مهندسی کشاورزی-علوم دامی
دانشگاه تربيت مدرس
گروه پژوهشی شتر مرغ
گروه پژوهشی شترمرغ
Abstract The aim of this study was to evaluate the effects of thermal manipulation (TM) during pre and post-hatch periods on thermotolerance of male broiler chickens exposed to chronic heat stress (CHS) during the finisher phase (34 ± 2°C, 6 h/day). Seven hundred fertile eggs of Ross 308 were assigned to the following groups: 1) control group incubated and housed in standard conditions, 2) pre-hatch treatment (PRE), the eggs were exposed to 39.5°C and 65% RH for 12 h, d from embryonic d 7 to 16 and after hatching the chicks where housed in standard conditions; 3 and 4) post-hatch TM at d 3 (PO3) and post-hatch TM at d 5 (PO5), which had the same incubation conditions as control and exposed to 36 to 38°C for 24 h at 3 and 5 days of age, respectively. TM in PRE group resulted in delay in the hatch time (6 h) along with reduction in body weight compared to control (P = 0.02). TM caused a significant reduction of facial surface temperature (FST) until d 28 (P < 0.02), but not significant during CHS. Body weight gain was suppressed in PO3 and PO5 groups at d 14 (P = 0.007) and compensated at d 28. However, TM led to higher BWG (P = 0.000) but lower FCR (P = 0.03) and mortality at the first week of CHS compared to control. European production efficiency index was higher in TM-treated chickens compared to control (P = 0.01). TM reduced the blood concentration of uric acid, total protein, T3, and T4 in which thyroid hormones in PO3 and PO5 treatments showed more reduction rather than other groups. In PRE group, chickens had lower abdominal fat pad than control (P = 0.0001). The relative weight of heart was decreased in TM groups (P = 0.001). It was concluded that TM may induce thermotolerance in growing broilers, possibly through the modification of physiological parameters of broilers especially during the first week of CHS
This investigation was carried out to study the influence of thermal manipulation (TM) during pre- and post-hatch periods on European production efficiency index (EPEI), intestinal morphology and microbiota, and long bone characteristics of male broilers subjected to the Chronic Heat Stress (CHS). Seven hundred fertile eggs were assigned to the following groups: 1) Control group incubated and housed in standard conditions, 2) Pre-Hatch Treatment (PRE), the eggs were exposed to 39.5◦C and 65% RH for 12 h/d from embryonic day 7 to 16 and after hatching the chicks were housed in standard conditions; 3) and 4) post- hatch TM at day 3 (PO3) and post-hatch TM at day 5 (PO5), which had the same incubation conditions as control and exposed to 36 to 38◦C for 24 h at 3 and 5 days of age, respectively. The mortality at the TM-treated groups were significantly (P ≤ 0.05) lower compared to control during CHS, and Post-hatch Group showed the lowest mortality. The EPEI was higher in TM-treated chickens compared to control (P ≤ 0.015). The TM has not any significant effect on intestinal microbiota (P ≥ 0.05). TM significantly increased the tibia length (P ≤ 0.05) and width (P ≤ 0.048). Thermal manipulation caused significant changes in the height and area of villus (P ≤ 0.05). TM-treated groups had higher villus height. It can be concluded that TM may improve the height of villus, long bone characteristics, and decrease mortality rate due to the adaptation and thermotolerance in broilers exposed to CHS
Heat stress is becoming one of the most significant environmental stressors challenging chickens worldwide. The detrimental effects of heat stress on broilers range from reduced growth and meat production to decreased meat quality. Thus, it is critical to know how heat stress can affect meat quality, which is the determining factor that influences the consumer acceptability and the price of meat products. Three primary mechanisms were suggested to explain this phenomenon: 1) Rapid drop in pH during and after slaughter due to the anaerobic metabolism that accelerates the accumulation of lactic acid while the temperature of muscle is high. The high temperature and low pH conditions facilitate the denaturation of sarcoplasmic proteins, which lowers the water-holding capacity of muscle; 2) Heat stress induces panting that increases the pH of the body fluid and initiate metabolic acidosis by activating enzymes related to anaerobic glycolysis in skeletal muscle. Also, the production of corticosterone hormone that increases the protein degradation in live animals; 3) The reactive oxygen species (ROS) produced by heat stress increases the oxidative stress in live animals, which can damage the structure and the functions of the enzymes that regulate sarcoplasmic calcium levels in muscles. Thus, the sarcoplasmic calcium level remains high. This induces constant muscle contractions mainly using the energy produced by the anaerobic metabolism, which will continue even after the animal has died. This review discusses the scientific evidence about how heat stress affects the quality of chicken meat.