Chronic Heat Stress Impairs the Quality of Breast-Muscle Meat in Broilers by Affecting Redox Status and Energy-Substance Metabolism

• Published in: Journal of agricultural and food chemistry Vol. 65; no. 51; pp. 11251 - 11258
• Main Authors: Lu, Zhuang, He, Xiaofang, Ma, Bingbing, Zhang, Lin, Li, Jiaolong, Jiang, Yun, Zhou, Guanghong, Gao, Feng
• Format: Journal Article
• Language: English
• Published: United States American Chemical Society 27.12.2017
• Subjects: breast meat; breast muscle; citrate (si)-synthase; drip loss; gene expression; glycolysis; heat; heat stress; intramuscular fat; lipids; meat quality; messenger RNA; mitochondria; oxidative stress; phosphorylation; pyruvate kinase; temperature; meat quality; broilers; chronic heat stress; mitochondria; energy metabolism
• ISSN: 0021-8561; 1520-5118; 1520-5118
• DOI: 10.1021/acs.jafc.7b04428

We investigated the molecular mechanisms by which chronic heat stress impairs the breast-meat quality of broilers. Broilers were assigned to three groups: the normal control (NC) group, heat-stress (HS) group, and pair-fed (PF) group. After 7 days of heat exposure (32 °C), the high temperature had caused oxidative stress; elevated the activity of citrate synthase (CS), the mRNA expression of M-CPT1, and the phosphorylation level of AMPKα; and reduced the mRNA expression of avUCP. After 14 days of heat exposure, the heat stress had increased the lightness and drip loss and decreased the pH and shear force of the breast meat. Additionally, the heat exposure had increased the mRNA expressions of FAS, ACC, and PDK4; the content of lipids; and the activities of lactic dehydrogenase and pyruvate kinase, and it had decreased the mRNA expression of M-CPT1 and the activity of CS. In conclusion, chronic heat stress impairs meat quality by causing mitochondria to malfunction and affecting energy-substance aerobic metabolism, resulting in increased glycolysis and intramuscular fat deposition.