Hypoxia during incubation and its effects on broiler's embryonic development.

In all vertebrates, hypoxia plays an important role in fetal development, driving vasculogenesis, angiogenesis, hematopoiesis, and chondrogenesis. Therefore, the ability to sense and respond to changes in the availability of oxygen (O2) is crucial for normal embryonic development as well as for developmental plasticity. Moderate levels of hypoxia trigger a regulated process which leads to adaptive responses. Regulation of angiogenesis by hypoxia is an important component of homeostatic control mechanisms that link the cardio-pulmonary-vascular O2 supply to metabolic demands in local tissues. Hypoxia leads to the activation of genes that are important for cell and tissue adaptation to low O2 conditions, such as hypoxia-inducible factor 1. Previous studies have shown a dose-response effect to hypoxia in chicken embryos, with lower and/or prolonged O2 levels affecting multiple mechanisms and providing a spectrum of responses that facilitate the ability to maintain O2 demand despite environmental hypoxia. In chicken embryos, mild to extreme hypoxia during embryogenesis improves chorioallantoic membrane and cardiovascular development, resulting in an increase in O2 carrying capacity and leading to developmental plasticity that may affect post-hatch chick performance and improve adaptation to additional environmental stresses at suboptimal environmental conditions.