The Effects of an Acute Bout of Neuromuscular Electrical Stimulation on Anabolic Signaling of the mTORC1 Pathway in Individuals with Chronic Stroke
MetadataShow full metadata
Stroke causes limited ability to produce voluntary muscle contraction and movement on one side of the body leading to further muscle wasting and weakness. Neuromuscular electrical stimulation (NMES) is often used to facilitate involuntary muscle contraction; however, the effect of NMES on muscle growth in hemiparetic muscle is not clear. PURPOSE: To determine the skeletal muscle anabolic response of an acute bout of NMES in individuals with chronic stroke and healthy older adults. METHODS: This study employed a two-group, pretest/posttest design. Ten individuals (59 ± 2.81 years old) were divided into two groups, a chronic stroke group (STROKE: n = 4) or a healthy older adult control group (CON: n = 6). A muscle biopsy was obtained from the vastus lateralis of the hemiparetic leg for STROKE and the right leg for CON before and 30 min after the NMES intervention. The NMES protocol consisted of a 60 Hz stimulation train of 10 seconds on and 15 seconds off which was repeated for 60 minutes. Phosphorylation of mTOR and p70S6K were analyzed using the SDS-PAGE Western blot technique. Phosphorylation is expressed as the ratio of phosphorylated to total protein content. Data were analyzed using two-way repeated measures analysis of variance. Data are reported as mean ± SE with statistical significance set at p < 0.05. RESULTS: An acute bout of NMES increased the phosphorylation of mTOR after stimulation (CON: 0.67 ± 0.10 vs. 1.01 ± 0.06; STROKE: 0.64 ± 0.15 vs. 0.99 ± 0.14; p < 0.01) and p70S6K (CON: 0.85 ± 0.13 vs. 2.18 ± 0.32; STROKE: 1.03 ± 0.29 vs. 2.56 ± 0.96; p < 0.01) from resting levels to 30 min following the NMES treatment, respectively. Phosphorylated protein content was not different between STROKE and CON (p > 0.05) following NMES. CONCLUSIONS: These findings suggest that NMES, in addition to facilitating muscle contraction, may initiate cellular processes that facilitate skeletal muscle growth and strengthening in healthy older and post-stroke populations.