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Studies have demonstrated that chronic heat stress can accelerate glycolysis, decrease glycogen content in muscle, and affect muscle quality. However, the consequences of chronic heat stress on glycogen synthesis, miRNA expression in pectoralis major (PM) muscle, and its regulatory functions remain unknown. In this study, high-throughput sequencing and cell experiments were used to explore the effects of chronic heat stress on miRNA expression profiles and the regulatory mechanisms of miRNAs in glycogen synthesis under chronic heat stress. In total, 144 cocks were allocated into 3 groups: the normal control (NC) group, the heat stress (HS) group, and the pair-fed (PF) group. In total, 30 differently expressed (DE) miRNAs were screened after excluding the effect of feed intake, which were mainly related to metabolism, signal transduction, cell growth and death. Furthermore, the gga-miR-212-5p/GYS1axis was predicted to participate in glycogen synthesis through the miRNA-mRNA analysis, and a dual-luciferase reporter test assay confirmed the target relationship. Mechanistically, chronic heat stress up-regulated gga-miR-212-5p, which could inhibit the expression of GYS1in the PM muscle. Knocking down gga-miR-212-5p alleviates the reduction of glycogen content caused by chronic heat stress; overexpression of gga-miR-212-5p can reduce glycogen content. This study provided another important mechanism for the decreased glycogen contents within the PM muscle of broilers under heat stress, which might contribute to impaired meat quality.

Heat stress (HS) largely impairs the quality of broiler breast meat through protein oxidative modification. This study aimed to investigate the carbonylation pattern of Ca2+channels and apoptotic proteins in the breast muscle of heat-stressed broilers. A total of 144 twenty-eight-day-old male Arbor Acres broilers were randomly divided into three treatment groups. The normal control (NC) group was kept at 22°C and provided with unlimited feed. The HS group was exposed to 32°C and provided with unlimited feed. The pair-fed (PF) group was kept at 22°C and given an amount of feed equivalent to that consumed by the HS group on the previous day. Results showed that broilers under HS conditions had a higher respiratory rate than those in NC and PF groups (P< 0.05). HS disrupted the morphology and structure of breast muscle fibers by decreasing the average diameters and average density of myofibers compared to the NC group (P< 0.05). HS increased the mean fluorescence intensity of the positive carbonyl signal in breast muscle compared with the NC group (P< 0.05). Besides, the pectoral Ca2+concentration in the sarcoplasmic reticulum, cytoplasm, and mitochondria was elevated by HS when compared with the NC group (P< 0.05). In comparison to the NC and PF groups, HS increased the apoptosis rate and caspase-3 activity in the breast muscle (P< 0.05). Furthermore, HS elevated the relative protein expressions of plasma membrane Ca2+-ATPase, Na+/Ca2+exchanger 1, and sarco/endoplasmic reticulum calcium transport ATPase 1 compared to the NC group (P< 0.05). Higher relative protein expression of μ-calpain and lower relative protein expression of cytosolic cytochrome complex were found in the HS group than the NC group (P< 0.05). HS decreased the carbonylation levels of transient receptor potential canonical 1 and inositol 1,4,5-trisphosphate receptor compared to the NC group (P< 0.05). Additionally, the carbonylation levels of cleaved caspase-3 and precursor caspase-9 were increased and decreased, respectively, by HS treatment compared to the NC group (P< 0.05). In conclusion, HS damages the myofiber based on Ca2+dyshomeostasis and apoptosis, which are potentially associated with protein carbonylation. These results shed new light on the possible mechanism behind the development of poor meat quality in broilers due to HS.