Johan Segers1, Ilse Vanhorebeek2, Daniel Langer3, Noppawan Charususin4, Weili Wei5, Bregje Frickx6, Inge Demeyere7, Beatrix Clerckx1, Michael Casaer8, Inge Derese2, Sarah Derde2, Lies Pauwels2, Greet Van den Berghe8, Greet Hermans9, Rik Gosselink10. 1. Department of Rehabilitation Sciences, Faculty of Kinesiology and Rehabilitation Sciences, KU Leuven, Herestraat 49, B-3000 Leuven, Belgium; Department of Intensive Care, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium. 2. Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, B-3000 Leuven, Belgium. 3. Department of Rehabilitation Sciences, Faculty of Kinesiology and Rehabilitation Sciences, KU Leuven, Herestraat 49, B-3000 Leuven, Belgium. 4. Department of Rehabilitation Sciences, Faculty of Kinesiology and Rehabilitation Sciences, KU Leuven, Herestraat 49, B-3000 Leuven, Belgium; Department of Physical therapy, Faculty of Allied Health Sciences, Thammasat University, Pathumthani, Thailand. 5. Department of Rehabilitation Sciences, Faculty of Kinesiology and Rehabilitation Sciences, KU Leuven, Herestraat 49, B-3000 Leuven, Belgium; Department of Respiratory and Critical Care, Tongji Hospital, Shangai, China. 6. Medical Intensive Care Unit, Department of General Internal Medicine, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium. 7. Department of Intensive Care, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium. 8. Department of Intensive Care, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium; Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, B-3000 Leuven, Belgium. 9. Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, B-3000 Leuven, Belgium; Medical Intensive Care Unit, Department of General Internal Medicine, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium. 10. Department of Rehabilitation Sciences, Faculty of Kinesiology and Rehabilitation Sciences, KU Leuven, Herestraat 49, B-3000 Leuven, Belgium; Department of Intensive Care, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium. Electronic address: Rik.Gosselink@kuleuven.be.
Abstract
PURPOSE: To investigate the effect of Neuromuscular Electrical Stimulation (NMES) on muscle thickness, strength and morphological and molecular markers of the quadriceps. MATERIALS AND METHODS:Adult critically ill patients with an expected prolonged stay receivedunilateral quadriceps NMES sessions for 7 consecutive days. Before and after the intervention period, quadriceps thickness was measured with ultrasound. After the intervention period, strength was assessed in cooperative patients and muscle biopsies were taken. Multivariable regression was performed to identify factors affecting muscle thickness loss. RESULTS:Muscle thickness decreased less in the stimulated leg (-6 ± 16% versus -12 ± 15%, p = 0.014, n = 47). Strength was comparable. Opioid administration, minimal muscle contraction and more muscle thickness loss in the non-stimulated muscle were independently associated with better muscle thickness preservation. Stimulated muscles showed a shift towards larger myofibers and higher MyHC-I gene expression. NMES did not affect gene expression of other myofibrillary proteins, MuRF-1 or atrogin-1. Signs of myofiber necrosis and inflammation were comparable for both muscles. CONCLUSIONS:NMES attenuated the loss of muscle mass, but not of strength, in critically ill patients. Preservation of muscle mass was more likely in patients receiving opioids, patients with a minimal muscle contraction during NMES and patients more prone to lose muscle mass. TRIAL REGISTRATION: clinicaltrials.govNCT02133300.
RCT Entities:
PURPOSE: To investigate the effect of Neuromuscular Electrical Stimulation (NMES) on muscle thickness, strength and morphological and molecular markers of the quadriceps. MATERIALS AND METHODS: Adult critically illpatients with an expected prolonged stay received unilateral quadriceps NMES sessions for 7 consecutive days. Before and after the intervention period, quadriceps thickness was measured with ultrasound. After the intervention period, strength was assessed in cooperative patients and muscle biopsies were taken. Multivariable regression was performed to identify factors affecting muscle thickness loss. RESULTS: Muscle thickness decreased less in the stimulated leg (-6 ± 16% versus -12 ± 15%, p = 0.014, n = 47). Strength was comparable. Opioid administration, minimal muscle contraction and more muscle thickness loss in the non-stimulated muscle were independently associated with better muscle thickness preservation. Stimulated muscles showed a shift towards larger myofibers and higher MyHC-I gene expression. NMES did not affect gene expression of other myofibrillary proteins, MuRF-1 or atrogin-1. Signs of myofiber necrosis and inflammation were comparable for both muscles. CONCLUSIONS: NMES attenuated the loss of muscle mass, but not of strength, in critically illpatients. Preservation of muscle mass was more likely in patients receiving opioids, patients with a minimal muscle contraction during NMES and patients more prone to lose muscle mass. TRIAL REGISTRATION: clinicaltrials.govNCT02133300.
Authors: Ismita Chhetri; Julie E A Hunt; Jeewaka R Mendis; Lui G Forni; Justin Kirk-Bayley; Ian White; Jonathan Cooper; Karthik Somasundaram; Nikunj Shah; Stephen D Patterson; Zudin A Puthucheary; Hugh E Montgomery; Benedict C Creagh-Brown Journal: J Clin Med Date: 2022-07-06 Impact factor: 4.964