PMID- 25296344
OWN - NLM
STAT- MEDLINE
DCOM- 20150223
LR  - 20151119
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Linking)
VI  - 128
IP  - 6
DP  - 2015 Mar
TI  - Neuromuscular electrical stimulation prevents muscle wasting in critically ill 
      comatose patients.
PG  - 357-65
LID - 10.1042/CS20140447 [doi]
AB  - 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.
FAU - Dirks, Marlou L
AU  - Dirks ML
AD  - *NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, 
      Maastricht, The Netherlands.
FAU - Hansen, Dominique
AU  - Hansen D
AD  - daggerJessa Hospital, Heart Centre Hasselt, Hasselt, and Rehabilitation Research 
      Center (REVAL), Hasselt University, Faculty of Medicine, Diepenbeek, Belgium.
FAU - Van Assche, Aime
AU  - Van Assche A
AD  - daggerJessa Hospital, Heart Centre Hasselt, Hasselt, and Rehabilitation Research 
      Center (REVAL), Hasselt University, Faculty of Medicine, Diepenbeek, Belgium.
FAU - Dendale, Paul
AU  - Dendale P
AD  - daggerJessa Hospital, Heart Centre Hasselt, Hasselt, and Rehabilitation Research 
      Center (REVAL), Hasselt University, Faculty of Medicine, Diepenbeek, Belgium.
FAU - Van Loon, Luc J C
AU  - Van Loon LJ
AD  - *NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, 
      Maastricht, The Netherlands.
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Muscle Proteins)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Biopsy
MH  - Conscious Sedation/adverse effects
MH  - Critical Care/methods
MH  - Critical Illness/*therapy
MH  - Electric Stimulation Therapy/*methods
MH  - Female
MH  - Gene Expression
MH  - Humans
MH  - Intensive Care Units
MH  - Male
MH  - Middle Aged
MH  - Muscle Fibers, Skeletal/pathology
MH  - Muscle Proteins/biosynthesis/genetics
MH  - Muscular Atrophy/etiology/pathology/*prevention & control
MH  - Phosphorylation
MH  - Quadriceps Muscle/pathology/physiopathology
MH  - RNA, Messenger/genetics
EDAT- 2014/10/09 06:00
MHDA- 2015/02/24 06:00
CRDT- 2014/10/09 06:00
PHST- 2014/10/09 06:00 [entrez]
PHST- 2014/10/09 06:00 [pubmed]
PHST- 2015/02/24 06:00 [medline]
AID - CS20140447 [pii]
AID - 10.1042/CS20140447 [doi]
PST - ppublish
SO  - Clin Sci (Lond). 2015 Mar;128(6):357-65. doi: 10.1042/CS20140447.