title: Neuromuscular electrical stimulation prevents muscle wasting in critically ill comatose patients.
abstract: Fully sedated patients, being treated in the intensive care unit (ICU), experience substantial skeletal muscle loss. Consequently, survival rate is reduced and full recovery after awakening is compromised. Neuromuscular electrical stimulation (NMES) represents an effective method to stimulate muscle protein synthesis and alleviate muscle disuse atrophy in healthy subjects. We investigated the efficacy of twice-daily NMES to alleviate muscle loss in six fully sedated ICU patients admitted for acute critical illness [n=3 males, n=3 females; age 63 ± 6 y; APACHE II (Acute Physiology and Chronic Health Evaluation II) disease-severity-score: 29 ± 2]. One leg was subjected to twice-daily NMES of the quadriceps muscle for a period of 7 ± 1 day whereas the other leg acted as a non-stimulated control (CON). Directly before the first and on the morning after the final NMES session, quadriceps muscle biopsies were collected from both legs to assess muscle fibre-type-specific cross-sectional area (CSA). Furthermore, phosphorylation status of the key proteins involved in the regulation of muscle protein synthesis was assessed and mRNA expression of selected genes was measured. In the CON leg, type 1 and type 2 muscle-fibre-CSA decreased by 16 ± 9% and 24 ± 7% respectively (P<0.05). No muscle atrophy was observed in the stimulated leg. NMES increased mammalian target of rapamycin (mTOR) phosphorylation by 19 ± 5% when compared with baseline (P<0.05), with no changes in the CON leg. Furthermore, mRNA expression of key genes involved in muscle protein breakdown either declined [forkhead box protein O1 (FOXO1); P<0.05] or remained unchanged [muscle atrophy F-box (MAFBx) and muscle RING-finger protein-1 (MuRF1)], with no differences between the legs. In conclusion, NMES represents an effective and feasible interventional strategy to prevent skeletal muscle atrophy in critically ill comatose patients.
authors.affiliation: *NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, The Netherlands.
authors.forename: Marlou L
authors.initials: ML
authors.lastname: Dirks
authors.affiliation: †Jessa Hospital, Heart Centre Hasselt, Hasselt, and Rehabilitation Research Center (REVAL), Hasselt University, Faculty of Medicine, Diepenbeek, Belgium.
authors.forename: Dominique
authors.initials: D
authors.lastname: Hansen
authors.affiliation: †Jessa Hospital, Heart Centre Hasselt, Hasselt, and Rehabilitation Research Center (REVAL), Hasselt University, Faculty of Medicine, Diepenbeek, Belgium.
authors.forename: Aimé
authors.initials: A
authors.lastname: Van Assche
authors.affiliation: †Jessa Hospital, Heart Centre Hasselt, Hasselt, and Rehabilitation Research Center (REVAL), Hasselt University, Faculty of Medicine, Diepenbeek, Belgium.
authors.forename: Paul
authors.initials: P
authors.lastname: Dendale
authors.affiliation: *NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, The Netherlands.
authors.forename: Luc J C
authors.initials: LJ
authors.lastname: Van Loon
mesh_terms: D000328:Adult; D000368:Aged; D001706:Biopsy; D016292:Procedural Sedation / Q000009:adverse effects; D003422:Critical Care / Q000379:methods; D016638:Critical Illness / Q000628:therapy*; D004599:Electric Stimulation Therapy / Q000379:methods*; D005260:Female; D015870:Gene Expression; D006801:Humans; D007362:Intensive Care Units; D008297:Male; D008875:Middle Aged; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D009124:Muscle Proteins / Q000096:biosynthesis / Q000235:genetics; D009133:Muscular Atrophy / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D010766:Phosphorylation; D052097:Quadriceps Muscle / Q000473:pathology / Q000503:physiopathology; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D009124:Muscle Proteins; D012333:RNA, Messenger