No abstract

Two experiments were conducted to investigate the effect of RH (35, 60, and 85%) on thermoregulation of broiler chickens at high (35 degrees C) and mild (30 degrees C) temperatures at the age of 4 wk. The effects of humidity on rectal temperature (RT) and plumage temperature at back (PBAT) and skin temperature at breast (SBRT) were determined at 1, 4, 8, 16, and 24 h after exposure. The RT, PBAT, and SBRT were all significantly increased by high temperature (35 degrees C). Humidity had a significant influence on RT at 35 degrees C but not at 30 degrees C. The peripheral temperatures (PBAT and SBRT) were significantly affected by humidity but responded differently at high (35 degrees C) compared with mild temperature (30 degrees C). In conclusion, high humidity above 60% impaired the heat transmission from body core to the periphery at 35 degrees C but facilitated it at 30 degrees C in 4-wk-old broiler chickens. The effect of humidity on nonevaporative heat loss was depended on air temperature, as nonevaporative heat loss was suppressed by high humidity (>60% RH) at high temperature but enhanced at the mild temperature. The effect of humidity on the relationship between peripheral and core temperature depends on ambient temperature as well as on the age of the broiler chicken. The disturbance of thermal balance could not be determined only by changes in RT or peripheral temperature at a single time point but could be determined by mean body temperature within a certain time frame.

Three trials were conducted to investigate the effect of RH (35, 60, and 85%) on thermoregulation of 1-wk-old broiler chickens at different temperatures (35, 30, and 25 degrees C). The response to humidity in rectal temperature and plumage temperature at the back and breast within 24 h after exposure were recorded at 5 time points (1,4,8,16, and 24 h). Humidity affected the thermoregulation of 1-wk-old broiler chickens by redistributing heat within the body at high, low, and thermoneutral temperatures. The redistribution of heat resulted in decreased rectal temperature and increased peripheral temperature, which were, respectively, beneficial and unfavorable at high and low temperatures. These results suggested that feedback effects of surface temperature on core temperature also exist in poultry, as already observed in mammals, and could be induced not only by changed ambient temperature but also by the changes in humidity at high temperature. The disturbance of thermal equilibrium could not be established solely by changes in RT, but rather core and surface temperatures had to be considered. The daily rhythms in rectal and surface temperatures were affected by humidity.

Three experiments were conducted to evaluate the effects of preslaughter physiological states mimicked by long- or short-term administration of corticosterone (CORT) and dietary energy sources on muscle glycogen contents and meat quality of broiler chickens. In experiment 1, the broilers were fed a high lipid diet (LD) or a normal diet (ND) that differed in carbohydrate (3.8%) and lipid (2.5%) contents from 21 d of age. From 28 d of age onwards, 50% of the chickens in each dietary treatment were subjected to CORT treatment (30 mg/kg of diet). At 7 and 11 d after CORT supplementation, musculus pectoralis major was sampled before and immediately after slaughter and analyzed for glycogen, pH, and R-value. In experiment 2, broilers, fed with the LD or ND diet from 21 d of age were subjected to 1 single s.c. injection of CORT (4 mg/kg of BW) for 3 h to mimicked acute stress at 46 d of age. In experiment 3, broiler chickens were supplied with water supplemented with glucose (30 g/L) for 1 wk before slaughter and were then subjected to the same CORT treatment as experiment 2. Blood and muscle samples were respectively obtained before and immediately after slaughter and analyzed for plasma glucose, urate and lactic acid, and muscle variables. Plasma concentrations of glucose and urate were significantly increased by acute CORT administration, whereas the lactic acid was not changed. Neither dietary energy source nor water glucose supplementation had any influence on the plasma variables. Dietary energy source or water glucose supplementation could not alter glycogen stores in musculus pectoralis major. Breast muscle glycogen stores were increased by stress mimicked by long-term CORT administration rather than by acute treatment. Preslaughter stress reactions had no relation to the depletion of breast muscle glycogen during the initial postmortem period. The initial breast muscle pH was significantly decreased by long-term CORT administration. The result suggests that short-term upregulation of circulating CORT is not involved in the elevated drip loss induced by preslaughter stress.