Muscle Weakness After COVID: Why It Happens and What to Know

Many people recovering from COVID-19 experience lingering symptoms, including muscle weakness. This can range from mild fatigue to significant difficulty with daily activities, affecting quality of life even after the infection has cleared. While not everyone experiences this symptom, it is common enough to raise concerns about its underlying causes and long-term implications.

Understanding why COVID-19 leads to muscle weakness involves multiple biological processes. Immune system activity, inflammation, and neuromuscular disruptions all contribute to post-infection changes in muscle function.

Post Infection Effects on Muscle Strength

Following a COVID-19 infection, many individuals report a decline in muscle strength that can persist for weeks or months. This reduction in physical capability is not just general fatigue but is often linked to measurable changes in muscle tissue. Studies have shown that individuals recovering from COVID-19 exhibit decreased muscle mass and function, a phenomenon observed in both hospitalized patients and those with milder cases. A 2021 study in The Journal of Cachexia, Sarcopenia and Muscle found that patients recovering from severe COVID-19 had significant reductions in skeletal muscle density, suggesting the virus may contribute to muscle degradation beyond what is typically seen with prolonged inactivity.

One primary factor influencing post-infection muscle strength is reduced physical activity during illness. Even in non-hospitalized cases, prolonged bed rest or decreased movement due to fatigue leads to muscle atrophy. Research has established that just one to two weeks of inactivity can result in a measurable decline in muscle mass and strength. A 2020 review in The Journal of Physiology highlighted that muscle protein synthesis rates drop significantly during immobility, leading to a net loss of muscle tissue. This effect is particularly pronounced in older adults, who already experience age-related muscle decline and may struggle to regain lost strength.

Beyond inactivity, disruptions in muscle protein turnover further contribute to muscle weakness. Muscle maintenance depends on a balance between protein synthesis and degradation, and when this equilibrium is disturbed, muscle loss accelerates. A 2022 study in Clinical Nutrition found that COVID-19 patients exhibited altered amino acid metabolism, impairing the body’s ability to rebuild muscle efficiently. Nutritional deficiencies, including reduced protein intake due to appetite loss or gastrointestinal symptoms, further delay recovery.

Immune System Activity and Tissue Damage

The immune response triggered by COVID-19 plays a major role in muscle weakness. When the body detects the virus, it releases pro-inflammatory cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β). While these molecules help fight the infection, they also contribute to systemic inflammation, which can harm muscle tissue. A 2021 study in Nature Reviews Immunology highlighted that excessive cytokine production in severe COVID-19 cases leads to a hyperinflammatory state known as a cytokine storm, associated with widespread tissue damage, including in skeletal muscles.

Inflammatory mediators disrupt normal muscle function by interfering with mitochondrial activity and protein synthesis. Mitochondria, which produce cellular energy, are particularly vulnerable to inflammation. Research published in Cell Metabolism in 2022 found that COVID-19 patients exhibited mitochondrial dysfunction characterized by reduced ATP production and increased oxidative stress, both of which impair muscle endurance and strength. This impairment can persist beyond the acute phase of infection, prolonging fatigue and muscle weakness.

Direct muscle damage has also been observed in COVID-19 patients. Muscle biopsies from hospitalized individuals have revealed signs of myositis, an inflammatory condition characterized by muscle fiber degeneration and immune cell infiltration. A 2021 study in The Lancet Rheumatology found evidence of necrotic fibers and capillary dysfunction in critically ill COVID-19 patients, indicating that the virus or immune response directly harms muscle integrity. Such structural damage impairs muscle contraction and regeneration, prolonging weakness.

Some studies have also detected viral RNA in muscle biopsies, raising concerns about localized viral effects on muscle health. A 2022 investigation in Frontiers in Immunology identified viral remnants in muscle tissue months after infection, suggesting lingering viral components may contribute to chronic inflammation and delayed recovery.

Neuromuscular Interactions Related to Weakness

Muscle weakness after COVID-19 is not solely due to structural muscle changes but also involves disruptions in neuromuscular communication. The nervous system coordinates muscle activation, and when signaling is impaired, muscles may exhibit reduced strength, slower response times, and increased fatigue. Evidence from post-viral syndromes, including those following other coronaviruses like SARS-CoV-1, suggests that viral infections can alter nerve function, leading to prolonged neuromuscular deficits.

COVID-19 can affect neuromuscular function by damaging peripheral nerves, which carry signals from the central nervous system to muscles. Case reports have documented post-COVID neuropathies, including Guillain-Barré Syndrome (GBS), where the immune system mistakenly attacks nerve fibers, leading to weakness and, in severe cases, paralysis. Even without overt neuropathic conditions, electrophysiological studies have shown impaired nerve conduction velocity and reduced motor unit recruitment, indicating that the virus may disrupt nerve signaling pathways at a subclinical level.

Dysfunction at the neuromuscular junction—the site where nerve signals are transmitted to muscles—may also contribute to post-COVID weakness. Some patients report symptoms resembling myasthenia gravis, a condition in which antibodies interfere with acetylcholine receptors, leading to muscle fatigue. While direct autoimmunity against these receptors has not been definitively linked to COVID-19, transient disruptions in neurotransmitter signaling have been observed in other viral illnesses, raising the possibility that SARS-CoV-2 may similarly affect neuromuscular transmission.

Role of Inflammatory Markers in Recovery

Recovery from post-COVID muscle weakness is influenced by persistent inflammatory markers. Even after the acute infection resolves, elevated levels of C-reactive protein (CRP), ferritin, and serum amyloid A can remain, indicating ongoing inflammation. A study in The Lancet Respiratory Medicine in 2022 found that individuals with lingering post-COVID symptoms often exhibited persistently high CRP levels, suggesting unresolved inflammation contributes to delayed muscle recovery.

Prolonged inflammation can impair muscle regeneration by disrupting satellite cell function, which is essential for muscle repair. Research in The Journal of Physiology has demonstrated that excessive IL-6 activity interferes with satellite cell function, delaying muscle fiber regeneration. This effect is especially concerning in older adults, who already experience reduced regenerative capacity.

Hormonal and Metabolic Influences

Hormonal imbalances following COVID-19 can also contribute to prolonged muscle weakness. Cortisol, testosterone, and insulin-like growth factor 1 (IGF-1) regulate muscle protein synthesis and energy metabolism, and disruptions in these hormones can lead to muscle atrophy and delayed recovery.

One notable change following COVID-19 is increased cortisol levels. While short-term elevations help regulate inflammation and mobilize energy, prolonged high cortisol can accelerate muscle breakdown. Additionally, COVID-19 has been linked to suppressed testosterone levels, particularly in male patients. A 2021 study in The Journal of Clinical Endocrinology & Metabolism found that hospitalized COVID-19 patients had significantly lower testosterone levels than healthy controls, with those experiencing severe weakness showing the greatest declines.

Metabolic disturbances also contribute to post-COVID muscle weakness. Mitochondrial dysfunction impairs cellular energy production, leading to decreased endurance and increased fatigue. Altered glucose metabolism and insulin resistance have been reported, further hindering muscle recovery.

Commonly Reported Symptoms and Severity Patterns

The severity of muscle weakness after COVID-19 varies widely. While hospitalized patients often report profound muscle loss, even individuals with mild or moderate cases can develop persistent muscular fatigue that impacts daily life.

Many recovering patients describe a sensation of heaviness in their limbs, making simple movements like climbing stairs or carrying objects more challenging. This is often accompanied by rapid fatigue during exertion, suggesting impairments in muscle endurance. Some individuals also report muscle pain, stiffness, or cramping, which may be linked to lingering inflammation or nerve-related dysfunction. A survey in JAMA Network Open in 2022 found that nearly 40% of individuals recovering from COVID-19 experienced muscle weakness lasting more than three months, with older adults and those with pre-existing metabolic conditions showing the most prolonged symptoms.

Long Term Changes in Muscle Composition

Persistent muscle weakness following COVID-19 may lead to lasting alterations in muscle composition. Emerging research suggests prolonged inflammation, metabolic disturbances, and reduced physical activity during recovery can contribute to shifts in muscle fiber type distribution and overall muscle quality.

One concern is increased muscle fibrosis, where normal muscle tissue is replaced with connective tissue. Fibrotic changes reduce muscle elasticity and strength, making it harder to regain pre-illness performance.

Another potential long-term effect is a shift in muscle fiber composition from type II (fast-twitch) fibers to type I (slow-twitch) fibers. Prolonged inactivity and metabolic stress can lead to a preferential loss of type II fibers, resulting in decreased muscle power and slower recovery times.