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1.
Crit Care ; 25(1): 381, 2021 11 08.
Article in English | MEDLINE | ID: covidwho-1506432

ABSTRACT

BACKGROUND: COVID-19 is primarily a respiratory disease; however, there is also evidence that it causes endothelial damage in the microvasculature of several organs. The aim of the present study is to characterize in vivo the microvascular reactivity in peripheral skeletal muscle of severe COVID-19 patients. METHODS: This is a prospective observational study carried out in Spain, Mexico and Brazil. Healthy subjects and severe COVID-19 patients admitted to the intermediate respiratory (IRCU) and intensive care units (ICU) due to hypoxemia were studied. Local tissue/blood oxygen saturation (StO2) and local hemoglobin concentration (THC) were non-invasively measured on the forearm by near-infrared spectroscopy (NIRS). A vascular occlusion test (VOT), a three-minute induced ischemia, was performed in order to obtain dynamic StO2 parameters: deoxygenation rate (DeO2), reoxygenation rate (ReO2), and hyperemic response (HAUC). In COVID-19 patients, the severity of ARDS was evaluated by the ratio between peripheral arterial oxygen saturation (SpO2) and the fraction of inspired oxygen (FiO2) (SF ratio). RESULTS: Healthy controls (32) and COVID-19 patients (73) were studied. Baseline StO2 and THC did not differ between the two groups. Dynamic VOT-derived parameters were significantly impaired in COVID-19 patients showing lower metabolic rate (DeO2) and diminished endothelial reactivity. At enrollment, most COVID-19 patients were receiving invasive mechanical ventilation (MV) (53%) or high-flow nasal cannula support (32%). Patients on MV were also receiving sedative agents (100%) and vasopressors (29%). Baseline StO2 and DeO2 negatively correlated with SF ratio, while ReO2 showed a positive correlation with SF ratio. There were significant differences in baseline StO2 and ReO2 among the different ARDS groups according to SF ratio, but not among different respiratory support therapies. CONCLUSION: Patients with severe COVID-19 show systemic microcirculatory alterations suggestive of endothelial dysfunction, and these alterations are associated with the severity of ARDS. Further evaluation is needed to determine whether these observations have prognostic implications. These results represent interim findings of the ongoing HEMOCOVID-19 trial. Trial registration ClinicalTrials.gov NCT04689477 . Retrospectively registered 30 December 2020.


Subject(s)
COVID-19/physiopathology , Intensive Care Units/trends , Microvessels/physiopathology , Respiratory Care Units/trends , Respiratory Distress Syndrome/physiopathology , Severity of Illness Index , Adult , Aged , Brazil/epidemiology , COVID-19/diagnosis , COVID-19/epidemiology , Female , Humans , Male , Mexico/epidemiology , Microcirculation/physiology , Middle Aged , Muscle, Skeletal/blood supply , Muscle, Skeletal/physiopathology , Prospective Studies , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/epidemiology , Spain/epidemiology
2.
Int J Mol Sci ; 22(21)2021 Oct 27.
Article in English | MEDLINE | ID: covidwho-1488608

ABSTRACT

Muscle fatigue (MF) declines the capacity of muscles to complete a task over time at a constant load. MF is usually short-lasting, reversible, and is experienced as a feeling of tiredness or lack of energy. The leading causes of short-lasting fatigue are related to overtraining, undertraining/deconditioning, or physical injury. Conversely, MF can be persistent and more serious when associated with pathological states or following chronic exposure to certain medication or toxic composites. In conjunction with chronic fatigue, the muscle feels floppy, and the force generated by muscles is always low, causing the individual to feel frail constantly. The leading cause underpinning the development of chronic fatigue is related to muscle wasting mediated by aging, immobilization, insulin resistance (through high-fat dietary intake or pharmacologically mediated Peroxisome Proliferator-Activated Receptor (PPAR) agonism), diseases associated with systemic inflammation (arthritis, sepsis, infections, trauma, cardiovascular and respiratory disorders (heart failure, chronic obstructive pulmonary disease (COPD))), chronic kidney failure, muscle dystrophies, muscle myopathies, multiple sclerosis, and, more recently, coronavirus disease 2019 (COVID-19). The primary outcome of displaying chronic muscle fatigue is a poor quality of life. This type of fatigue represents a significant daily challenge for those affected and for the national health authorities through the financial burden attached to patient support. Although the origin of chronic fatigue is multifactorial, the MF in illness conditions is intrinsically linked to the occurrence of muscle loss. The sequence of events leading to chronic fatigue can be schematically denoted as: trigger (genetic or pathological) -> molecular outcome within the muscle cell -> muscle wasting -> loss of muscle function -> occurrence of chronic muscle fatigue. The present review will only highlight and discuss current knowledge on the molecular mechanisms that contribute to the upregulation of muscle wasting, thereby helping us understand how we could prevent or treat this debilitating condition.


Subject(s)
Muscle Fatigue/physiology , Muscle Proteins/metabolism , Muscle, Skeletal/physiology , Autophagy , COVID-19/physiopathology , Critical Illness , Humans , Insulin Resistance , Lysosomes/metabolism , Muscle Fatigue/drug effects , Muscle, Skeletal/physiopathology , Muscular Atrophy/etiology , Sarcopenia/physiopathology
3.
Biomed Res Int ; 2021: 2624860, 2021.
Article in English | MEDLINE | ID: covidwho-1484096

ABSTRACT

Background: People with multiple sclerosis (MS) suffer from symptoms related to neural control, such as reduced central activation, lower muscle activity, and accentuated spasticity. A forced 9-week home confinement related to COVID-19 in Spain may have worsened these symptoms. However, no study has demonstrated the impact of home confinement on neuromuscular mechanisms in the MS population. This study was aimed at analyzing the effects of a 9-week home confinement on central activation, muscle activity, contractile function, and spasticity in MS patients. Methods: Eighteen participants were enrolled in the study. Left and right knee extensor maximum voluntary isometric contraction (MVIC), maximal neural drive via peak surface electromyography (EMG) of the vastus lateralis, central activation ratio (CAR), and muscle contractile function via electrical stimulation of the knee extensor muscles, as well as spasticity using the pendulum test, were measured immediately before and after home confinement. Results: Seventeen participants completed the study. CAR significantly decreased after lockdown (ES = 1.271, p < 0.001). Regarding spasticity, there was a trend to decrease in the number of oscillations (ES = 0.511, p = 0.059) and a significant decrease in the duration of oscillations (ES = 0.568, p = 0.038). Furthermore, in the left leg, there was a significant decrease in the first swing excursion (ES = 0.612, p = 0.027) and in the relaxation index (ES = 0.992, p = 0.001). Muscle contractile properties, MVIC, and EMG variables were not modified after confinement. Conclusions: The results suggest that a home confinement period of 9 weeks may lead to an increase in lower limb spasticity and a greater deficit in voluntary activation of the knee extensors.


Subject(s)
COVID-19 , Multiple Sclerosis/physiopathology , Muscle, Skeletal/physiopathology , Communicable Disease Control , Electric Stimulation , Electromyography , Female , Humans , Isometric Contraction , Knee/physiology , Male , Middle Aged , Muscle Contraction , Muscle Spasticity , Muscle, Skeletal/physiology , Quadriceps Muscle/physiology
4.
Skelet Muscle ; 11(1): 10, 2021 04 21.
Article in English | MEDLINE | ID: covidwho-1197351

ABSTRACT

BACKGROUND: SARS-CoV2 virus could be potentially myopathic. Serum creatinine phosphokinase (CPK) is frequently found elevated in severe SARS-CoV2 infection, which indicates skeletal muscle damage precipitating limb weakness or even ventilatory failure. CASE PRESENTATION: We addressed such a patient in his forties presented with features of severe SARS-CoV2 pneumonia and high serum CPK. He developed severe sepsis and acute respiratory distress syndrome (ARDS) and received intravenous high dose corticosteroid and tocilizumab to counter SARS-CoV2 associated cytokine surge. After 10 days of mechanical ventilation (MV), weaning was unsuccessful albeit apparently clear lung fields, having additionally severe and symmetric limb muscle weakness. Ancillary investigations in addition with serum CPK, including electromyogram, muscle biopsy, and muscle magnetic resonance imaging (MRI) suggested acute myopathy possibly due to skeletal myositis. CONCLUSION: We wish to stress that myopathogenic medication in SARS-CoV2 pneumonia should be used with caution. Additionally, serum CPK could be a potential marker to predict respiratory failure in SARS-CoV2 pneumonia as skeletal myopathy affecting chest muscles may contribute ventilatory failure on top of oxygenation failure due to SARS-CoV2 pneumonia.


Subject(s)
COVID-19/physiopathology , Creatine Kinase/blood , Muscle, Skeletal/physiopathology , Muscular Diseases/physiopathology , Quadriplegia/physiopathology , Respiratory Distress Syndrome/physiopathology , Adenosine Monophosphate/analogs & derivatives , Adenosine Monophosphate/therapeutic use , Adult , Alanine/analogs & derivatives , Alanine/therapeutic use , Antibodies, Monoclonal, Humanized/therapeutic use , Anticoagulants/therapeutic use , Antiviral Agents/therapeutic use , COVID-19/complications , COVID-19/therapy , Critical Illness , Dexamethasone/therapeutic use , Electromyography , Glucocorticoids/therapeutic use , Heparin, Low-Molecular-Weight/therapeutic use , Humans , Intensive Care Units , Magnetic Resonance Imaging , Male , Methicillin-Resistant Staphylococcus aureus , Muscle, Skeletal/diagnostic imaging , Muscle, Skeletal/pathology , Muscular Diseases/blood , Muscular Diseases/diagnosis , Muscular Diseases/etiology , Neural Conduction , Pulmonary Embolism/diagnosis , Pulmonary Embolism/drug therapy , Pulmonary Embolism/etiology , Pulmonary Embolism/physiopathology , Quadriplegia/etiology , Respiration, Artificial , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy , SARS-CoV-2 , Severity of Illness Index , Staphylococcal Infections/complications , Staphylococcal Infections/diagnosis , Staphylococcal Infections/drug therapy , Ventilator Weaning
5.
Neurophysiol Clin ; 51(2): 183-191, 2021 Mar.
Article in English | MEDLINE | ID: covidwho-1087170

ABSTRACT

OBJECTIVE: To assess whether patients with acute inflammatory demyelinating polyneuropathy (AIDP) associated with SARS-CoV-2 show characteristic electrophysiological features. METHODS: Clinical and electrophysiological findings of 24 patients with SARS-CoV-2 infection and AIDP (S-AIDP) and of 48 control AIDP (C-AIDP) without SARS-CoV-2 infection were compared. RESULTS: S-AIDP patients more frequently developed respiratory failure (83.3% vs. 25%, P=0.000) and required intensive care unit (ICU) hospitalization (58.3% vs. 31.3%, P=0.000). In C-AIDP, distal motor latencies (DMLs) were more frequently prolonged (70.9% vs. 26.2%, P=0.000) whereas in S-AIDP distal compound muscle action potential (dCMAP) durations were more frequently increased (49.5% vs. 32.4%, P=0.002) and F waves were more often absent (45.6% vs. 31.8%, P=0.011). Presence of nerves with increased dCMAP duration and normal or slightly prolonged DML was elevenfold higher in S-AIDP (31.1% vs. 2.8%, P=0.000);11 S-AIDP patients showed this pattern in 2 nerves. CONCLUSION: Increased dCMAP duration, thought to be a marker of acquired demyelination, can also be oserved in critical illness myopathy. In S-AIDP patients, an increased dCMAP duration dissociated from prolonged DML, suggests additional muscle fiber conduction slowing, possibly due to a COVID-19-related hyperinflammatory state. Absent F waves, at least in some S-AIDP patients, may reflect α-motor neuron hypoexcitability because of immobilization during the ICU stay. These features should be considered in the electrodiagnosis of SARS-CoV-2 patients with weakness, to avoid misdiagnosis.


Subject(s)
COVID-19/complications , COVID-19/physiopathology , Guillain-Barre Syndrome/etiology , Guillain-Barre Syndrome/physiopathology , Action Potentials , Adult , Aged , Aged, 80 and over , Critical Care/statistics & numerical data , Electrodiagnosis , Electrophysiological Phenomena , Female , Hospitalization/statistics & numerical data , Humans , Male , Middle Aged , Motor Neurons , Muscle, Skeletal/physiopathology , Neural Conduction , Respiratory Insufficiency/etiology , Sensory Receptor Cells
6.
Shock ; 56(3): 360-367, 2021 09 01.
Article in English | MEDLINE | ID: covidwho-1028641

ABSTRACT

PURPOSE: Rhabdomyolysis (RM) has been associated with many viral infectious diseases, and associated with poor outcomes. We aim to evaluate the clinical features and outcomes of RM in patients with coronavirus disease 2019 (COVID-19). METHOD: This was a single-center, retrospective, cohort study of 1,014 consecutive hospitalized patients with confirmed COVID-19 at the Huoshenshan Hospital in Wuhan, China, between February 17 and April 12, 2020. RESULTS: The overall incidence of RM was 2.2%. Compared with patients without RM, those with RM tended to have a higher risk of deterioration. Patients with RM also constituted a greater percentage of patients admitted to the intensive care unit (90.9% vs. 5.3%, P < 0.001) and a greater percentage of patients undergoing mechanical ventilation (86.4% vs. 2.7% P < 0.001). Moreover, patients with RM had laboratory test abnormalities, including the presence of markers of inflammation, activation of coagulation, and kidney injury. Patients with RM also had a higher risk of in-hospital death (P < 0.001). Cox's proportional hazard regression model analysis confirmed that RM indicators, including peak creatine kinase levels > 1,000 IU/L (HR = 6.46, 95% CI: 3.02-13.86) and peak serum myoglobin concentrations > 1,000 ng/mL (HR = 9.85, 95% CI: 5.04-19.28), were independent risk factors for in-hospital death. Additionally, patients with COVID-19 that developed RM tended to have delayed viral clearance. CONCLUSION: RM might be an important contributing factor to adverse outcomes in COVID-19 patients. The early detection and effective intervention of RM may help reduce mortality among COVID-19 patients.


Subject(s)
COVID-19/complications , COVID-19/mortality , Hospital Mortality , Rhabdomyolysis/complications , Rhabdomyolysis/mortality , Adolescent , Adult , Aged , Aged, 80 and over , China/epidemiology , Female , Hospitalization , Humans , Incidence , Intensive Care Units , Male , Middle Aged , Muscle, Skeletal/physiopathology , Proportional Hazards Models , Respiration, Artificial , Retrospective Studies , SARS-CoV-2 , Treatment Outcome , Young Adult
7.
J Neurol Sci ; 420: 117271, 2021 01 15.
Article in English | MEDLINE | ID: covidwho-1023663

ABSTRACT

More than half of patients who recover from COVID-19 experience fatigue. We studied fatigue using neuropsychological and neurophysiological investigations in post-COVID-19 patients and healthy subjects. Neuropsychological assessment included: Fatigue Severity Scale (FSS), Fatigue Rating Scale, Beck Depression Inventory, Apathy Evaluation Scale, cognitive tests, and computerized tasks. Neurophysiological examination was assessed before (PRE) and 2 min after (POST) a 1-min fatiguing isometric pinching task and included: maximum compound muscle action potential (CMAP) amplitude in first dorsal interosseous muscle (FDI) following ulnar nerve stimulation, resting motor threshold, motor evoked potential (MEP) amplitude and silent period (SP) duration in right FDI following transcranial magnetic stimulation of the left motor cortex. Maximum pinch strength was measured. Perceived exertion was assessed with the Borg-Category-Ratio scale. Patients manifested fatigue, apathy, executive deficits, impaired cognitive control, and reduction in global cognition. Perceived exertion was higher in patients. CMAP and MEP were smaller in patients both PRE and POST. CMAP did not change in either group from PRE to POST, while MEP amplitudes declined in controls POST. SP duration did not differ between groups PRE, increased in controls but decreased in patients POST. Patients' change of SP duration from PRE to POST was negatively correlated to FSS. Abnormal SP shortening and lack of MEP depression concur with a reduction in post-exhaustion corticomotor inhibition, suggesting a possible GABAB-ergic dysfunction. This impairment might be related to the neuropsychological alterations. COVID-19-associated inflammation might lead to GABAergic impairment, possibly representing the basis of fatigue and explaining apathy and executive deficits.


Subject(s)
Action Potentials/physiology , COVID-19/complications , Executive Function/physiology , Fatigue/virology , Muscle, Skeletal/physiopathology , Aged , Aged, 80 and over , COVID-19/physiopathology , COVID-19/psychology , Evoked Potentials, Motor/physiology , Fatigue/physiopathology , Fatigue/psychology , Female , Humans , Male , Middle Aged , Motor Cortex/physiopathology , Neuropsychological Tests , Transcranial Magnetic Stimulation
8.
Int J Mol Sci ; 21(21)2020 Oct 24.
Article in English | MEDLINE | ID: covidwho-895370

ABSTRACT

Severe acute respiratory syndrome coronavirus (SARS-CoV-2) has produced significant health emergencies worldwide, resulting in the declaration by the World Health Organization of the coronavirus disease 2019 (COVID-19) pandemic. Acute respiratory syndrome seems to be the most common manifestation of COVID-19. A high proportion of patients require intensive care unit admission and mechanical ventilation (MV) to survive. It has been well established that angiotensin-converting enzyme type 2 (ACE2) is the primary cellular receptor for SARS-CoV-2. ACE2 belongs to the renin-angiotensin system (RAS), composed of several peptides, such as angiotensin II (Ang II) and angiotensin (1-7) (Ang-(1-7)). Both peptides regulate muscle mass and function. It has been described that SARS-CoV-2 infection, by direct and indirect mechanisms, affects a broad range of organ systems. In the skeletal muscle, through unbalanced RAS activity, SARS-CoV-2 could induce severe consequences such as loss of muscle mass, strength, and physical function, which will delay and interfere with the recovery process of patients with COVID-19. This article discusses the relationship between RAS, SARS-CoV-2, skeletal muscle, and the potentially harmful consequences for skeletal muscle in patients currently infected with and recovering from COVID-19.


Subject(s)
Coronavirus Infections/metabolism , Muscle, Skeletal/physiopathology , Muscular Atrophy/etiology , Pneumonia, Viral/metabolism , Renin-Angiotensin System , Animals , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/physiopathology , Humans , Muscle, Skeletal/metabolism , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/physiopathology
9.
Med Hypotheses ; 144: 110002, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-610333

ABSTRACT

Straying away from a sedentary lifestyle is essential, especially in these troubled times of a global pandemic to reverse the ill effects associated with the health risks as mentioned earlier. In the view of anticipated effects on immune system and prevention against influenza and Covid-19, globally moderate to vigorous exercises are advocated wearing protective equipment such as facemasks. Though WHO supports facemasks only for Covid-19 patients, healthy "social exercisers" too exercise strenuously with customized facemasks or N95 which hypothesized to pose more significant health risks and tax various physiological systems especially pulmonary, circulatory and immune systems. Exercising with facemasks may reduce available Oxygen and increase air trapping preventing substantial carbon dioxide exchange. The hypercapnic hypoxia may potentially increase acidic environment, cardiac overload, anaerobic metabolism and renal overload, which may substantially aggravate the underlying pathology of established chronic diseases. Further contrary to the earlier thought, no evidence exists to claim the facemasks during exercise offer additional protection from the droplet transfer of the virus. Hence, we recommend social distancing is better than facemasks during exercise and optimal utilization rather than exploitation of facemasks during exercise.


Subject(s)
COVID-19/prevention & control , Exercise , Hypercapnia/etiology , Hypoxia/etiology , Masks/adverse effects , Pulmonary Ventilation , Air Microbiology , Anaerobiosis , Brain/physiopathology , COVID-19/immunology , COVID-19/transmission , Carbon Dioxide/blood , Exercise/physiology , Guidelines as Topic , Heart/physiopathology , Humans , Hypercapnia/blood , Hypercapnia/immunology , Hypercapnia/physiopathology , Hypoxia/blood , Hypoxia/immunology , Hypoxia/physiopathology , Kidney/physiopathology , Muscle, Skeletal/physiopathology , Oxygen/blood , Oxygen Consumption , SARS-CoV-2/isolation & purification , World Health Organization
11.
J Bone Joint Surg Am ; 102(14): 1197-1204, 2020 07 15.
Article in English | MEDLINE | ID: covidwho-594092

ABSTRACT

Coronavirus disease 2019 (COVID-19) is an emerging pandemic disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the majority of patients who become infected with SARS-CoV-2 are asymptomatic or have mild symptoms, some patients develop severe symptoms that can permanently detract from their quality of life. SARS-CoV-2 is closely related to SARS-CoV-1, which causes severe acute respiratory syndrome (SARS). Both viruses infect the respiratory system, and there are direct and indirect effects of this infection on multiple organ systems, including the musculoskeletal system. Epidemiological data from the SARS pandemic of 2002 to 2004 identified myalgias, muscle dysfunction, osteoporosis, and osteonecrosis as common sequelae in patients with moderate and severe forms of this disease. Early studies have indicated that there is also considerable musculoskeletal dysfunction in some patients with COVID-19, although long-term follow-up studies have not yet been conducted. The purpose of this article was to summarize the known musculoskeletal pathologies in patients with SARS or COVID-19 and to combine this with computational modeling and biochemical signaling studies to predict musculoskeletal cellular targets and long-term consequences of the SARS-CoV-2 infection.


Subject(s)
Coronavirus Infections/complications , Musculoskeletal System/physiopathology , Pneumonia, Viral/complications , Angiotensin-Converting Enzyme 2 , Betacoronavirus , Bone and Bones/physiopathology , COVID-19 , Computer Simulation , Humans , Joints/physiopathology , Muscle Weakness/virology , Muscle, Skeletal/physiopathology , Myalgia/virology , Pandemics , Peptidyl-Dipeptidase A/genetics , SARS-CoV-2 , Serine Endopeptidases/genetics
12.
Eur J Sport Sci ; 21(4): 614-635, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-245123

ABSTRACT

The COVID-19 pandemic is an unprecedented health crisis as entire populations have been asked to self-isolate and live in home-confinement for several weeks to months, which in itself represents a physiological challenge with significant health risks. This paper describes the impact of sedentarism on the human body at the level of the muscular, cardiovascular, metabolic, endocrine and nervous systems and is based on evidence from several models of inactivity, including bed rest, unilateral limb suspension, and step-reduction. Data form these studies show that muscle wasting occurs rapidly, being detectable within two days of inactivity. This loss of muscle mass is associated with fibre denervation, neuromuscular junction damage and upregulation of protein breakdown, but is mostly explained by the suppression of muscle protein synthesis. Inactivity also affects glucose homeostasis as just few days of step reduction or bed rest, reduce insulin sensitivity, principally in muscle. Additionally, aerobic capacity is impaired at all levels of the O2 cascade, from the cardiovascular system, including peripheral circulation, to skeletal muscle oxidative function. Positive energy balance during physical inactivity is associated with fat deposition, associated with systemic inflammation and activation of antioxidant defences, exacerbating muscle loss. Importantly, these deleterious effects of inactivity can be diminished by routine exercise practice, but the exercise dose-response relationship is currently unknown. Nevertheless, low to medium-intensity high volume resistive exercise, easily implementable in home-settings, will have positive effects, particularly if combined with a 15-25% reduction in daily energy intake. This combined regimen seems ideal for preserving neuromuscular, metabolic and cardiovascular health.


Subject(s)
Communicable Disease Control/methods , Energy Metabolism , Exercise/physiology , Health Behavior , Muscle, Skeletal , Pandemics , Sedentary Behavior , Adipose Tissue/metabolism , Cardiovascular System/metabolism , Endocrine System , Energy Intake , Humans , Insulin Resistance , Muscle, Skeletal/metabolism , Muscle, Skeletal/physiopathology , Muscular Atrophy , Oxygen/metabolism , Physical Distancing , Physical Exertion/physiology , Resistance Training , SARS-CoV-2
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