Abstract
Normally, preslaughter acute heat stress could accelerate postmortem glycolysis and impair chicken breast (pectoralis major muscle) quality. However, previous studies indicated that it might be different when the acute heat stress temperature rises to an extreme range (above 35°C). Therefore, this study's objectives were to compare the pH decline, glycolytic enzyme activity, and AMP-activated protein kinase (AMPK) phosphorylation at early postmortem among three extreme acute heat stress temperature settings: a control group (36°C) and two experimental groups (38°C and 40°C). Although the temperature did not affect glycogen phosphorylase a and pyruvate kinase activity, there was a decrease in pH decline rate, phosphofructokinase-1 activity, and phospho-AMPK-α[Thr172] within 4h postmortem when temperature increased from 36 to 40°C. Temperature also affected hexokinase activity, with the 36°C-group having the highest activity. The results of the current study, for the first time, indicated that postmortem metabolic rate in chicken breast muscle could be changed by acute heat stress temperature setting at extreme range.
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