Cardiorespiratory and thermal responses to hypercapnia of broiler chicks exposed to CO2 in the incubation

The concentration of gases in the incubator influences gas exchange of the embryo. It is known that high concentrations of CO₂ in the air can reduce the time for hatching and result in heavier hatched chicks. However, it is not clear the late-life consequences of an early life CO₂ exposure of chickens. The CO₂ concentration can be increased in warehouses because of the high density setting. We aimed to evaluate the cardiorespiratory and thermal responses to hypercapnia of chicks exposed to CO₂ during incubation period. The eggs were incubated with 0 and 1% CO₂ during the first ten days of incubation. With ten days old, males and females, were exposed to hypercapnia (7% CO₂) and pulmonary ventilation, arterial pH and gases, mean arterial blood pressure (MAP) and heart rate, body temperature (T_b), metabolic rate (VO2) were measured. Male incubated with 1% CO₂ hypercapnia presented higher ventilation than in normocapnia. Conversely, ventilation of females in hypercapnia was not influenced by incubation condition. Blood gases chicks, males and females, incubated 1% of CO₂ were lower in hypercapnia. Hypercapnia induced bradycardia in all groups (p < 0.001), but the CO₂ exposure during incubation period did not alter the cardiovascular responses to hypercapnia in post-hatch animals. There were no significant effects of incubation treatment or gender in the MAP, T_b and VO2 of animals in normocapnia and hypercapnia. Hypercapnia causes an increase of VE/VO2 in both gender regardless of treatment during incubation. In conclusion, the hypercapnia triggers cardiorespiratory responses in chicks incubated with CO₂ regardless of gender, but the effect of CO₂ incubation is more pronounced in male chicks which presented an attenuated ventilatory response to hypercapnia.