OP019 EXPLORATION OF WHAT LEVEL OF PROTEIN IS NEEDED FOR MUSCLE MASS ACCRETION DURING WEIGHT LOSS WITH RESISTANCE TRAINING IN OBESE ELDERLY

Abstract

Rationale: Recent studies from our laboratory have indicated that glycine represents an effective anti-inflammatory agent that attenuates muscle loss in tumour-bearing mice. However, it remains to be established whether glycine affects skeletal muscle directly. The aim was to investigate how muscle cell health, metabolism and inflammation are affected by glycine. Methods: After differentiation, C2C12 myotubes were incubated with either 2.5mM glycine or 2.5mM alanine and exposed to 1) lipopolysaccharide (LPS, 1mg/mL) for 24 h to induce an inflammatory response and wasting; or 2) serum free media (SFM) for 48 h to induce wasting. Myotube diameter was assessed and changes in intracellular [Ca2+] were monitored by loading cells with Fluo-4/AM and imaging using confocal microscopy Protein synthesis was determined using SunSET methodology. Insulin-mediated glucose uptake was determined using fluorescent deoxyglucose and anabolic signalling was assessed using routine western blot analyses. One way ANOVA was used to identify differences between groups. Results: Serum withdrawal reduced protein synthesis in myotubes by 25% (P < 0.05). Interestingly, glycine treatment completely prevented this decrease. LPS-treated myotubes were 25% smaller, had an 80% higher intracellular [Ca2+], and a 40% reduction in insulin-mediated glucose uptake compared with control cells (P < 0.05). Glycine treatment reduced the loss of myotube diameter by 50% and improved insulinmediated glucose uptake and Akt phosphorylation by 40% and 10%, respectively (P < 0.05). Conclusion: Glycine protects muscle cells from various catabolic stimuli in vitro, thereby maintaining protein synthesis, anabolic signalling and insulin-mediated glucose transport. These findings suggest a direct protective effect of glycine on skeletal muscle.