetic cost a potential losing game. We implemented near continuous measurements of body temperature in zebra finches (Taeniopygia guttata) as a proxy for the energetic cost with particular interests in the body temperature from activation of the humoral IR until the peak of antibody release several days later. At the peak of the antibody release we additionally measured oxygen consumption (open-flow respirometry) and markers of oxidative stress (dROMs, OXY). Birds with activated IR defended a higher night time body temperature during the first four nights after an immune challenge in comparison to controls, implying increased night time energy use. At the peak of antibody production, we did not find differences in night time body temperature and oxygen consumption but observed a differentiated results for oxygen consumption during day time. Immune challenged females had significantly higher oxygen consumption than other groups. Moreover, we found that activation of the humoral IR increases oxidative damage, a potential cost of defending higher night time body temperature crucial at the early stage of the IR. The costs generated by the immune system appear to consist of two components energetic and non-energetic, and these may appear separated in time.