Washington, In a recent study published in Reviews in Medical Virology, researchers reviewed the mechanisms of muscle tissue injury, aggravating conditions, and associated sequelae in long coronavirus disease 2019 (COVID-19).
In long COVID-19, musculoskeletal system involvement secondary to the hyper inflammatory state is characterized by the persistence of clinical symptoms such as myalgia, fatigue, muscle weakness, and decline in functional and physical performance, even after four weeks of symptom onset. In addition, mitochondrial damage, hypoxemia, and dysregulation of the renin-angiotensin system (RAS) occur.
COVID-19-associated hospitalization, immobility and drugs, cerebrovascular disorders, and involvement of the central and peripheral nervous systems aggravate muscle damage, which is characterized by reduced protein synthesis and decreased muscle mass. An in-depth understanding of the pathophysiology of muscle dysfunction could aid in the development of novel muscle management strategies to curb COVID-19-associated sequelae.
In the present study, researchers elucidated the mechanisms of the impact of long COVID-19 on the musculoskeletal system.
COVID-19 results in severe hypoxemia and requirements of oxygen supplementation and mechanical ventilation. Diffuse alveolar injury with subsequent aggregation of inflammatory substances, deposition of fibrin and collagen, compromised gaseous exchange, and reduced permeability of alveolar capillaries takes place.
SARS-CoV-2 invades the CNS via the hematogenous route, which involves viral binding to the endothelial cells of the blood-brain barrier (BBB), an infection of immune-regulatory cells, olfactory neurons, and the liquor route, wherein infected lymphocytes get attached to endothelial cells of the cerebrospinal fluid (CSF) and reach the glial cells and neurons.
Studies have reported an association between COVID-19 and the cerebrovascular derangements, with hemorrhagic and ischemic stroke, endothelial cell inflammation, and coagulopathy. These effects are associated increase in angiotensin II (Ang II) expression, which causes clot formation, fluid retention, vasoconstriction, and hypertension.
COVID-19 associated PNS damage involves neuromuscular junction dysfunctions, myopathies, and polyneuropathies. The hypoxia increases vascular permeability, leading to vasogenic edema. COVID-19, associated with Guillain-Barré syndrome (GBS), is an example of the PNS involvement of COVID-19, in which flaccid paralysis of lower limb muscles develops rapidly post symptom onset.
Long COVID-19 patients have substantially increased creatine kinase (CK), cholesterol C-reactive protein (CRP), lactate dehydrogenase (LDH), ferritin, and cortisol, which affect ATP production and cause increased muscle fatigue and thereby decreased ability to perform routine functions. COVID-19 associated sarcopenia causes physical and functional muscular deterioration in muscle volume and strength with decreased satellite cells and activation of anabolic mechanisms. Further, type 2 diabetes mellitus and obesity exacerbate long COVID-19 complications. Muscle fatigue in long COVID-19 is also associated with cognitive deficits, dyspnea, and reduced lung capacity.
Overall, the review highlights the inflammation, RAS- and hypoxia-associated decrease in muscle mass, strength, size, and volume in long COVID-19, potentiated by prolonged immobilization, drug use, and comorbidities. The review underscores the importance of physical exercise, nutritional monitoring, and other muscle management strategies for long COVID-19 patients.
Source: Oman News Agency
