Abstract

Studies have been demonstrating in poultry, the existence of at least two causes for the formation of PSE meat: genetic through the sensibility towards halothane and the environmental factor in particular the temperature as the main factor. Thus the objective of this work was to evaluate halothane as stressor agent for broiler concomitantly to evaluating the PSE incidence by submitting these birds to thermal stress. In this experiment, 24 broilers of commercial lineage were divided in 6 animals for 4 treatments: HHH, broilers submitted to halothane test and slaughtered 1h after this test; HET broilers submitted to halothane at 35°C/1h after 48h of halothane test followed by the birds slaughtering; EET, broilers submitted to thermal stress and slaughtered immediately after this treatment, and finally the control treatment (CCC) where broilers were not submitted to halothane test nor to thermal stress as control. The initial pH of Pectoralis major m, was evaluated 30 min post mortem and the pH final, color, (L*, a*, b*) water holding capacity (WHC), and R value analysis were carried out after 24h of storage of fillet samples at 40C. The pH24h was higher (p ? 0.05) for CCC samples in comparison to other treatments and R value was higher for birds under HET and EET treatments in comparison to CCC (p ? 0.05) suggesting that the rigor mortis was more rapid in samples from birds submitted to thermal stress. The HHH, HET, and EET treatments presented 4 birds each with PSE meat and 2 broilers from CCC treatment originated PSE meat showing the influence not only halothane but also the thermal stress over broilers welfare. Finally, results demonstrated that halothane is a stressor agent as well as the thermal stress and both promoted dramatic biochemical changes bringing about the formation of broiler PSE meat.

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