Resistance training in humans and mechanical overload in rodents do not elevate muscle protein lactylation.

Although several reports have hypothesized that exercise may increase skeletal muscle protein lactylation, empirical evidence in humans is lacking. Thus, we adopted a multi-faceted approach to examine if acute and subchronic resistance training (RT) altered skeletal muscle protein lactylation levels. In mice, we also sought to examine if surgical ablation-induced plantaris hypertrophy coincided with increases in muscle protein lactylation. To examine acute responses, participants' blood lactate concentrations were assessed before, during, and after eight sets of an exhaustive lower body RT bout (n = 10 trained college-aged men). Vastus lateralis biopsies were also taken before, 3-h post, and 6-h post-exercise to assess muscle protein lactylation. To identify training responses, another cohort of trained college-aged men (n = 14) partook in 6 weeks of lower-body RT (3x/week) and biopsies were obtained before and following the intervention. Five-month-old C57BL/6 mice were subjected to 10 days of plantaris overload (OV, n = 8) or served as age-matched sham surgery controls (Sham, n = 8). Although acute resistance training significantly increased blood lactate responses ∼7.2-fold (p < 0.001), cytoplasmic and nuclear protein lactylation levels were not significantly altered at the post-exercise time points, and no putative lactylation-dependent mRNA was altered following exercise. Six weeks of RT did not alter cytoplasmic protein lactylation (p = 0.800) despite significantly increasing VL muscle size (+3.5%, p = 0.037), and again, no putative lactylation-dependent mRNA was significantly affected by training. Plantaris muscles were larger in OV versus Sham mice (+43.7%, p < 0.001). However, cytoplasmic protein lactylation was similar between groups (p = 0.369), and nuclear protein lactylation was significantly lower in OV versus Sham mice (p < 0.001). The current null findings, along with other recent null findings in the literature, challenge the thesis that lactate has an appreciable role in promoting skeletal muscle hypertrophy.

Effects of 405 ± 5-nm LED Illumination on Environmental Stress Tolerance of Salmonella Typhimurium in Sliced Beef.

Salmonella Typhimurium is a widely distributed foodborne pathogen and is tolerant of various environmental conditions. It can cause intestinal fever, gastroenteritis and bacteremia. The aim of this research was to explore the effect of illumination with 405 nm light-emitting diodes (LEDs) on the resistance of S. Typhimurium to environmental stress. Beef slices contaminated with S. Typhimurium were illuminated by 405 nm LEDs (18.9 ± 1.4 mW/cm2) for 8 h at 4 °C; controls were incubated in darkness at 7 °C. Then, the illuminated or non-illuminated (control) cells were exposed to thermal stress (50, 55, 60 or 65 °C); oxidative stress (0.01% H2O2 [v/v]); acid stress (simulated gastric fluid [SGF] at pH 2 or 3); or bile salts (1%, 2%, or 3% [w/v]). S. Typhimurium treated by 405 nm LED irradiation showed decreased resistance to thermal stress, osmotic pressure, oxidation, SGF and bile salts. The transcription of eight environmental tolerance-related genes were downregulated by the illumination. Our findings suggest the potential of applying 405 nm LED-illumination technology in the control of pathogens in food processing, production and storage, and in decreasing infection and disease related to S. Typhimurium.

Survival and Environmental Stress Resistance of Cronobacter sakazakii Exposed to Vacuum or Air Packaging and Stored at Different Temperatures.

The aim of this study was to evaluate the survival of Cronobacter sakazakii exposed to vacuum or air packaging, then stored at 4, 10, or 25°C, and the environmental stress resistance of vacuum-packaged or air-packaged bacterial cells were determined by subjecting the cells to reconstituted infant formula at 50°C, in acid (simulated gastric fluid, pH = 3.5), and in bile salt [bile salt solution, 5% (wt/vol)]. A cocktail culture of C. sakazakii desiccated on the bottom of sterile petri plates was air-packaged or vacuum-packaged and then stored at 4, 10, or 25°C for 10 days. The viable cell populations during storage were examined, and the vacuum-packaged and air-packaged cells (stored at 10°C for 4 days) were subsequently exposed to heat, acid, or bile salt. The results show that the populations of vacuum-packaged and air-packaged C. sakazakii were reduced by 1.6 and 0.9 log colony-forming units (CFU)/ml at 4°C and by 1.6 and 1.3 log CFU/ml at 25°C, respectively, in 10 days. At 10°C, significant reductions of 3.1 and 2.4 log CFU/ml were observed for vacuum-packaged and air-packaged cells, respectively. Vacuum packaging followed by storage at 10°C for 4 days caused significant decreases in the resistance of C. sakazakii to heat, acid, and bile salt conditions compared with air packaging. These results suggest that the application of vacuum packaging for powdered infant formula could be useful to minimize the risk of C. sakazakii.