ABSTRACT
Intensive Care Unit-Acquired Weakness (ICU-AW) is a generalized and symmetric neuromuscular dysfunction associated with critical illness and its treatments. Its incidence is approximately 80% in intensive care unit patients, and it manifests as critical illness polyneuropathy, critical illness myopathy, and muscle atrophy. Intensive care unit patients can lose an elevated percentage of their muscle mass in the first days after admission, producing short- and long-term sequelae that affect patients' quality of life, physical health, and mental health. In 2019, the world was faced with coronavirus disease 2019 (COVID-19), caused by the acute respiratory syndrome coronavirus 2. COVID-19 produces severe respiratory disorders, such as acute respiratory distress syndrome, which increases the risk of developing ICU-AW. COVID-19 patients treated in intensive care units have shown early diffuse and symmetrical muscle weakness, polyneuropathy, and myalgia, coinciding with the clinical presentation of ICU-AW. Besides, these patients require prolonged intensive care unit stays, invasive mechanical ventilation, and intensive care unit pharmacological therapy, which are risk factors for ICU-AW. Thus, the purposes of this review are to discuss the features of ICU-AW and its effects on skeletal muscle. Further, we will describe the mechanisms involved in the probable development of ICU-AW in severe COVID-19 patients.
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.