A single session of neuromuscular electrical stimulation does not augment postprandial muscle protein accretion

The loss of muscle mass and strength that occurs with aging, termed sarcopenia, has been ( at least partly ) attributed to an impaired muscle protein synthetic response to food intake. Previously, we showed that neuromuscular electrical stimulation ( NMES ) can stimulate fasting muscle protein synthesis rates and prevent muscle atrophy during disuse. We hypothesized that NMES prior to protein ingestion would increase postprandial muscle protein accretion. Eighteen healthy elderly ( 69 ± 1 yr ) males participated in this study. After a 70-min unilateral NMES protocol was performed, subjects ingested 20 g of intrinsically l-[1-13C]phenylalanine-labeled casein. Plasma samples and muscle biopsies were collected to assess postprandial mixed muscle and myofibrillar protein accretion as well as associated myocellular signaling during a 4-h postprandial period in both the control ( CON ) and stimulated ( NMES ) leg. Protein ingestion resulted in rapid increases in both plasma phenylalanine concentrations and l-[1-13C]phenylalanine enrichments, which remained elevated during the entire 4-h postprandial period ( P < 0.05 ). Mixed-muscle protein-bound l-[1-13C]phenylalanine enrichments increased significantly over time following protein ingestion, with no differences between the CON ( 0.0164 ± 0.0019 MPE ) and NMES ( 0.0164 ± 0.0019 MPE ) leg ( P > 0.05 ). In agreement, no differences were observed in the postprandial rise in myofibrillar protein bound l-[1-13C]phenylalanine enrichments between the CON and NMES legs ( 0.0115 ± 0.0014 vs. 0.0133 ± 0.0013 MPE, respectively, P > 0.05 ). Significant increases in mTOR and P70S6K phosphorylation status were observed in the NMES-stimulated leg only ( P < 0.05 ). We conclude that a single session of NMES prior to food intake does not augment postprandial muscle protein accretion in healthy older men.