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-C-13] 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-C-13]phenylalanine enrichments, which remained elevated during the entire 4-h postprandial period (P < 0.05). Mixed-muscle protein-bound L-[1-C-13] 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-C-13] 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.