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Muscle weakness can be caused by a variety of factors, including aging, fatigue, and underlying health conditions. Recent studies have identified a possible link between COVID-19 and muscle weakness, particularly in individuals experiencing long COVID. University of Malta researchers found that SARS-CoV-2, the virus responsible for COVID-19, attaches to the ACE2 (angiotensin-converting enzyme 2) receptor, leading to a breakdown in communication between nerves and muscles. This discovery provides valuable insights into the development of treatments for individuals suffering from long-term COVID-19 complications.
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What You'll Learn
ACE2 receptor targeted by SARS-CoV-2
COVID-19 can cause muscle weakness, which can be a result of direct damage to motor neurons and muscles by the virus or the body's immune response. In addition, COVID-19 causes inflammation throughout the body, which can lead to muscle pain and soreness.
ACE2, or Angiotensin-converting enzyme 2, is a receptor targeted by SARS-CoV-2, the virus that causes COVID-19. ACE2 is an enzyme that plays a crucial role in the cardiovascular system and the lungs. It is usually associated with hypertension and other cardiovascular system disorders. The SARS-CoV-2 virus binds to ACE2 receptors on the surface of skeletal muscle cells, allowing it to enter and infect the cell.
ACE2 is also known to have a protective effect on the lungs and the cardiovascular system. It produces Ang 1-7, which protects lung cells by antagonizing the actions of Ang II, preventing lung cell death. Ang 1-7 also has a protective function in the vasculature, providing vasodilation and cell protection.
When SARS-CoV-2 binds to ACE2, it can disrupt the production of Ang 1-7, leading to a loss of its protective functions. This disruption can result in an imbalance, causing unchecked effects of Ang II and upregulation of the RAS/Ang II pathway. Increased Ang II levels contribute to vasoconstriction, thrombophilia, microthrombosis, alveolar epithelial injury, and respiratory failure.
Understanding the interaction between SARS-CoV-2 and ACE2 is crucial for developing targeted interventions and treatments for COVID-19. Researchers are investigating various therapeutic strategies, such as inhibiting SARS-CoV-2 spike protein activation, virus endocytosis, and sustaining ACE2/Angiotensin-(1-7)/Mas receptor pathway activation.
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Breakdown in communication between nerves and muscles
COVID-19 infection can cause muscle weakness, which may be prolonged. In some cases, the virus or the immune response to it can directly damage motor neurons and adjacent muscles. This damage to the nervous system can result in neurological symptoms such as 'brain fog' and even acute Guillain-Barré syndrome.
Myasthenia gravis is a condition caused by an error in nerve-to-muscle communication. It is characterised by the interruption of signals between the nerve and muscle at the neuromuscular junction. This junction is the critical region where muscles and nerves communicate. When electrical impulses travel down a nerve to trigger muscle movement, the nerve endings release a neurotransmitter called acetylcholine, which binds to receptors on the muscle and causes it to contract. In myasthenia gravis, antibodies block, alter, or destroy these receptors, preventing the muscle from contracting.
Myasthenia gravis can be diagnosed through repetitive nerve stimulation, single-fibre electromyography (considered the most sensitive test), and blood tests. Single-fibre electromyography can detect impaired nerve-to-muscle transmission, even in mild cases. Blood tests can reveal elevated levels of acetylcholine receptor antibodies or anti-MuSK antibodies, although some cases of myasthenia gravis are seronegative.
COVID-19 infection can precipitate the onset of myasthenia gravis, and patients may present with classic symptoms such as ptosis and fluctuating muscle weakness. Therefore, when examining patients with post-COVID muscle weakness, it is crucial to identify myasthenia and assess specific symptoms.
Additionally, the regrowth of nerve fibres following COVID-19-induced damage takes 2–3 years, and patients may need to be supported to live within the limitations imposed by their muscle weakness.
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Muscle weakness after recovery from COVID-19
Muscle weakness is a common symptom of COVID-19, and it can persist during recovery, even after the infection has cleared. This reduction in physical capability is not just general fatigue but is often linked to measurable changes in muscle tissue.
During an acute COVID-19 infection, motor neurons and adjacent muscles can be directly damaged by the virus or the immune response. This damage impairs muscle contraction and regeneration, prolonging weakness. In addition, the immune response triggered by COVID-19 can also harm muscle tissue. When the body detects the virus, it releases pro-inflammatory cytokines, which help fight the infection but also contribute to systemic inflammation. This inflammation can cause muscle pain and soreness, particularly in the legs.
COVID-19 can also cause respiratory muscle weakness, reduced exercise capacity, and impaired lung functions in the long term. A study found that 41% of post-COVID-19 patients reported respiratory muscle weakness, with low exercise capacity and abnormal lung functions. Another study found that 8 out of 10 adults who get COVID-19 experience fatigue during their illness, and this can continue as one of the symptoms of post-COVID syndrome.
To manage muscle weakness after COVID-19, it is important to support the body's natural healing process. This may include rest, elevating the legs, using ice packs, gentle massages, and light stretching. Maintaining gentle levels of activity while avoiding overexertion is recommended. Nutritional deficiencies, including reduced protein intake, can delay recovery, so ensuring adequate nutrition is important. B vitamins are essential for nerve regrowth, so supplementation may be beneficial.
If you are experiencing muscle weakness after recovering from COVID-19, it is important to seek medical advice, as further investigations may be required to identify any underlying causes or conditions.
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Muscle weakness during COVID-19
Muscle weakness is a common symptom of COVID-19, and it can persist long after the initial infection, affecting everyday functioning and quality of life. This symptom has been dubbed "long COVID" and is experienced by around one-third of COVID-19 survivors.
COVID-19 can cause muscle weakness through various mechanisms. One key mechanism is the virus's ability to attach itself to the ACE2 receptor on skeletal muscle cells, allowing it to enter and infect the cell. This interference with the ACE2 receptor results in a breakdown of communication between nerves and muscles, impairing the body's ability to build and maintain muscle mass. Additionally, an overactive immune response to the virus can lead to excessive inflammation, a condition known as a "cytokine storm," which can also contribute to muscle weakness and pain.
The immune response to the virus can also result in damage to motor neurons and adjacent muscles, leading to acute conditions such as Guillain-Barré syndrome and prolonged muscle weakness. Furthermore, COVID-19 can cause damage to the anterior spinal cord, resulting in myelopathy, which can present with muscle wasting and brisk reflexes. Specific plexopathies, such as brachial neuritis and lumbosacral plexopathy, have also been reported following COVID-19 infection.
The regrowth of nerve fibres following COVID-19-induced nerve damage can take 2–3 years. During this recovery period, patients may experience muscle weakness, fatigue, and brain fog due to central nervous system inflammation. It is important to note that graded exercise programs are not recommended for patients with long COVID, as rest and gentle activity are crucial for managing symptoms and avoiding "boom-bust" cycles.
Vitamin D and B vitamin deficiencies have also been identified as modifiable causes of muscle weakness in long COVID patients. Therefore, identifying and treating these deficiencies can be an important part of managing muscle weakness in this context.
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Muscle weakness due to medication
Muscle weakness can be a symptom of many illnesses, including COVID-19. During an acute COVID-19 infection, the virus or the immune response can directly damage motor neurons and adjacent muscles, leading to muscle weakness. This can also result in myelopathy, which affects the upper and lower limbs. In addition, COVID-19 can cause inflammation throughout the body, leading to muscle pain and soreness.
However, muscle weakness can also be a side effect of certain medications. This is known as drug-induced myopathy, which is characterised by muscle weakness, pain, inflammation, stiffness, spasms, and cramps. The following types of medications have been associated with drug-induced myopathy:
- Cholesterol-lowering drugs, such as statins (e.g., simvastatin and atorvastatin) and fibrates (e.g., fenofibrate and gemfibrozil). Statins are among the most commonly prescribed medications for managing cholesterol, and muscle weakness is a common side effect. Combining a statin with other cholesterol medications can be dangerous and may increase the risk of muscle breakdown (rhabdomyolysis).
- Antiarrhythmic medications used to treat heart rhythm problems, such as amiodarone and procainamide.
- Corticosteroids, such as prednisone, especially when taken in high doses or for prolonged periods. Corticosteroids can cause muscle weakness by altering muscle fibre behaviour and lowering potassium levels, which are essential for muscle function.
- Antiepileptic drugs, such as lamotrigine and phenytoin.
- Omeprazole, which is used to treat gastroesophageal reflux disease (GERD).
- Antiretroviral drugs like zidovudine (AZT), which is an older HIV medication known for causing muscle weakness.
- Fluoroquinolone antibiotics, such as levofloxacin and ciprofloxacin, which are used to treat bacterial infections.
It is important to note that not everyone who takes these medications will develop myopathy or experience muscle weakness. If you are concerned about potential side effects, consult your doctor or pharmacist to discuss the risks and benefits of your medication.
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Frequently asked questions
Yes, COVID-19 can cause muscle weakness. It is one of the many signs of COVID-19, including coughing, fever and fatigue.
Angiotensin-converting enzyme 2 (ACE2) exists in two forms: one anchored to cell membranes (mACE2) and the other as a soluble variant (sACE2). SARS-CoV-2, the virus that causes COVID-19, latches onto the ACE2 receptor, acting as a doorway for the virus to infect cells. When the ACE2 receptor is hijacked by the virus, it can lead to a breakdown in communication between nerves and muscles, resulting in muscle weakness.
It is estimated that around one-third of individuals who recover from COVID-19 experience lingering symptoms such as fatigue, breathlessness, "brain fog", and muscle weakness.
There is currently no specific treatment for muscle weakness caused by COVID-19. However, physical therapy and exercises can help individuals regain their muscle strength. Researchers are working on developing medications to treat individuals who have not completely recovered from COVID-19 and experience persistent symptoms, including muscle weakness.
