Heat stress is one of the most important environmental stressors for the poultry industry in the world. Reduced growth rate, low feed efficiency, impaired immunological responses, changes in intestinal microflora, and deterioration of meat quality are the consequences of acute or chronic heat stress. In terms of meat quality, 3 primary mechanisms have been suggested to explain this phenomenon: 1) rapid drop in pH during and after slaughter due to the glycogen conversion to increase in lactic acid accumulation especially when the muscle temperature is high, a combination of high temperature and low pH that facilitates the denaturation of sarcoplasmic proteins resulting in lower water-holding capacity of muscle; 2) acceleration of panting to dissipate body heat, which increases CO2 exhalation and pH drop in blood, initiates metabolic acidosis in skeletal muscle. Increase in panting is also associated with a high release of corticosteroid hormones; 3) the reactive oxygen species produced by heat stress increases the oxidative stress in the birds, which can damage the structure and functions of the enzymes that regulate sarcoplasmic calcium levels in muscles. Overall, these changes in the muscle cells accentuate energy expenditure due to constant muscle contractions. This review discusses the scientific evidence about how heat stress affects the quality of chicken meat through the acid/base status, oxidative reactions, and changes in hormonal secretions.

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.

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