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.

1. The experiment was conducted to investigate the effects of dietary sodium butyrate on the growth performance and immune response of broiler chickens. In experiment 1, 240 1-d-old chickens were allocated into 4 dietary groups (0, 0·25, 0·50 or 1·00 g sodium butyrate/kg) with 6 replicates each. In experiment 2, 120 1-d-old chickens were fed a control diet (without sodium butyrate) or 1·00 g sodium butyrate/kg diet. Half of the chickens fed on each diet were injected intra-peritoneally with 0·5 g/kg body weight of Escherichia coli lipopolysaccharide (LPS) at 16, 18 and 20 d of age. 2. There was no effect of dietary sodium butyrate on growth performance. On d 21, serum interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) were decreased in chickens given 1·00 g sodium butyrate/kg, serum superoxide dismutase (SOD) and catalase activities were significantly increased, and malondialdehyde (MDA) was decreased by dietary sodium butyrate at 0·50 or 1·00 g/kg. On d 42, serum IL-6 was markedly decreased by dietary sodium butyrate, while 1·00 g sodium butyrate/kg greatly reduced MDA and increased catalase. 3. LPS challenge significantly reduced the growth performance of chickens. Serum IL-1β, IL-6, TNF-α, corticosterone, alpha-1 acid glycoprotein (AGP) and prostaglandin E(2) (PGE(2)) were increased in LPS-challenged chickens. Dietary sodium butyrate supplementation maintained the body weight gain and feed intake. Sodium butyrate supplementation inhibited the increase in IL-6 and AGP in serum at 16 d of age and TNF-α, corticosterone, AGP and PGE(2) at 20 d of age. Similar inhibitory effects of sodium butyrate in serum glucose and total protein concentrations were also found at 20 d of age. 4. The results indicated that dietary sodium butyrate supplementation can improve the growth performance in chickens under stress and that this may be used to moderate the immune response and reduce tissue damage.

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.

A total of 320 male Arbor Acres broiler chickens (28 days old) were randomly allotted to one of the three experimental diets supplemented with 0 (160 birds), 600 (80 birds) or 1200 mg/kg (80 birds) creatine monohydrate (CMH) for 14 days. On the morning of 42 day, after an 8-h fast, the birds of CMH-free group were divided into two equal groups, and all birds of these four groups were transported according to the follow protocol: 0.75-h transport without CMH supplementation (as a lower stress control group), 3-h transport without CMH supplementation, 3-h transport with 600 or 1200 mg/kg CMH supplementation. Each treatment group was composed of 8 replicates with 10 birds each. The results showed that supplementation of CMH for 14 days before slaughter did not affect the overall growth performance and carcass traits of stressed broilers (P>0.05). A 3-h transport decreased plasma glucose concentration, elevated plasma corticosterone concentration, increased bird live weight loss, breakdown of muscle glycogen, as well as the accumulation of muscle lactate (P<0.05), which induced some detrimental changes to breast meat quality (lower ultimate pH and higher drip loss, P<0.05). Nevertheless, supplementation of 1200 mg/kg CMH reduced chicken weight loss, decreased the contents of lactate and glycolytic potential in pectoralis major of 3-h transported broilers (P<0.05), which is beneficial to maintain breast meat quality by reducing the drip loss (P<0.05). These findings suggest that the reduction of muscle glycolysis is probably the reason for maintainance of meat quality by supplementation of CMH in transported broilers.

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Chronic heat exposure impairs the performance, intestinal morphology and appetite, which may be correlated with the increased secretion or gene expression of appetite-related hormones and genes, and the higher expression of nutrient-sensing receptors (T1R1 and T1R3) in broilers. © 2018 Society of Chemical Industry.

To investigate the mitochondrial decay and oxidative damage resulting from aging, the activities/ kinetics of the mitochondrial complexes were examined in the brains of young and old rats as well as in old rats fed R-α-lipoic acid plus acetyl-L-carnitine (LA/ALC). The brain mitochondria of old rats, compared with young rats, had significantly decreased endogenous antioxidants and superoxide dismutase activity; more oxidative damage to lipids and proteins; and decreased activities of complex I, IV and V. Complex I showed a decrease in binding affinity (increase in K m ) for substrates. Feeding LA/ALC to old rats partially restored age-associated mitochondrial dysfunction to the levels of the young rats. These results indicate that oxidative mitochondrial decay plays an important role in brain aging and that a combination of nutrients targeting mitochondria, such as LA/ALC, could ameliorate mitochondrial decay through preventing mitochondrial oxidative damage.