Abstract

Physiological mechanisms were measured in embryos from turkey hens of different ages to determine associations with declines in hatchability as breeder hens age. As the hens aged from 32 to 54 wk of age, embryonic viability declined (P < 0.05). The greatest proportional increase (P < 0.01) in embryonic mortality of aging hens occurred at the plateau stage in oxygen consumption or immediately thereafter at pipping. Eggshell conductance constants increased (P < 0.01) as hens aged but did not change after mid-lay, suggesting an alteration in respiration for the embryos in eggs produced by older hens compared to eggs produced by the same hens at younger ages. The alteration may cause embryos in eggs from older hens to reach the plateau stage in oxygen consumption (approximately 25 to 26 d of incubation) earlier in development than embryos from young hens. Hepatic and cardiac glycogen concentrations were greatest (P < 0.001) in embryos from hens at the youngest age and then declined (P < 0.05) as the hens aged. Embryonic blood plasma glucose concentrations declined (P < 0.05) similarly. Plasma thyroxine (T4) and triiodothyronine (T3) concentrations were measured in embryos from the hens at different ages as well. Increased (P < 0.05) T4 was evidenced in embryos from the youngest hens, whereas increased (P < 0.05) T3 activity was evident in embryos from hens of older ages. It was concluded that the decline in hatchability seen as turkey breeder hens age may have a basis in the differences seen in the physiology of hatching in embryos. Specifically, thyroid influences on growth and carbohydrate metabolism may be involved in decreased embryonic viability.

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