Effects of neuromuscular electrical stimulation on muscle layer thickness of knee extensor muscles in intensive care unit patients: a pilot study

Gruther, Wolfgang; Kainberger, Franz; Fialka‐Moser, Veronika; Paternostro-Sluga, Tatjana; Quittan, Michael; Spiss, Christian K.; Crevenna, Richard

doi:10.2340/16501977-0564

Cited by 129 publications

(195 citation statements)

References 29 publications

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“…In non-ICU patient populations, EMS has been shown to increase muscle strength and exercise tolerance (637). Preliminary results in small samples of critically ill patients were promising and found that EMS preserved muscle mass (237,272,474), reduced muscle catabolism (73), and exerted shortterm systemic microcirculatory effects (238). In another eight patients with septic shock however, 7 days of EMS did not preserve muscle volume (555).…”

Section: Electrical Muscle Stimulationmentioning

confidence: 92%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

300

329

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Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. Some ICUAW forms require stringent diagnostic features; CIM is marked by membrane hypoexcitability, severe atrophy, preferential myosin loss, ultrastructural alterations, and inadequate autophagy activation while myopathies in pure sepsis do not reproduce marked myosin loss. Reduced membrane excitability results from depolarization and ion channel dysfunction. Mitochondrial dysfunction contributes to energy-dependent processes. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Myosin loss is more pronounced than actin loss in CIM. Protein quality control is altered by inadequate autophagy. Ca 2ϩ dysregulation is present through altered Ca 2ϩ homeostasis. We highlight clinical hallmarks, trigger factors, and potential mechanisms from human studies and animal models that allow separation of risk factors that may trigger distinct mechanisms contributing to weakness. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. Future challenges include identification of primary/secondary events during the time course of critical illness, the interplay between membrane excitability, bioenergetic failure and differential proteolysis, and finding new therapeutic targets by help of tailored animal models.

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Section: Electrical Muscle Stimulationmentioning

confidence: 92%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

300

329

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“…Prolonged application of NMES has been reported to attenuate the loss of muscle mass and/or strength in patients recovering from surgery (60,66,69), patients suffering from severe cardiovascular complications (6,58,67), or patients treated in the intensive care unit (25,32). Despite the proposed benefits of NMES in a clinical setting, there is little evidence for the proposed impact of NMES on muscle protein synthesis (27,28).…”

mentioning

confidence: 99%

Neuromuscular electrical stimulation increases muscle protein synthesis in elderly type 2 diabetic men

Wall

Dirks

Verdijk

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Wall BT, Dirks ML, Verdijk LB, Snijders T, Hansen D, Vranckx P, Burd NA, Dendale P, van Loon LJ. Neuromuscular electrical stimulation increases muscle protein synthesis in elderly type 2 diabetic men. Am J Physiol Endocrinol Metab 303: E614-E623, 2012. First published June 26, 2012 doi:10.1152/ajpendo.00138.2012.-Physical activity is required to attenuate the loss of skeletal muscle mass with aging. Short periods of muscle disuse, due to sickness or hospitalization, reduce muscle protein synthesis rates, resulting in rapid muscle loss. The present study investigates the capacity of neuromuscular electrical stimulation (NMES) to increase in vivo skeletal muscle protein synthesis rates in older type 2 diabetes patients. Six elderly type 2 diabetic men (70 Ϯ 2 yr) were subjected to 60 min of one-legged NMES. Continuous infusions with L-[ring-13 C6]phenylalanine were applied, with blood and muscle samples being collected regularly to assess muscle protein synthesis rates in both the stimulated (STIM) and nonstimulated control (CON) leg during 4 h of recovery after NMES. Furthermore, mRNA expression of key genes implicated in the regulation of muscle mass were measured over time in the STIM and CON leg. Muscle protein synthesis rates were greater in the STIM compared with the CON leg during recovery from NMES (0.057 Ϯ 0.008 vs. 0.045 Ϯ 0.008%/h, respectively, P Ͻ 0.01). Skeletal muscle myostatin mRNA expression in the STIM leg tended to increase immediately following NMES compared with the CON leg (1.63-vs.

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“…В этом аспекте интересно исследование W. Gruther и соавт. [39], в котором изучали эффекты ЭСМ, помимо групп пассивных тренировок и контроля, также и у пациентов, которые находились в ОРИТ в течение различного времени -менее 7 и более 14 дней. После курса ЭСМ у пациентов, находившихся на момент начала пассивных тренировок менее 7 дней, не бы-ло отличий в толщине мышечного слоя (p=0,457) по срав-нению с группой контроля.…”

Section: клинические и научные перспективы дальнейшего использования unclassified

“…Напротив, у пациентов, находившихся в ОРИТ более 2 нед, в результате ЭСМ мышечный слой был боль-ше в группе пассивных тренировок по сравнению с груп-пой контроля. Кроме того, отмечена значимая динамика толщины мышечного слоя до и после ЭСМ (p=0,036), в то время как в контрольной группе она осталась неизменной (p=0,162) [39]. K. Iwatsu и соавт.…”

Section: клинические и научные перспективы дальнейшего использования unclassified

Rehabilitation in the intensive care unit: electrical stimulation of skeletal muscles

Безденежных¹,

Сумин²

2016

Kardiol. serdechno-sosud. khir.

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Effects of neuromuscular electrical stimulation on muscle layer thickness of knee extensor muscles in intensive care unit patients: a pilot study

Abstract: Neuromuscular electrical stimulation appears to be a useful adjunct to revert muscle wasting in intensive care unit long-term patients; however, larger studies with a larger sample size are needed to confirm these promising, but preliminary, results.

Cited by 129 publications

References 29 publications

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Neuromuscular electrical stimulation increases muscle protein synthesis in elderly type 2 diabetic men

Rehabilitation in the intensive care unit: electrical stimulation of skeletal muscles

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