scholarly journals Skeletal Muscle Wasting and Function Impairment in Intensive Care Patients With Severe COVID-19

2021 ◽  
Vol 12 ◽  
Author(s):  
Mario Chueire de Andrade-Junior ◽  
Isabel Chateaubriand Diniz de Salles ◽  
Christina May Moran de Brito ◽  
Laerte Pastore-Junior ◽  
Renato Fraga Righetti ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Intensive Care ◽  
Muscle Strength ◽  
Muscle Wasting ◽  
Rectus Femoris ◽  
Quadriceps Muscle ◽  
Anterior Compartment ◽  
Intensive Care Patients ◽  
Skeletal Muscle Wasting ◽  
And Function

Background: Intensive care patients commonly develop muscle wasting and functional impairment. However, the role of severe COVID-19 in the magnitude of muscle wasting and functionality in the acute critical disease is unknown.Objective: To perform a prospective characterization to evaluate the skeletal muscle mass and functional performance in intensive care patients with severe COVID-19.Methods: Thirty-two critically ill patients (93.8% male; age: 64.1 ± 12.6 years) with the diagnosis of the severe COVID-19 were prospectively recruited within 24 to 72 h following intensive care unit (ICU) admission, from April 2020 to October 2020, at Hospital Sírio-Libanês in Brazil. Patients were recruited if older than 18 years old, diagnosis of severe COVID-19 confirmed by RT-PCR, ICU stay and absence of limb amputation. Muscle wasting was determined through an ultrasound measurement of the rectus femoris cross-sectional area, the thickness of the anterior compartment of the quadriceps muscle (rectus femoris and vastus intermedius), and echogenicity. The peripheral muscle strength was assessed with a handgrip test. The functionality parameter was determined through the ICU mobility scale (IMS) and the International Classification of Functioning, Disability and Health (ICF). All evaluations were performed on days 1 and 10.Results: There were significant reductions in the rectus femoris cross-section area (−30.1% [95% IC, −26.0% to −34.1%]; P < 0.05), thickness of the anterior compartment of the quadriceps muscle (−18.6% [95% IC, −14.6% to 22.5%]; P < 0.05) and handgrip strength (−22.3% [95% IC, 4.7% to 39.9%]; P < 0.05) from days 1 to 10. Patients showed increased mobility (0 [0–5] vs 4.5 [0–8]; P < 0.05), improvement in respiratory function (3 [3–3] vs 2 [1–3]; P < 0.05) and structure respiratory system (3 [3–3] vs 2 [1–3]; P < 0.05), but none of the patients returned to normal levels.Conclusion: In intensive care patients with severe COVID-19, muscle wasting and decreased muscle strength occurred early and rapidly during 10 days of ICU stay with improved mobility and respiratory functions, although they remained below normal levels. These findings may provide insights into skeletal muscle wasting and function in patients with severe COVID-19.

scholarly journals Angiotensin II suppresses autophagy and disrupts ultrastructural morphology and function of mitochondria in mouse skeletal muscle

2019 ◽  
Vol 126 (6) ◽  
pp. 1550-1562 ◽  
Author(s):  
Kleiton Augusto Santos Silva ◽  
Thaysa Ghiarone ◽  
Kathy Schreiber ◽  
DeAna Grant ◽  
Tommi White ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Protein Expression ◽  
Chronic Diseases ◽  
Muscle Wasting ◽  
Beclin 1 ◽  
Ang Ii ◽  
Autophagosome Formation ◽  
Skeletal Muscle Wasting ◽  
And Function

Angiotensin II (ANG II)-induced skeletal muscle wasting is characterized by activation of the ubiquitin-proteasome system. However, the potential involvement of proteolytic system macroautophagy/autophagy in this wasting process remains elusive. Autophagy is precisely regulated to maintain cell survival and homeostasis; thus its dysregulation (i.e., overactivation or persistent suppression) could lead to detrimental outcomes in skeletal muscle. Here we show that infusion of ANG II for 7 days in male FVB mice suppressed autophagy in skeletal muscle. ANG II blunted microtubule-associated protein 1 light chain 3B (LC3B)-I-to-LC3B-II conversion (an autophagosome marker), increased p62/SQSTM1 (an autophagy cargo receptor) protein expression, and decreased the number of autophagic vacuoles. ANG II inhibited UNC-51-like kinase 1 via inhibition of 5′-AMP-activated kinase and activation of mechanistic target of rapamycin complex 1, leading to reduced phosphorylation of beclin-1Ser14 and Autophagy-related protein 14Ser29, suggesting that ANG II impairs autophagosome formation in skeletal muscle. In line with ANG II-mediated suppression of autophagy, ANG II promoted accumulation of abnormal/damaged mitochondria, characterized by swelling and disorganized cristae and matrix dissolution, with associated increase in PTEN-induced kinase 1 protein expression. ANG II also reduced mitochondrial respiration, indicative of mitochondrial dysfunction. Together, these results demonstrate that ANG II reduces autophagic activity and disrupts mitochondrial ultrastructure and function, likely contributing to skeletal muscle wasting. Therefore, strategies that activate autophagy in skeletal muscle have the potential to prevent or blunt ANG II-induced skeletal muscle wasting in chronic diseases. NEW & NOTEWORTHY Our study identified a novel mechanism whereby angiotensin II (ANG II) impairs mitochondrial energy metabolism in skeletal muscle. ANG II suppressed autophagosome formation by inhibiting the UNC-51-like kinase 1(ULK1)-beclin-1 axis, resulting in accumulation of abnormal/damaged and dysfunctional mitochondria and reduced mitochondrial respiratory capacity. Therapeutic strategies that activate the ULK1-beclin-1 axis have the potential to delay or reverse skeletal muscle wasting in chronic diseases characterized by increased systemic ANG II levels.

scholarly journals Skeletal muscle wasting in chronic kidney disease: the emerging role of microRNAs

2019 ◽  
Vol 35 (9) ◽  
pp. 1469-1478 ◽  
Author(s):  
Kate A Robinson ◽  
Luke A Baker ◽  
Matthew P M Graham-Brown ◽  
Emma L Watson
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Muscle Growth ◽  
Exciting Field ◽  
Skeletal Muscle Wasting ◽  
And Function

Abstract Skeletal muscle wasting is a common complication of chronic kidney disease (CKD), characterized by the loss of muscle mass, strength and function, which significantly increases the risk of morbidity and mortality in this population. Numerous complications associated with declining renal function and lifestyle activate catabolic pathways and impair muscle regeneration, resulting in substantial protein wasting. Evidence suggests that increasing skeletal muscle mass improves outcomes in CKD, making this a clinically important research focus. Despite extensive research, the pathogenesis of skeletal muscle wasting is not completely understood. It is widely recognized that microRNAs (miRNAs), a family of short non-coding RNAs, are pivotal in the regulation of skeletal muscle homoeostasis, with significant roles in regulating muscle growth, regeneration and metabolism. The abnormal expression of miRNAs in skeletal muscle during disease has been well described in cellular and animal models of muscle atrophy, and in recent years, the involvement of miRNAs in the regulation of muscle atrophy in CKD has been demonstrated. As this exciting field evolves, there is emerging evidence for the involvement of miRNAs in a beneficial crosstalk system between skeletal muscle and other organs that may potentially limit the progression of CKD. In this article, we describe the pathophysiological mechanisms of muscle wasting and explore the contribution of miRNAs to the development of muscle wasting in CKD. We also discuss advances in our understanding of miRNAs in muscle–organ crosstalk and summarize miRNA-based therapeutics currently in clinical trials.

The ubiquitin–proteasome system and skeletal muscle wasting

2005 ◽  
Vol 41 (1) ◽  
pp. 173 ◽  
Author(s):  
Didier Attaix ◽  
Sophie Ventadour ◽  
Audrey Codran ◽  
Daniel Béchet ◽  
Daniel Taillandier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Wasting ◽  
Ubiquitin Proteasome System ◽  
Skeletal Muscle Wasting ◽  
Ubiquitin Proteasome

scholarly journals Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 588
Author(s):  
Hayden W. Hyatt ◽  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Chronic Diseases ◽  
Muscle Mass ◽  
Cancer Chemotherapy ◽  
Muscle Wasting ◽  
The Body ◽  
Common Denominator ◽  
Skeletal Muscle Wasting ◽  
Vital Functions

Skeletal muscle is the most abundant tissue in the body and is required for numerous vital functions, including breathing and locomotion. Notably, deterioration of skeletal muscle mass is also highly correlated to mortality in patients suffering from chronic diseases (e.g., cancer). Numerous conditions can promote skeletal muscle wasting, including several chronic diseases, cancer chemotherapy, aging, and prolonged inactivity. Although the mechanisms responsible for this loss of muscle mass is multifactorial, mitochondrial dysfunction is predicted to be a major contributor to muscle wasting in various conditions. This systematic review will highlight the biochemical pathways that have been shown to link mitochondrial dysfunction to skeletal muscle wasting. Importantly, we will discuss the experimental evidence that connects mitochondrial dysfunction to muscle wasting in specific diseases (i.e., cancer and sepsis), aging, cancer chemotherapy, and prolonged muscle inactivity (e.g., limb immobilization). Finally, in hopes of stimulating future research, we conclude with a discussion of important future directions for research in the field of muscle wasting.

scholarly journals Volitional rehabilitative assessments in patients admitted in a post-intensive care step down unit. A feasibility study

2017 ◽  
Vol 87 (1) ◽  
Author(s):  
Mara Paneroni ◽  
Francesco D' Abrosca ◽  
Georges Fokom ◽  
Laura Comini ◽  
Michele Vitacca
Keyword(s):  
Intensive Care ◽  
Muscle Strength ◽  
Outcome Measures ◽  
Quadriceps Muscle ◽  
Disability Score ◽  
Icu Patients ◽  
Motor Disability ◽  
Peripheral Muscle ◽  
Teres Major ◽  
Step Down

<p>A high variability in functional tests and activities used during the pulmonary rehabilitation has been observed in post-intensive care unit (ICU) patients, and the best battery of tests to adopt has not been described yet. We tested in patients admitted in a post-ICU Step Down Unit the ability to perform the more frequent functional volitional tests. The relations of each single volitional test with general disability and dyspnea at discharge were also evaluated. Ten volitional tests including: bedside spirometry test (ST: FEV<sub>1</sub>%, FVC%), maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), Peak Expiratory Flow during Cough (PCEF), Quadriceps Muscle Strength (QMS), latissimus Dorsi and teres Major Strength (DMS), Brachial biceps Muscle Strength (BMS), effort tolerance measured by sit-to-stand test, Takahashi test and 6-Min Walking Test (6MWT), were evaluated in post-ICU patients at entry and discharge from in-hospital rehabilitation. General disability was assessed by Barthel Index, while dyspnea by Borg scale. At admission, &gt;70% of subjects performed muscle strength test, while &lt;25% performed respiratory and effort tolerance tests. At discharge, feasibility of spirometry, respiratory muscle strength and effort tolerance tests improved (all, p&lt;0.001); 6MWT was the least feasible. At discharge, cardiorespiratory patients were more capable to perform tests compared to neurological ones. All outcome measures, with exception of FEV<sub>1</sub>%, and FVC%, were significantly related to the disability score. Peripheral muscle exercises showed the highest feasibility, spirometry and leg effort tolerance the lowest. Motor disability was explained mainly by the peripheral muscle strength. The study of non-volitional outcome measures and tests linked to a protocol-driven intervention should be performed in this specific population.</p>

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