This study investigated the effects of acute heat stress and slaughter processing on poultry meat quality and carbohydrate metabolism. Broilers (200) were randomly divided into 2 groups receiving heat stress (HS; 36°C for one h), compared to a non-stressed control (C). At slaughter, each group was further divided into 2 groups for slaughter processing (L = laboratory; F = commercial factory). L group breasts were removed immediately after bleeding without carcass scalding or defeathering, and stored at 4°C. F group broilers were scalded (60°C, 45 s) after bleeding and defeathering. Then the breasts were removed and cooled in ice water until the core temperature was ≤4°C. Rates of Pectoralis core temperature and pH decline were changed by slaughter processing, but only HS affected ultimate pH in group L. HS muscles had higher L* values (P < 0.05) than controls at 24 h postmortem. Laboratory processing "hot-deboning" increased drip loss, which resulted in a lower cooked loss (P < 0.05). Postmortem glycolysis was affected only by HS. The speed of lactic acid accumulation and glycogen degradation was faster in the HS group than controls at 5 min postmortem. During storage the glycolysis rates were not different (P > 0.05). Sarcoplasmic protein solubility was higher in F processed birds (P < 0.05). HS decreased the solubility of myofibrillar and total protein in the L-slaughtered birds. Thus, HS caused a higher frequency of accelerated muscle glycolysis than controls. Factory processing (chilling) could not completely eliminate the effects of accelerated glycolysis caused by pre-slaughter HS.

Objective: To establish a new psoas muscle depletion index (PDI) from healthy young donors and to explore the correlation between the PDI and the severity of cirrhosis in patients with endstage liver disease (ESLD). Methods: Clinical data of 461 healthy donors were collected during the period 2014-2019, and clinical data of 331 patients with ESLD were collected during the period 2014-2018. The patients were divided into four groups by PDI severity: PDI ≥ 0.90, PDI = 0.75-0.90, PDI = 0.50-0.75 and PDI ≤ 0.50 (Gsev). Differences in international normalised ratio (INR), total bilirubin and serum creatinine levels, and Child-Pugh (CP) and model for end-stage liver disease (MELD) scores were compared. The sarcopenia incidence according to the PDI and the psoas muscle index (PMI) in different weight groups were also compared. Results: Gsev had the highest CP (10.2 ± 2.1) and MELD (20.1 ± 7.4) scores and total bilirubin (166.3 ± 192.0 umol/L) and blood creatinine (92.9 ± 90.2 umol/L) levels and the lowest haemoglobin (93.8 ± 21.7 g/L) and blood albumin (30.9 ± 5.8 g/L) levels. Gsev showed significant changes in INR (1.74 ± 0.65) and blood sodium (135.3 ± 5.65 mmol/L). If PDI <0.75 was used as the diagnostic criterion for sarcopenia, the incidence was 53.3% in patients weighing >90 kg and 53.6% in those weighing <60 kg. This differed from the PMI, with an incidence of 3.3% in patients weighing >90 kg. Conclusions: The PDI had no significant correlation with body height, body weight or body mass index (BMI) in healthy individuals and patients with ESLD. The PDI was significantly correlated with the severity of cirrhosis and loss of skeletal muscle.