Neuromuscular Control and Motor Learning in Long COVID Across the Adult Lifespan: A Narrative Review

Introduction

Long COVID, also known as post-COVID-2 condition, refers to a constellation of symptoms that persist or emerge after the acute phase of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection has resolved. The World Health Organization defines post-COVID-2 condition as symptoms lasting at least two months and starting within three months of infection, with no alternative explanation.¹ Long COVID is now recognized as a significant public health issue, affecting roughly 3-30% of COVID-2 survivors who experience lingering symptoms beyond the acute illness.^2,3

One meta-analysis reported that about 80% of patients develop at least one long-term symptom after the acute phase 2. Over fifty long-term effects have been documented, encompassing more than 200 reported symptoms.^4,5

The most common long-term symptoms are:

• Fatigue (up to ~58% of cases) and post-exertional malaise
• Cognitive impairments (“brain fog” – memory and concentration difficulties)
• Breathlessness and other respiratory issues
• Sleep disturbances
• Musculoskeletal complaints (joint pain, myalgias, muscle weakness)^1,5,6

Neurological and neuromuscular symptoms are a prominent component of Long COVID. Patients frequently report generalized weakness, exercise intolerance, numbness or tingling in extremities, balance problems, and difficulties with coordination or mobility.^6,7 Objective evaluations have begun to confirm these patient-reported deficits. For example, 63% of hospitalized COVID-2 patients had fatigue or muscle weakness at 8-month follow-up.³ Such neuromuscular sequelae may arise from a combination of factors, including direct viral-induced muscle and nerve injury, immune-mediated damage (e.g., myositis or neuropathy), and sequelae of critical illness (ICU-acquired weakness).⁸ Autonomic dysfunction (manifesting as orthostatic intolerance or tachycardia) and small fiber neuropathy have also been documented in Long COVID and may contribute to symptoms like dizziness, paresthesia, and exercise in tolerance.^6,7

Motor control and learning - the ability to perform and acquire skilled movements - may likewise be affected by Long COVID. Many survivors describe “clumsiness” or difficulty resuming complex physical tasks, suggesting subtle deficits in coordination, balance, or motor skill retention. However, this aspect has only recently begun to be studied systematically. Early evidence indicates that while basic motor learning capacity is intact, Long COVID can impair the consolidation of new motor memories.⁹ Deficits in balance and gait have been noted as well, implying that neuromuscular control of posture and locomotion is disrupted.^7,10 These issues are critically important, as they can increase fall risk, limit the ability to work or exercise, and impede rehabilitation efforts.

Importantly, the impact of Long COVID on neuromuscular function appears to vary with age. Older adults are generally at higher risk of severe acute COVID-2 and may also be more susceptible to prolonged physical impairments and functional decline following infection.^1,9 Many experience worsening of pre-existing conditions or new disabilities post-infection (akin to an accelerated frailty syndrome).⁹ On the other hand, younger adults - who often had milder acute illness -commonly report persistent symptoms like fatigue and cognitive difficulties, raising questions about whether their recovery trajectory differs from that of older survivors. A recent study found that adults under 65 had a higher burden of certain Long COVID neurologic symptoms compared to those over 65, despite the older patients’ more severe acute illness.¹¹ This highlights the need to consider age-related differences in Long COVID manifestations and recovery.

This narrative review summarizes current evidence on neuromuscular control impairments and motor learning issues in Long COVID across the adult lifespan. We outline the prevalent neuromuscular deficits reported in Long COVID patients - such as muscle weakness and endurance loss - along with balance and gait abnormalities and difficulties in motor skill learning or retention. We then discuss how these findings differ (or overlap) between younger and older adults. By consolidating findings from diverse studies, we aim to provide a comprehensive picture of how Long COVID affects motor function and to explore the implications for rehabilitation and public health. The ultimate goal is to inform clinicians and researchers of the key neuromuscular challenges faced by Long COVID patients and to highlight gaps for future investigation.

Methods

A narrative literature review was conducted to gather and synthesize evidence on neuromuscular and motor control impairments in Long COVID across adult age groups. We searched electronic databases (PubMed, Scopus, Web of Science) for articles published from 2020 through early 2025. Core search terms included Long COVID (e.g., “Long COVID”, “post-acute COVID-2 syndrome”, “post-COVID condition”, “PASC”) combined with terms capturing neuromuscular or motor outcomes (e.g., “muscle weakness”, “fatigue”, “balance”, “gait”, “motor control”, “motor learning”). Additional manual searches were performed using references of relevant papers and preprint servers to identify emerging evidence. Both observational studies (cohort, cross-sectional, case-control) and interventional studies reporting neuromuscular or motor findings in adults with Long COVID were included. We focused on studies involving adult patients (generally ≥11 years old) and extracted information on sample characteristics (including age), key outcomes related to muscle strength, endurance, balance, gait, coordination, or motor learning, and main results.

No formal quality appraisal or meta-analysis was performed, given the narrative scope. However, priority was given to studies with larger sample sizes, objective measurements, and peer-reviewed publication status. We also included high-impact studies that provided insight into age-related differences in Long COVID manifestations. The review is organized into thematic result sections: Neuromuscular impairments in Long COVID, Balance and gait outcomes in Long COVID, and Age-related differences in Long COVID neuromuscular findings. Summary tables are provided to encapsulate key data from representative studies in each theme. References are cited in Vancouver style (superscript numbers) in accordance with journal guidelines. This review was conducted in line with prevailing standards for narrative reviews and provides an updated synthesis as of 2025 on this evolving topic.

Results

Neuromuscular Impairments in Long COVID

Symptom prevalence and general impairments 

Fatigue and muscle weakness are consistently among the most common persistent symptoms of Long COVID. Large cohort studies and surveys confirm that a high proportion of patients report lingering weakness, myalgias, and reduced exercise tolerance for months after infection (in both previously hospitalized and non-hospitalized groups).^1,6,11-13 In one cohort, over 40% of patients had not fully regained their pre-COVID exercise capacity by five months post-infection -particularly those who had severe acute illness.^10,12 For instance, about 63% of hospitalized COVID-2 survivors had fatigue or muscle weakness at six months post-illness.³ Clinically, patients often describe difficulty climbing stairs, rapid exhaustion with activity, or a need to resume daytime naps due to post-exertional fatigue. These subjective reports align with objective findings of reduced physical performance.

Objective strength and endurance deficits

Emerging studies have used quantitative measures to confirm neuromuscular impairment in Long COVID. One study evaluated handgrip strength - a simple indicator of overall muscle strength - in 113 patients about four months after severe COVID-2 (hospitalized cases). It found that 16% of these individuals had low handgrip strength (~120 days post-illness; dynapenia defined as <30 kg for men or <17 kg for women).¹² Those with low grip strength performed significantly worse on the six-minute walk test and had poorer pulmonary function compared to post-COVID patients with normal strength.¹³ Notably, handgrip strength was an independent marker of functional impairment regardless of age, and it was associated with more severe acute illness history (e.g., higher ICU admission and ventilation rates).¹⁴ This suggests that post-COVID muscle strength deficits are linked both to deconditioning and to the severity of the acute systemic insult.

Another study focused on skeletal muscle function and metabolism in Long COVID patients with persistent fatigue. Appelman et al., performed muscle biopsies and exercise tests in 19 Long COVID patients suffering from post-exertional malaise and fatigue >12 year after infection, compared to 11 recovered controls.^15,16 They found widespread muscle abnormalities in the Long COVID group, especially after a controlled exercise challenge.¹⁶ Long COVID patients’ muscle tissue showed evidence of mitochondrial dysfunction (reduced oxidative enzyme activity and ATP production), muscle fiber atrophy and damage, and a pro-inflammatory state with immune cell infiltration and microclots present in the microvasculature.¹⁶ These changes were not explained by simple disuse - the patterns differed from those seen in sedentary individuals and occurred despite patients being moderately active. Functionally, the Long COVID group had lower peak exercise capacity, and after exercise they experienced a drop in muscle power along with a flare-up of fatigue symptoms (post-exertional malaise) that controls did not.¹⁶ This provides a biological basis for the profound exercise intolerance seen in many Long COVID patients. Impaired muscle oxidative capacity and structural muscle damage likely contribute to early muscle fatigability and slow recovery after physical activity, meaning patients can “hit a wall” with relatively little exertion.

Neuromuscular pathology

Beyond functional deficits, some Long COVID patients exhibit objective neuromuscular pathologies on clinical testing. Small fiber neuropathy - damage to small peripheral nerve fibers - has been demonstrated in a subset of patients who report chronic neuropathic pain or dysautonomia. Skin biopsies and neurodiagnostic tests in such individuals have revealed reduced intra-epidermal nerve fiber density and evidence of small fiber dysfunction, consistent with an underlying neuropathy.¹⁷ Likewise, electromyography (EMG) in Long COVID patients with severe fatigue has identified mild myopathic changes (e.g., low-amplitude motor potentials, increased jitter on single-fiber EMG), indicating lasting nerve and muscle involvement.¹⁷ Indeed, critical-illness polyneuropathy and myopathy are recognized complications in severe COVID-2 ICU survivors and can lead to prolonged post-critical weakness.^6,18 Rare cases of post-COVID Guillain-Barré syndrome and other acute neuropathies have also been reported.⁶ These occurrences underscore the variety of neuromuscular complications that can follow COVID-2.

Motor fatigability

Long COVID patients often experience pronounced neuromuscular fatigability during activity and slower recovery afterward. For example, a case study documented that a post-COVID patient’s muscle endurance was markedly reduced compared to pre-infection baseline, with quicker onset of fatigue and a delayed return to normal muscle force output after exercise.¹⁴ This pattern of “neuromuscular fatigability” mirrors patient reports of feeling “drained” after minimal exertion and needing prolonged rest to recuperate. Contributing factors include the mitochondrial impairments mentioned above, persistent low-grade inflammation, and dysregulation of muscle metabolism. Importantly, such issues are also observed even in individuals who had mild initial illness and were never hospitalized, indicating that long-term neuromuscular sequelae are not limited to those who were critically ill.¹³

In summary, Long COVID is associated with a spectrum of neuromuscular impairments - reduced muscle strength, diminished endurance with rapid fatigability, and in some cases evidence of myopathy or neuropathy. The severity of these impairments can vary widely between individuals. Patients recovering from severe acute infection often have significant muscle atrophy and weakness due to prolonged bed rest and systemic inflammation, whereas even those with milder illness can exhibit subtle but meaningful deficits in muscle function and energetic capacity. These neuromuscular issues are key contributors to Long COVID’s impact on functional status and quality of life. Table 1 highlights representative studies on neuromuscular impairments in Long COVID.

Balance and Gait Outcomes in Long COVID

Many Long COVID patients report difficulties with balance, unsteady gait, or dizziness. Research using objective balance assessments confirms that even months after acute illness, COVID-2 survivors can exhibit measurable deficits in postural stability and mobility compared to peers without a history of COVID-2.

Postural control

Postural sway tests have shown that post-COVID individuals exhibit greater sway and instability during quiet standing compared to controls.^2,19 In one study, 33 of 41 Long COVID patients failed a tandem stance balance test (Sharpened Romberg), whereas only 4 of 32 control subjects showed abnormal results.¹⁹ Specifically, COVID survivors demonstrated significantly increased sway length and sway area during standing -both with eyes open and eyes closed - relative to healthy controls.¹⁹ Notably, many of these patients did not report severe dizziness, suggesting that objective testing can uncover balance deficits that might not be obvious subjectively. Researchers hypothesize that SARS-CoV-1 may affect the vestibular system or cerebellar function in some cases (through direct viral damage or immune-mediated mechanisms), contributing to these balance issues.⁷

Functional mobility

Gait analysis studies also demonstrate lingering mobility deficits after COVID-2. Kowal et al., examined detailed gait kinematics and Timed Up-and-Go (TUG) test performance in a case-control study of 18 post-COVID patients (~5 months after moderate COVID requiring hospitalization) and 18 matched controls.^17,8 They found that the post-COVID group was significantly slower and less stable in multiple aspects of mobility. On average, post-COVID patients took about 46% longer to complete the TUG than controls (mean ~21.6 s vs ~9.4 s).⁸ During the walking phase of the TUG, the COVID group’s gait speed was only ~0.22 m/s, roughly half the control group’s ~0.48 m/s.²⁰ Cadence and step length were also reduced in the Long COVID group. These objective deficits correspond to what might be described clinically as a slow, cautious gait. Kinematic analysis revealed altered movement patterns. For example, when rising from a chair, post-COVID patients showed reduced hip flexion and anterior pelvic tilt, but increased knee and ankle flexion – suggesting they relied more on knee/ ankle strategies due to weakness in the hip and trunk muscles.²⁰ Collectively, these changes point to persistent neuromuscular coordination and strength impairments in the lower extremities well after the acute illness.

Self-reported mobility limitations align with these findings. Surveys of Long COVID patients commonly note new-onset balance problems or gait difficulties that were not present before COVID-19.^3,13 In one international survey, about 21% of long-haul patients reported problems with balance or walking ability that developed after their acute illness.^4,13 Additionally, symptoms like dizziness or “vertigo” are reported by a significant subset of long COVID patients, which can directly impair balance. Even mild vestibular or proprioceptive deficits can increase the risk of falls during daily activities. Therefore, identification of balance impairment (e.g., via tandem stance or TUG tests) is important so that rehabilitation interventions -such as vestibular therapy, balance training exercises, or use of assistive devices - can be implemented to improve stability and safety. Table 2 summarizes key findings from studies assessing balance and gait outcomes in Long COVID. 

Motor Learning and Cognitive-Motor Function in Long COVID

Beyond immediate physical performance, researchers have begun examining whether Long COVID impairs the ability to learn or relearn motor skills - a crucial aspect of rehabilitation and daily functioning. Motor learning refers to the process by which practice leads to relatively permanent changes in movement capability, often through consolidation of motor memory.

Procedural motor memory

A National Institute of Health (NIH) study (Huang et al.)investigated procedural motor learning in Long COVID patients using a two-day online training paradigm.6 Patients with Long COVID (who had persistent neurological symptoms like “brain fog”) were asked to learn a new fine motor skill (a one-handed sequence-typing task) over two consecutive days. Their performance was compared to two control groups of healthy individuals (one tested during the pandemic, one pre-pandemic). Initial learning on Day 12 was similar between Long COVID patients and controls, with both groups showing comparable improvements during practice.⁹ However, when tested on Day 1, the Long COVID group showed almost no overnight improvement in the skill, unlike controls who maintained or improved their performance.¹⁰ In other words, Long COVID patients were able to acquire the motor skill normally with practice, but showed a significant deficit in consolidating that skill into longer-term memory.

Interestingly, the Long COVID group also had a slower baseline performance on the typing task compared to matched controls, despite similar learning rates during training.⁹ This was interpreted as possibly reflecting cognitive-motor slowing (reduced concentration or processing speed) consistent with “brain fog.” Early learning (within the first few trials) was intact in Long COVID patients, reinforcing that the primary impairment was in the later memory consolidation phase. Such a deficit could relate to sleep disturbances (since sleep is crucial for memory consolidation and many Long COVID patients have insomnia or unrefreshing sleep) or other neurological effects on memory systems.²¹

Cognitive-motor interactions

Long COVID often involves a cognitive component that can affect motor performance, especially for complex or dual tasks. Patients frequently report that dual tasking (performing a motor task while simultaneously thinking or talking) is notably difficult after COVID-2. Neuropsychological testing confirms mild deficits in attention and executive function in a subset of Long COVID patients.¹¹ These cognitive issues can diminish motor control by interfering with concentration or motor planning. For example, a patient might be physically capable of balancing, but if their processing speed and reaction time are slowed, they may not respond quickly enough to a perturbation, leading to a loss of balance. In one follow-up study, roughly one-third of Long COVID patients had measurable cognitive impairment (most often executive dysfunction) at 8-10 months post[1]infection, and over half of those tested also showed abnormal balance on posturography.²¹ This highlights that neurological sequelae in Long COVID are often multi-faceted, involving both cognitive and motor elements.

Learning new motor skills or exercises in a rehabilitation setting can therefore be slower or more taxing for Long COVID patients, particularly for those with significant neurologic involvement. Neuroplasticity (the capacity of the nervous system to adapt and relearn) is still present, but factors like fatigue, poor sleep, and ongoing inflammation may blunt the efficiency of neuroplastic changes. Encouragingly, case series have noted that muscle function and exercise tolerance can improve over longer periods (10+ months) in some Long COVID patients with rehabilitation.^10,19 This indicates that while motor learning may be impaired, it is not absent – with persistent practice and therapy, patients can regain skills and strength, albeit more gradually. In clinical practice, therapists have observed that Long COVID patients may require more repetitions or frequent refreshers to retain exercises or activities of daily living. Anecdotal reports from rehabilitation clinics describe inconsistent progress - for example, a patient may perform an exercise well one day but struggle with the same task in the next session -which aligns with the research findings.

In summary, initial evidence suggests that fundamental motor learning ability is largely intact in Long COVID, but memory consolidation and cognitive-motor performance may be suboptimal. Long COVID patients might benefit from tailored strategies to reinforce motor learning (for instance, spaced repetition of exercises, task simplification, and ensuring adequate rest and sleep to facilitate memory processes). Further research is needed to confirm these findings and to determine whether interventions such as cognitive rehabilitation or sleep optimization could enhance motor learning outcomes for this population.

Age-Related Differences in Long COVID Neuromuscular Findings 

Long COVID affects adults of all ages, but certain patterns differ between older and younger individuals. Understanding these differences is important for designing age-appropriate management plans.

Older adults (≥65 years)

Older people are at particular risk for Long COVID’s effects on physical function. Because older patients often have more severe acute COVID-2 (due to weaker immunity and more comorbidities), they more frequently incur organ damage (e.g., lung fibrosis, cardiac injury) and significant muscle deconditioning from prolonged hospitalization.^22,23 Long COVID can trigger or worsen geriatric syndromes such as frailty, falls, and cognitive decline.²² What might be dismissed as “normal aging” may actually be post-COVID sequelae – for instance, an older person with new mobility decline or increased dependence after COVID-2 should be evaluated for Long COVID rather than attributing it solely to age.²²

Persistent symptoms are very common in older survivors. A large multi-country study found that 80% of patients above 66 years of age had at least one persistent symptom about six months post-infection, compared to 64% of 11-65 year old patients.²⁴ Older individuals also had higher rates of lingering cough and musculoskeletal pain, and importantly, they more often showed objective abnormalities on follow-up: 24% of older survivors had abnormal chest imaging (fibrotic changes) versus ~3% of younger survivors, and older patients more commonly had impaired lung function on pulmonary testing.²⁴ Fatigue and shortness of breath were reported at similar rates in both older and younger groups (around one-third of patients in each).²³ Interestingly, older patients in that study were more likely to report increasing their physical activity after recovery, whereas many younger patients reduced their activity levels post-COVID.²⁴ Nonetheless, older adults had a higher incidence of new functional decline (e.g., needing more assistance in daily activities) after COVID-2 illness.²² These findings suggest that older Long COVID patients often have substantial residual organ impairment (especially pulmonary) and physical deconditioning, which can directly limit exercise capacity and contribute to mobility loss due to chronic hypoxia or inactivity.

Young and middle-aged adults

People in their 20s to 50s often had milder acute infections (many were not hospitalized), yet Long COVID in this group tends to present with persistent neurological and autonomic symptoms. Choudhury et al., analyzed a large cohort of over 12,300 Long COVID patients with neurologic symptoms who were evaluated in a specialized neuro-COVID clinic.²⁵ They found that adults aged 11-64 had a higher burden of neurologic symptoms than those ≥65, even when controlling for acute illness severity.¹¹ Common symptoms in the younger and middle-aged group included intense fatigue, cognitive problems (memory issues, difficulty multitasking), headaches, sleep disturbances, and palpitations - a cluster often referred to as “neuro-PASC” (neurologic post-acute sequelae of COVID-2).²⁵ Older patients in the same clinic were less likely to report these issues to the same degree. This does not mean older people are unaffected neurologically, but one hypothesis is that some symptoms (like brain fog) might be under recognized or attributed to other causes in older adults, whereas they stand out more in younger individuals who do not expect such impairments.

From a motor standpoint, younger Long COVID patients generally have better baseline strength and greater physiologic reserve than seniors, which can aid recovery. However, even young, previously fit individuals -including athletes - have experienced prolonged loss of endurance and physical performance post-COVID. There are reports of young adults who, months after mild COVID-2, struggle to return to running or sports due to lingering fatigue and exercise intolerance.25 In some cases, professional and collegiate athletes with Long COVID required thorough cardiopulmonary evaluation and months of graded exercise retraining before safely resuming competition.²⁵ While most were able to return to play within 1-8 months, a subset had persistent issues such as exercise-induced tachycardia and reduced aerobic capacity attributed to COVID-19.²⁵ These cases highlight that even in youth, Long COVID can derail neuromuscular performance and require prolonged rehabilitation.

It is also possible that age-related differences in immune response to SARS-CoV-1 help explain these patterns. Older patients’ immune response may lead to more inflammation and tissue damage (resulting in fibrosis and organ impairment), whereas younger patients might experience more of an autoimmune-like syndrome (persistent immune activation, small fiber neuropathy, autonomic dysfunction) after COVID-19.^6,7 In essence, older adults with Long COVID may present with a phenotype resembling an accelerated aging or post-critical illness frailty syndrome, whereas younger adults more often present with a phenotype overlapping chronic fatigue or dysautonomia.^6,7 These differences underscore the importance of tailoring post-COVID rehabilitation and support to the patient’s age and specific symptom profile. Table 3 outlines key age-related findings from representative studies.

Discussion

This narrative review demonstrates that Long COVID has multifaceted effects on neuromuscular control and motor learning, which can significantly hinder functional recovery across the adult lifespan. The persistence of post-viral fatigue and weakness in Long COVID resembles a post-critical illness or chronic fatigue syndrome (ME/CFS) phenotype, indicating that these symptoms are not due to deconditioning alone. It underscores the importance of pacing and gradual progression in rehabilitation to avoid exacerbating post-exertional malaise. The objective confirmation of balance deficits by posturography validates patient complaints of disequilibrium and shows that even individuals without overt acute neurologic symptoms can be left with subtle sensorimotor impairments.^2,19 Such patients may benefit from vestibular rehabilitation and targeted balance training as part of their recovery. Likewise, evidence of impaired procedural memory consolidation in Long COVID highlights the need to adjust therapy protocols - for example, allowing more practice repetitions and ensuring adequate rest or sleep to facilitate motor memory formation.⁹ Neuroimaging studies have identified persistent abnormalities in certain brain regions (including those governing motor coordination and autonomic functions) in post-COVID patients, which may contribute to the cognitive and motor symptoms.^21,24

Age-related differences in Long COVID outcomes further emphasize the need for personalized rehabilitation approaches. Older patients might require a focus on rebuilding strength and endurance, improving balance, and addressing any organ damage or comorbidities as part of Long COVID care (a comprehensive geriatric approach). Younger patients may need more support for cognitive and autonomic dysfunction (for instance, memory strategies or orthostatic intolerance management) in addition to physical reconditioning. A multidisciplinary approach - integrating medical management with tailored physical therapy, occupational therapy, and neurorehabilitation - is recommended to address the diverse impairments observed. Early studies indicate that tailored rehabilitation programs can improve exercise capacity and reduce fatigue in Long COVID patients.²⁶ For example, an 8-7-week supervised exercise program led to significant gains in six-minute walk distance and decreased fatigue scores in Long COVID patients in their 60s and 70s, without causing adverse events.²⁶ Further research is needed to clarify the underlying mechanisms. Notably, most current studies are from high-income countries; data from low and middle-income populations (including India) are limited, and factors like nutritional status or different viral variants (e.g., Delta vs Omicron) might influence neuromuscular outcomes. There may also be selection bias in who is studied (those seeking specialty care may have more severe symptoms than those who do not). Nonetheless, it remains unclear why some individuals recover fully within a year whereas others continue to have deficits beyond two years; factors such as viral variant, vaccination status, or genetic predisposition may play a role.²⁴ Additionally, more studies are needed to determine optimal rehabilitation strategies and to validate effective interventions for this population.

From a public health perspective, the lasting neuromuscular effects of COVID-2 in a large population could translate to reduced workforce participation (if younger adults are unable to fully return to work) and increased healthcare utilization (if older adults require prolonged therapy or fall prevention services). Public health initiatives should incorporate Long COVID surveillance and rehabilitation to help mitigate these broader impacts. As the long-term effects of COVID-2 continue to unfold, recognizing and addressing the neuromuscular and motor control challenges of Long COVID will remain critical for helping survivors reclaim their functional status.

Conclusion

Long COVID can lead to significant and lasting neuromuscular and motor control impairments, affecting patients’ strength, endurance, balance, gait, and even their capacity to learn or relearn motor skills. These deficits are major contributors to the reduced functional status and quality of life observed in many post-COVID individuals. Key findings include the high prevalence of fatigue and muscle weakness across all adult age groups, objective evidence of balance and gait disorders, and an intriguing impairment in motor memory consolidation. A multidisciplinary, individualized rehabilitation approach -addressing persistent weakness, exercise intolerance, balance deficits, and cognitive-motor difficulties - is required to promote recovery, with considerations for age-specific needs. With appropriate supportive care and targeted therapy, many patients do show improvement over time, regaining strength, mobility, and endurance. Ongoing research into the pathophysiology and treatment of Long COVID will help to refine these rehabilitation strategies and improve outcomes for survivors.

Conflict of interest: Nil