The effect of physical and breathing exercises on functional outcomes in patients with myasthenia gravis

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Introduction

Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disease that attacks the neuromuscular junction in skeletal muscles, characterized by fluctuating muscle weakness that worsens with activity and significantly impairs patients’ quality of life (QoL) [1, 2]. This condition primarily involves the extraocular, oropharyngeal, and limb muscles and can extend to the respiratory muscles, causing myasthenic crisis, which is a medical emergency [2]. Although MG is rare, advances in diagnostic methods have led to an increasing incidence and prevalence of this condition worldwide. A recent systematic review estimated a mean incidence of 15.7 cases per million per year and a prevalence of 173.3 cases per million, representing more than a two-fold increase compared to data from 14 years earlier [3, 4].

The burden of MG extends beyond neuromuscular symptoms, encompassing considerable decline in physical function, social life, vitality, and emotional well-being. These negative effects are more pronounced in women, patients with severe disease, and individuals with low socioeconomic status. Mental comorbidities, including anxiety, depression, and chronic fatigue, along with low social support, further worsen patients’ overall condition. In addition, MG substantially affect family planning, employment, and financial stability, underscoring the necessity of a multidimensional management approach [1].

While pharmacological therapy and surgical interventions such as thymectomy remain central to MG management, optimal care also requires integrated rehabilitative strategies, particularly for patients with mild to moderate symptoms. Evidence suggests that moderate-intensity physical exercise, respiratory training, and balance exercises can improve muscle strength, functional capacity, and QoL without aggravating the symptoms. Respiratory rehabilitation has been shown to prevent respiratory complications common in MG, while psychosocial interventions, including group therapy, may alleviate fatigue and reduce social isolation [5–8].

However, current evidence base for exercise and respiratory rehabilitation in MG is still limited and lacks standardization. Existing studies are constrained by small sample sizes, short intervention duration, and heterogeneous protocols, with only a few addressing functional, cardiorespiratory, and psychosocial outcomes comprehensively. Consequently, there is no consensus on safe and effective exercise recommendations for MG patients [9–13].

To date, no review has specifically examined the role of physical and respiratory exercise as integral components of MG rehabilitation. Therefore, this narrative review aims to synthesize the current evidence on the effects of exercise-based interventions on physical function, respiratory capacity, and QoL in patients with MG. The findings are expected to provide clinicians, particularly in Physical Medicine and Rehabilitation, with a practical reference for developing evidence-based rehabilitative strategies in clinical practice.

Methods

This narrative review was conducted by synthesizing evidence from relevant articles obtained through a structured search of PubMed and Web of Science databases, and the Google Scholar search engine. Additional references were identified by manually searching the citation lists of included studies and by reviewing relevant textbooks and grey literature to enrich the discussion.

The search strategy employed a combination of Medical Subject Headings (MeSH) terms and text words, including: “early physical therapy” OR “early rehabilitation” OR “early mobility” OR “pulmonary rehabilitation” OR “exercise” OR “exercise therapy” OR “endurance training” OR “respiratory rehabilitation” OR “respiration” OR “respiratory function tests” OR “muscle strength” OR “lung function” OR “tidal volume” OR “vital capacity” OR “quality of life” OR “respiratory insufficiency” OR “cycle ergometer*” AND “myasthenia gravis” OR “myasthenia crisis” OR “myasthenic” OR “myasthenias” AND “rehabilitation” OR “therapeutics*”.

The inclusion criteria were articles published in English or Indonesian and the studies discussing the role of physical or breathing exercise in patients with MG. All study designs (randomized controlled trials, observational studies, case series, and relevant reviews) that contributed to the study objectives were included. Articles without full-text were excluded.

The selection process involved two steps: (1) screening titles and abstracts to assess relevance, followed by (2) full-text review of potentially eligible articles. Disagreements were resolved by discussion among the authors. Ultimately, the most relevant studies that fulfilled the objectives of this review were synthesized narratively.

Results

The search process yielded several potentially relevant articles. After removing duplicates and applying inclusion and exclusion criteria, seven articles were identified as directly addressing the effects of physical or breathing exercises on functional outcomes in patients with MG. These studies included a variety of designs, predominantly intervention-based studies, and were supplemented by supportive literature from reviews and textbooks.

The included evidence was narratively summarized to provide a comprehensive overview of the clinical impact and disability burden of MG, the role of physical exercise in improving muscle strength, functional capacity, and QoL, and the role of breathing exercise in preventing respiratory complications and enhancing respiratory function. This synthesis provides an integrated discussion of the therapeutic potential of rehabilitation strategies in MG, highlighting current evidence while identifying remaining gaps in knowledge.

Functional impairments associated with myasthenia gravis

Dyspnea

Dyspnea in patients with MG generally reflects respiratory muscle weakness. However, subjective complaints of breathlessness without other bulbar symptoms rarely indicate a life-threatening myasthenic crisis. Comprehensive evaluation, including pulmonary function testing, is essential, particularly when symptoms occur during physical activity. Subjective dyspnea without objective evidence of muscle weakness typically does not constitute a basis for therapeutic escalation [3].

Patients with MG may exhibit shallow breathing and hyperventilation at rest and during light activity. Exacerbating factors include deconditioning, weight gain, obstructive sleep apnea, and anxiety, often worsened by corticosteroid use. Interventions such as physical exercise and respiratory muscle training (e.g., diaphragmatic breathing and pursed-lip breathing) have been shown to improve respiratory muscle endurance and reduce the perception of breathlessness [3].

In generalized MG, diaphragmatic weakness can cause life-threatening respiratory insufficiency. This condition typically presents as a restrictive pattern on spirometry with reduced maximal voluntary ventilation (MVV), known as the myasthenic pattern. Even in well-controlled patients, obstructive patterns may be observed, with lower forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) ratios compared to controls. Dyspnea during strenuous activity is frequently attributed to ventilatory muscle weakness and contributes to reduced functional capacity and limitations in activities of daily living [8].

Fatigue, fatigability, and exercise intolerance

Fatigue in MG is multifactorial and may occur even in the absence of prominent neuromuscular weakness. Central mechanisms involving regulation by the central nervous system play a role in limiting physical activity as a protective response against muscle damage, but this also perpetuates a cycle of inactivity, muscle loss, and chronic fatigue. Contributing factors include long-term corticosteroid use, weight gain, and comorbidities such as thyroid disease, diabetes, cancer, and pulmonary disorders [14].

Psychosocial factors, including sleep disturbances, depression, and hormonal fluctuations (particularly in women), also contribute to fatigue. Although the causal relationship between fatigue and depression remains unclear, with two conditions often overlap. To date, there is no evidence-based pharmacological therapy available for MG-related fatigue, making physical and psychological interventions the mainstay of management [14].

Fatigue frequently persists despite improvement in muscle strength; thus, escalation of immunosuppressive therapy is not recommended solely for fatigue management. Its assessment relies heavily on subjective questionnaires, and no consensus exists regarding the most reliable objective measurement tool. Fatigue in MG is affected by muscle weakness, physical inactivity, depression, poor sleep hygiene, comorbidities, and disease severity [14].

Fatigability, or progressive decline in physical performance, can be assessed using the 6-minute walk test and the arm movement test. This decline correlates with acetylcholine receptor antibodies levels but not with body mass index. In contrast, subjective fatigue perception often does not correlate with fatigability test outcomes, highlighting the complex mechanisms underlying fatigue in MG [8].

Fatigue affects up to 80% of MG patients across disease stages and may result from a combination of muscle weakness, sleep disorders, weight gain, physical deconditioning, mood disturbances, medication effects, and mild cognitive impairment (“cognitive fogginess”). Fatigue without hallmark MG symptoms does not require immunotherapy escalation. Management strategies include cognitive-behavioral therapy, aerobic exercise, weight reduction, sleep assessment, pain management, and treatment of mood disorders [3].

Exercise intolerance in MG, caused by proximal muscle weakness, fatigability, and respiratory muscle dysfunction, promotes a sedentary lifestyle that worsens risks of obesity, respiratory infections, osteoporosis, and increases fall and fracture risk. This vicious cycle leads to further decline in physical fitness and persistent fatigue [8].

Peripheral skeletal muscle weakness

Muscle weakness in MG results from impaired postsynaptic neuromuscular transmission due to acetylcholine receptor antibodies. This reduces muscle activation and manifests clinically as isometric weakness in large muscle groups, such as shoulder abductors, knee extensors, and ankle extensors. Muscle strength correlates with clinical scales such as the Quantitative Myasthenia Gravis Score, and Myasthenia Gravis Composite score. Fluctuating and progressive weakness, particularly in generalized MG, is a major cause of functional disability affecting activities of daily living [15].

Respiratory muscle dysfunction

Respiratory muscle dysfunction is a key marker of severity and prognosis in MG, particularly in generalized MG. Impaired neuromuscular transmission in inspiratory and expiratory muscles, including diaphragm and intercostal muscles, leads to reduced resopiratory capacity, tidal volume, and cough reflex. This increases the risk of hypoventilation, aspiration, respiratory infections, and myasthenic crisis requiring mechanical ventilation. Risk factors include muscle-specific tyrosine kinase antibodies, history of thymoma, older age, and respiratory comorbidities [16].

Respiratory dysfunction significantly impacts daily activities and QoL, with patients experiencing dyspnea even during light activity, fatigue, and anxiety about disease exacerbation. Consequences extend to social and occupational domains, leading to decreased participation and higher hospitalization rates. Sleep-disordered breathing, including nocturnal hypoventilation and obstructive sleep apnea, is also common [16].

Respiratory muscle function is assessed using maximum inspiratory pressure (MIP) and FVC, particularly in the supine position, as an indicator of diaphragmatic weakness. Impaired expiratory strength reduces cough effectiveness, increasing risks of atelectasis and aspiration pneumonia. Management strategies include regular respiratory monitoring, patient education, long-term immunomodulatory therapy, and rehabilitative interventions [16].

Limitations in activity, social participation, and QoL

Patients with MG experience limitations in functional activities such as walking long distances, climbing stairs, lifting objects, and performing household chores. Muscle weakness increases energy expenditure even for simple tasks, thereby accelerating fatigue. Performance on functional tests such as the 30-Second Chair Stand Test and 400-Meter Walk Test demonstrates reduced mobility and independence. High levels of subjective fatigue are often reported despite the absence of objective fatigability, underscoring the central role of body perception and psychosocial factors [15].

Difficulties in chewing solid foods and dyspnea at rest are key determinants of low QoL in MG. Weakness of masticatory muscles leads to altered eating patterns and malnutrition risk, while breathlessness reduces physical activity and social interaction. Other predictors of poor QoL include older age, longer disease duration, generalized MG, high disability scores, and use of high-dose corticosteroids. Poor response to repetitive nerve stimulation (RNS) at diagnosis further worsens QoL outcomes [17].

MG also has a significant psychological impact. Patients may develop depression, anxiety, chronic fatigue, and sleep disturbances, particularly in refractory cases, among women, and in cases with positive acetylcholine receptor antibodies. These psychological conditions often worsen during active disease phases, further impairing daily functioning. Psychosocially targeted interventions remain limited, emphasizing the need for a holistic approach to MG management [8, 18, 19].

Social participation and work productivity are also affected by fluctuating symptoms and fatigue. Many patients report restrictions in mobility, domestic activities, interpersonal relationships, and experience job loss or reduced working hours before retirement age [19]. Social stigma, dependency, and isolation further exacerbate participation restrictions [20].

Data from L. O’Connor et al. demonstrate that approximately 78% of daily time in MG patients is spent sitting or being inactive, leading to decreased participation in recreational, social, and family activities. Active social engagement is strongly associated with better cognitive, psychological, and emotional outcomes [8].

To address participation limitations, a multidisciplinary approach is essential, encompassing functional rehabilitation, psychosocial counseling, workplace adaptations, and community support. Participation assessment should be an integral component of MG evaluation to design targeted rehabilitation interventions [8].

The effects of physical and respiratory training on functional outcomes in myasthenia gravis

Exercise protocol

The exercise interventions applied in patients with MG (Table 1) included aerobic exercise (AE), resistance exercise (RE), balance and stretching exercises, respiratory exercises, and inspiratory muscle training (IMT). Evidence regarding structured physical or respiratory training in MG remains limited, and no standardized protocol has been established to date. Reported programs have been delivered either under direct supervision or through remote monitoring using diaries, phone follow-ups, or laboratory results [9–13].

 

Table 1. Physical and breathing exercises in rehabilitation of patients with MG

Component	AE [9, 10, 12, 21, 22]	RE [13]	Breathing exercise [9, 11]	IMT [10]	Balance and stretching [13]
Frequency	·                  3×/week (cycle ergometer, 8 weeks) [9] ·                  1×/day (walking, 7 days) [10, 21] ·                  2×/week (interval bike, 12 weeks) [12, 22]	2×/week during 12 weeks [13]	·                  1×/day during 7 days ·                  (rebreathing) [11] ·                  Every day (deep breathing and pursed-lip breathing) [9]	2×/day during 6 weeks [10]	2×/week during 12 weeks [13]
Intensity	·                  Heart rate rest + 30% [9] ·                  50–70% heart rate reserve (rate of perceived exertion 11–12) [10] ·                  80% maximum heart rate (interval 2’) [12, 13]	Individual load, 2 sets × 10 repetition maximum, monitored by a physiotherapist [13]	Respiratory rate 25–35×/minutes, up to the maximum limit that can be maintained for 5–8 minutes [11]	Start 30% MIP, increase every 2 weeks: 35% → 40% → 45% MIP [10]
Time	·                  30 minutes (cycle ergometer: 5’ warm-up, 20’ inti, 5’ cool-down) [9] ·                  30 minutes walking (5’ slow — 2’ fast — 5’ slow) [10]	± 40–45 minutes per session [13]	·                  10 minutes (rebreathing) [11] ·                  5–15 minutes (deep breathing and pursed-lip breathing) [9]	10–15 minutes/ session (6 sets × 5 breaths, including warm-up and cool-down) [10]	± 15 minutes (2 balance + 6 stretching) [13]
Type	·                  Walking and extremity ·                  movement [10] ·                  Cycle ergometer (steady and interval) [9]	Large muscle exercise: biceps curl, latissimus dorsi pulldown, leg press, etc. [13] Using heavy equipment & body weight [13]	·                  Rebreathing bag (50–60% vital capacity) [11] ·                  Deep breathing and pursed-lip breathing [9]	Threshold IMT: inhale — hold — exhale [10]	Static balance exercises and muscle stretching [13]
Volume	·                  90 minutes/week (cycling, 3×/week) [9] ·                  210 minutes/week (walking) [10] ·                  25 minutes/session (interval bike × 2/week) [12]	140 repetition/ session × 2×/week × 12 weeks [13]	70 minutes/week (10’ × 7 days) – (deep breathing and pursed-lip breathing) not counted explicitly [9]	± 140–210 minutes/week (2 session × 10–15’ × 7 days) [10]	± 15 minutes × 2x/week × 12 weeks = 360 minutes in total [13]
Progression	Adjusted bicycle load (heart rate or metronome) [9, 12]	The training load is increased gradually on an individual level [13]	·                  Respiratory rate adjusted until tolerance threshold is reached [9] ·                  VT adjusted based on the patient’s ability [11]	The load is gradually increased based on %MIP every 2 weeks [10]	No progression

 

Respiratory muscle endurance training (RMET) was implemented using a normocapnic hyperpnea method (rebreathing technique for controlled hyperpnea). The program consisted of two phases: an intensive 4-week training phase followed by a 12-month maintenance phase (Table 2) [12]. Conventional breathing exercises, such as deep breathing and pursed-lip breathing, were mainly educational and were not always structured quantitatively [9, 10].

 

Table 2. Respiratory muscle exercise endurance training [11]

Component	Phase 1: intensive training	Phase 2: maintenance training
Frequency	5 sessions per week (a total of 20 sessions over 4 weeks)	5 sessions per 2 weeks (reduced frequency)
Intensity	Ventilation target: 50–60% MVV for 15 seconds Tidal volume: 50–60% of vital capacity Respiratory rate: 25–35/minute	The intensity remains the same, but is adjusted if conditions worsen or improve
Time	30 minutes per session. If unable, 2 × 15 minutes at the beginning of the exercise	30 minutes per session
Type	RMET (normocapnic hyperpnea training with portable rebreathing device)	RMET (normocapnic hyperpnea training with portable rebreathing device)
Volume	150 minutes per week × 4 weeks = 600 minutes total	75 minutes per 2 weeks × 52 weeks = 1.950 minutes in 12 months
Progression	Gradual tidal volume adjustment ± 200–300 ml based on ability. If necessary, increase the respiratory rate by 1–2 breaths per minute	No explicit progression is mentioned, but targets are maintained and adjusted if necessary

 

In another study, a combined intervention of physical training and behavioral therapy was conducted once weekly for 30 minutes over 10 weeks. Training intensity was individualized based on patient tolerance, and the study included nine stable MG patients with fatigue as the primary complaint [21]. Another trial delivered AE and RE based on established guidelines, with a frequency of twice weekly for 12 weeks. Sessions lasted 75 minutes, performed at moderate intensity [22].

Effects of exercise on functional outcomes

Effects on pulmonary function

RMET over 13 months did not produce significant changes in vital capacity, FEV1, or peak expiratory flow (PEF), which were within normal limits at baseline. However, MVV for 15 seconds increased significantly, with a trend toward improvement in MIP and MEP in the intervention group. These findings indicate enhanced endurance and ventilatory efficiency despite stable baseline pulmonary function [11].

Adaptive changes in breathing pattern were also observed, including reduced respiratory frequency and prolonged expiratory time at rest, reflecting improved ventilatory control and reduced work of breathing [11]. N. Amalina et al. (2024) reported that low-intensity AE using a stationary cycle for eight weeks significantly improved FVC and FEV1 compared with controls. This effect was attributed to improved alveolar compliance, recruitment of previously inactive alveoli, and increased thoracic cavity expansion induced by repeated aerobic activity. Improvements were also linked to enhanced respiratory muscle strength and greater expiratory muscle contribution. Notably, the lack of change in the FEV1/FVC ratio likely reflected a larger increase in FVC relative to FEV1 [9].

Similarly, C.L. Chang et al. (2025) demonstrated that combined IMT and AE over six weeks significantly improved pulmonary function, with an increase in FVC of 0.21 ± 0.24 L (p < 0.001) and an FEV1 gain of 0.19 ± 0.34 L, while controls showed a decline. These effects were attributed to diaphragm hypertrophy, enhanced respiratory muscle blood flow, and activation of auxiliary respiratory muscles such as the rectus abdominis and internal intercostals [10]. In contrast, M.A. Rahbek et al. (2017) reported stable aerobic capacity (VO₂peak) following eight weeks of progressive AE and RE, likely due to limited intervention duration, small sample size, and reduced exercise tolerance from respiratory muscle weakness [12]. E. Westerberg et al. (2017) similarly found no significant changes in PEF or RNS, reinforcing that supervised training does not compromise respiratory safety in MG patients [22].

Effects on dyspnea

RMET reduced the perception of breathing effort during exercise. In the intervention group, perceived effort at the halfway point decreased from 72.8% to 65.4%, while in the control group it increased. This suggests improved respiratory efficiency and reduced dyspnea. Mechanistically, these effects were linked to optimized breathing patterns, reduced respiratory muscle fatigue, and improved ventilatory coordination [10]. This is consistent with findings reported by C.L. Chang et al. (2025), where Modified Borg Scale scores declined significantly in the IMT+AE group (p < 0.001), explained by improved respiratory muscle strength, enhanced neuromotor control, and attenuated reflex sympathetic activation [10].

Effects on fatigue, fatigability, and exercise intolerance

RMET significantly extended time-to-exhaustion from 10.5 to 29.5 minutes after 12 months, accompanied by reduced perceived exertion during training [11]. Combined IMT and AE increased exercise capacity, demonstrated by improved 6-minute walk test performance and reduced Borg scores, reflecting enhanced respiratory muscle strength and ventilatory efficiency [10]. M.E. Farrugia et al. (2018) assessed fatigue using modified fatigue impact scale, the visual analogue fatigue scale and the fatigue severity scale, showing transient improvements during intervention that were not sustained at follow-up [21]. Progressive resistance training reduced muscular fatigability, with one reported case of transient bulbar symptom exacerbation not requiring program discontinuation [12]. Clinical fatigue did not worsen, Myasthenia Gravis Composite scores remained stable, and Exercise Self-Efficacy Score improved, reflecting increased exercise confidence [22]. Notably, fatigue severity scale scores did not change significantly, likely due to limited sensitivity in MG populations [13].

Effects on peripheral muscle strength

RMET improved peripheral muscle performance, evidenced by an increase in squat repetitions from 21 to 30 per minute after 12 months [11]. This suggests improved oxygen delivery and reduced systemic fatigue. Progressive RE enhanced knee extensor strength by 10%, whereas AE alone had no significant effect, highlighting the role of RE in strengthening proximal muscles commonly affected in MG [12]. E. Westerberg et al. (2017, 2018) reported increased quadriceps compound muscle action potential amplitudes and resistance load capacity, with significant improvements in functional measures such as the 30-Second Chair Stand Test and muscle thickness on ultrasound, despite no significant changes in static hand-held dynamometry [13, 22].

Effects on respiratory muscle function

Breathing exercises yielded significant improvements in respiratory muscle capacity and efficiency. S. Freitag et al. (2018) reported increases in time-to-exhaustion and MVV for 15 seconds and reduced variability in minute ventilation, mediated by diaphragm strengthening and improved ventilatory control [11]. N. Amalina et al. (2024) and C.L. Chang et al. (2025) also reported gains in MIP and MEP, reflecting activation of primary respiratory muscles [9, 10]. Importantly, E. Westerberg et al. (2018) found no decline in respiratory safety parameters (PEF) and RNS, supporting the safety of structured exercise programs in MG patients [13].

Effects on psychological function

Exercise had favorable effects on psychological well-being. S. Freitag et al. (2018) observed improved perceived physical fitness and reduced respiratory symptoms, while M.E. Farrugia et al. (2018) found non-significant but favorable changes in Hospital Anxiety and Depression Scale that regressed at follow-up. Patients also reported psychosocial benefits from group interaction and normalization of their symptoms [11, 21]. E. Westerberg et al. (2017) demonstrated improvements in Exercise Self-Efficacy Score, though scores plateaued in later trials, likely due to a ceiling effect [13, 22].

Effects on activities, social participation, and quality of life

Exercise positively influenced activity and participation outcomes. S. Freitag et al. (2018) documented improvements in MG functional scores, squat repetitions, and bulbar/ocular symptoms [11]. MG QoL scores declined after intervention, though worsened at follow-up [21]. Fatigue and depression strongly correlated with reduced QoL, highlighting the multidimensional impact of exercise. Progressive resistance training produced significant improvements in functional tests, whereas aerobic training effects were less pronounced [12]. E. Westerberg et al. (2017, 2018) reported gains in 6-minute walk test, 30-Second Chair Stand Test, and body composition, with MG QoL showing non-significant but positive trends [13, 22]. Collectively, these findings suggest that exercise enhances functional capacity and participation without compromising QoL.

Safety issues

Across studies, exercise interventions were generally safe and well-tolerated in stable MG patients (Table 3). In S. Freitag et al. (2018), 12 of 18 participants completed 13 months of RMET; dropouts were mainly due to severe comorbidities, with no major MG exacerbations reported. Mild transient muscle weakness was observed but required no medical intervention [11]. Similarly, E. Westerberg et al. (2018) reported no withdrawals due to MG relapse, with stable MG Composite, Quantitative Myasthenia Gravis Score, PEF, and RNS results and no laboratory evidence of muscle damage [13]. N. Amalina et al. (2024) confirmed the safety of low-intensity cycling, with dropouts driven by logistical rather than medical reasons [9]. E. Westerberg et al. (2017) and C.L. Chang et al. (2025) further confirmed safety at moderate intensities, while M.E. Farrugia et al. (2018) observed no acute exacerbations during a combined physical and psychological rehabilitation program [10, 21, 22]. One case of bulbar symptom exacerbation was reported in M.A. Rahbek et al. (2017), but overall clinical stability was maintained [12].

 

Table 3. Adverse events during exercise rehabilitation in patients with MG

Source	Adverse events
M.A. Rahbek et al. (2017) [12]	Progressive AE and RE at moderate to high intensities were generally safe. One patient experienced exacerbation of bulbar symptoms leading to discontinuation, but clinical status remained stable based on Quantitative Myasthenia Gravis Scores
E. Westerberg et al. (2017) [22]	Moderate-intensity exercise programs were safe in patients with mild MG (Class I–II), without triggering exacerbations or muscle injury
S. Freitag et al. (2018) [11]	No worsening of MG symptoms was observed. Some patients reported temporary muscle weakness, but none required medical intervention or withdrawal
E. Westerberg et al. (2018) [13]	No patients discontinued exercise due to MG exacerbation
M.E. Farrugia et al. (2018) [21]	One patient dropped out after the first session. No acute exacerbations or treatment changes occurred during the intervention
N. Amalina et al. (2024) [9]	No adverse effects were reported. Dropouts were attributed to non-medical reasons such as distance and time constraints
C.L. Chang et al. (2025) [10]	The combination of IMT and AE was well tolerated, with no adverse events or increases in pathological biomarkers

 

Conclusion

Physical and breathing exercise interventions in MG consistently demonstrated benefits across multiple functional outcomes, including pulmonary function, dyspnea, fatigue, peripheral and respiratory muscle strength, psychological health, and daily activity participation. Mechanisms include enhanced respiratory muscle strength, improved ventilatory efficiency, motor unit recruitment, and favorable psychosocial adaptations. Progressive resistance training reduced muscular fatigability and improved neuromuscular adaptation, while aerobic and respiratory training enhanced endurance and reduced symptom burden. Importantly, structured exercise programs were safe, with no evidence of disease exacerbation or pathological biomarker elevation. Collectively, exercise can be recommended as an integral component of comprehensive rehabilitation strategies in stable MG patients, supporting both physiological and psychosocial recovery.

About the authors

Lucky Nurdiansyah

Universitas Padjadjaran; Dr. Hasan Sadikin General Hospital

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0009-0008-5054-0941

MD, Department of physical medicine and rehabilitation, Faculty of medicine

Indonesia, Bandung; Bandung

Arnengsih Nazir

Universitas Padjadjaran; Dr. Hasan Sadikin General Hospital

Author for correspondence.
Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0001-8600-1925

MD, PhD, cardiorespiratory consultant, Department of physical medicine and rehabilitation, Faculty of medicine

Indonesia, Bandung; Bandung

Dian Marta Sari

Universitas Padjadjaran; Unpad University Hospital

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0003-2720-4532

MD, PhD, cardiorespiratory consultant, Department of physical medicine and rehabilitation, Faculty of Medicine

Indonesia, Bandung; Sumedang

Reinata Digjaya

Rumah Sakit Tentara Dustira — Cimahi

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0009-0001-3067-8846

MD, Medical department

Indonesia, Cimahi Tengah

References

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