Stress inevitably occurs from the farm to abattoir in modern livestock husbandry. The effects of stress on the behavioral and physiological status and ultimate meat quality have been well documented. However, reports on the mechanism of stress effects on physiological and biochemical changes and their consequent effects on meat quality attributes have been somewhat disjointed and limited. Furthermore, the causes of variability in meat quality traits among different animal species, muscle fibers within an animal, and even positions within a piece of meat in response to stress are still not entirely clear. This review 1st summarizes the primary stress factors, including heat stress, preslaughter handling stress, oxidative stress, and other stress factors affecting animal welfare; carcass quality; and eating quality. This review further delineates potential stress‐induced pathways or mediators, including AMP‐activated protein kinase‐mediated energy metabolism, crosstalk among calcium signaling pathways and reactive oxygen species, protein modification, apoptosis, calpain and cathepsin proteolytic systems, and heat shock proteins that exert effects that cause biochemical changes during the early postmortem period and affect the subsequent meat quality. To obtain meat of high quality, further studies are needed to unravel the intricate mechanisms involving the aforementioned signaling pathways or mediators and their crosstalk.

Indigenous chickens possess desirable characteristics and account for considerable proportions of the total chicken production in China. The current study examined the growth performance, carcass characteristics and muscle metabolites among a crossbred broiler and two indigenous, yellow-feathered chickens (Mahuang and Tuer) with different ages (60 and 75 days). Results indicated that the crossbred broiler had better feed efficiency, higher breast and thigh muscle yield, as well as a lower abdominal fat percentage than Mahuang and Tuer chickens (p < 0.05). Gas chromatography–mass spectrometry-based metabolomics and multivariate analysis revealed sugars, amino acids and organic acids were the predominant metabolites that differed among the three chicken breeds. Growth performance and carcass traits of yellow-feathered chickens exhibited significant differences with the extension of the feeding period (p < 0.05). Moreover, differential metabolites reflected altered aminoacyl-tRNA biosynthesis, ATP-binding cassette transporters, pantothenate and CoA biosynthesis, as well as glutathione metabolism in yellow-feathered chickens affected by age. Collectively, this study contributes to a deeper understanding of the production efficiency and chemical composition of precursor flavor in Chinese indigenous, yellow-feathered chicken.

Objective: This work was conducted to investigate the effects of oxidative stress on meat quality, mitochondrial function, calcium metabolism and ferroptosis of broilers.Methods: In this study, a total of 144 one-day-old male Ross 308 chicks were divided into 3 groups (control group, saline group, and hydrogen peroxide [H2O2] group) with 6 replicates of 8 broilers each. The study lasted for 42 d. The broilers in the saline and H2O2 groups were intraperitoneally injected with 0.75% saline and 10.0% H2O2 on the 16th and 37th day of the experimental period respectively, the injection volumes were 1.0 mL/kg of broiler body weight. On the 42nd day of the experimental period, two chicks were randomly selected from each cage, a total of thirty-six chicks were stunned by electric shock and slaughtered to collect breast muscle samples.Results: The H2O2 exposure reduced pH value, increased drip loss and shear force of breast meat (p<0.05), impaired the ultrastructure and function of mitochondria. The H2O2 exposure damaged the antioxidant system in mitochondria, excessive reactive oxygen species carbonylation modified calcium channels on mitochondria, which impaired the activities of key enzymes on calcium channel, resulted in the increased calcium concentration in cytoplasm and mitochondria (p<0.05). In addition, the H2O2 exposure increased the iron content and lipid peroxidation (p<0.05), which induced ferroptosis.Conclusion: Oxidative stress could impair meat quality by causing mitochondrial dysfunction, resulting in calcium metabolism disorder and ferroptosis.

The current study is designed to investigate dietary guanidinoacetic acid (GAA) supplementation on the growth performance, intestinal histomorphology, and jejunum mucosal barrier function of broilers that are subjected to chronic heat stress (HS). A total of 192 male broilers (28-d old) were randomly allocated to four groups. A chronic HS model (at a temperature of 32 °C and 50%–60% relative humidity for 24 h daily) was applied in the experiment. Normal control (NC, ad libitum feeding, 22 °C), HS group (HS, ad libitum feeding, 32 °C), pair-fed group (PF, received food equivalent to that consumed by the HS group on the previous day, 22 °C), guanidinoacetic acid group (HG, ad libitum feeding, supplementing the basal diet with 0.6 g/kg GAA, 32 °C). The experiment lasted from 28 to 35 and 28 to 42 d of age of broilers. Our results showed that broilers subjected to HS had lower average daily feed intake and average daily gain (P < 0.05), higher feed-to-gain ratio and relative length of the small intestine (P < 0.05), as well as lower relative weight and weight per unit length of the small intestine (P < 0.05). HS damaged the small intestinal histomorphology by decreasing the small intestinal VH and the VH/CD (P < 0.05). Compared with the HS group, supplementation with 0.6 g/kg GAA increased jejunal VH and VH/CD (P < 0.05), but decreased relative weight and relative length of the small intestine (P < 0.05). Moreover, in comparison with NC, HS elevated intestinal permeability (D-Lactic acid concentration and diamine oxidase activity) and mRNA expression levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α (P < 0.05), reduced jejunal mucus thickness, number of goblet cells, IgA⁺cell density, and mucin2 mRNA expression level of broilers (P < 0.05). Compared with the HS group, dietary GAA elevated jejunal mucus thickness, goblet cell number and IgA⁺ cell density (P < 0.05), and up-regulated jejunal mRNA expression of interleukin-1β and tumor necrosis factor-α (P < 0.05). In conclusion, HS impaired growth performance, and the intestinal mucosal barrier function of broilers. Dietary supplementation with 0.6 g/kg GAA alleviated HS-induced histomorphology changes of small intestine and jejunal mucosal barrier dysfunction. With the global warming getting worse, heat stress (HS) has been a serious problem faced by poultry industry. As one of the main target organs, the intestine is easily affected by HS. Broilers are particularly sensitive to hot temperatures, and HS occurs when temperatures rise above the optimum (16–26 °C). Moreover, ambient humidity below 40% and above 80% also affects broilers adversely. HS can impair intestinal morphology and function of the intestinal barrier. The intestinal mucosal barrier not only plays key roles in nutrient digestion and absorption but also serves as the innate defense barrier fending off noxious substances within the intestinal luminal environment. Therefore, protecting intestinal mucosal barrier from HS is important to animal health. Nutrient regulation is an economical and effective method to alleviate HS of intensively-farmed broiler chickens. The results of current study demonstrated that chronic HS impaired the growth performance and intestinal mucosal barrier function of broilers, while dietary supplementation with 0.6 g/kg guanidinoacetic acid improved intestinal histomorphology and alleviated intestinal barrier dysfunction of broilers subjected to chronic HS, which is beneficial for improving health of broilers.