Centro Fisioterapia e Osteopatia Martinelli Gianluca

03/12/2025

🧠 𝙀𝙭𝙚𝙧𝙘𝙞𝙨𝙚 𝙄𝙣𝙩𝙚𝙣𝙨𝙞𝙩𝙮 𝙈𝙖𝙩𝙩𝙚𝙧𝙨: 𝙁𝙞𝙣𝙙𝙞𝙣𝙜 𝙩𝙝𝙚 𝙊𝙥𝙩𝙞𝙢𝙖𝙡 𝘿𝙤𝙨𝙚 𝙛𝙤𝙧 𝘽𝙧𝙖𝙞𝙣 𝙃𝙚𝙖𝙡𝙩𝙝

▪️ Aerobic exercise is a recognized medical intervention effective in preventing and managing chronic conditions, including dementia, by protecting against age-related brain atrophy and cognitive decline.
▪️ The key molecular link mediating this neuroprotective effect is muscle–brain crosstalk, facilitated by factors released from skeletal muscle during contraction, known as myokines.

💬 𝗠𝘆𝗼𝗸𝗶𝗻𝗲𝘀: 𝗠𝗼𝗹𝗲𝗰𝘂𝗹𝗮𝗿 𝗠𝗲𝘀𝘀𝗲𝗻𝗴𝗲𝗿𝘀

▪️ Neuroprotective myokines—including FNDC5/Irisin, Cathepsin B (CTSB), and Vascular Endothelial Growth Factor (VEGF), along with metabolites in the kynurenine pathway—are upregulated during exercise.
▪️ These factors ultimately enhance the expression of Brain-Derived Neurotrophic Factor (BDNF), a pivotal neurotrophin crucial for neurogenesis, synaptic plasticity, learning, and memory, predominantly expressed in the hippocampus.

⚡𝗧𝗵𝗲 𝗖𝗲𝗻𝘁𝗿𝗮𝗹 𝗤𝘂𝗲𝘀𝘁𝗶𝗼𝗻 𝗼𝗳 𝗜𝗻𝘁𝗲𝗻𝘀𝗶𝘁𝘆

▪️ While the neuroprotective effects of exercise are clear, the most effective “dose” of aerobic exercise to promote beneficial changes in these myokine pathways is currently unknown.
▪️ Most existing evidence stems from moderate-intensity exercise studies, and research on high-intensity exercise (like High-Intensity Interval Training or HIIT) is scarce.
▪️ The review emphasizes that intensity matters, highlighting the need for standardized intensity classifications (e.g., Low, Moderate, High, based on metabolic thresholds) to effectively compare research findings.

🔬 𝗜𝗻𝘁𝗲𝗻𝘀𝗶𝘁𝘆 𝗮𝗻𝗱 𝗞𝗲𝘆 𝗣𝗮𝘁𝗵𝘄𝗮𝘆𝘀: 𝗪𝗵𝗮𝘁 𝘁𝗵𝗲 𝗘𝘃𝗶𝗱𝗲𝗻𝗰𝗲 𝗦𝗵𝗼𝘄𝘀

▪️ FNDC5/Irisin: There is emerging evidence suggesting that high-intensity exercise may have a superior impact on circulating Irisin levels compared to lower intensities.
▪️ Moderate- to high-intensity training has also been shown to be superior (≈ 2-fold) to low-intensity training in increasing FNDC5 protein levels in rodent skeletal muscle.

▪️ CTSB: This protease promotes adult hippocampal neurogenesis (AHN) and neural debris clearance.
▪️ Moderate-intensity exercise increases CTSB in muscle and plasma, but research on high-intensity exercise effects is lacking.

▪️ Kynurenine Metabolites: The balance between neuroprotective Kynurenic Acid (KA) and neurotoxic Quinolinic Acid (QA) is critical.
▪️ High-intensity training is hypothesized to be superior in promoting neuroprotective metabolites (via PGC-1α activation), but current human studies show no difference in key metabolite levels between low- and high-intensity exercise.

▪️ Adult Hippocampal Neurogenesis (AHN): In contrast to myokine upregulation, low- to moderate-intensity training appears to be the strongest stimulus to enhance AHN (cell proliferation and maturation) in rodents, often improving AHN to a greater extent than high-intensity training.

🎯 𝘾𝙤𝙣𝙘𝙡𝙪𝙨𝙞𝙤𝙣 𝙖𝙣𝙙 𝙁𝙪𝙩𝙪𝙧𝙚 𝘿𝙞𝙧𝙚𝙘𝙩𝙞𝙤𝙣

▪️ The current evidence is insufficient to draw definitive conclusions on the optimal intensity for maximizing neuroprotective myokine benefits.
▪️ Future research must utilize well-controlled studies, such as work-matched training interventions, and standardize intensity definitions to accurately determine the optimal exercise dose.
▪️ Understanding how exercise intensity regulates myokines holds significant promise in offering therapeutic avenues to alleviate the burden of neurodegenerative conditions like dementia.

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⚠️Disclaimer: Sharing a study or a part of it is NOT an endorsement. Please read the original article and evaluate critically.⚠️

Link to Article 👇

30/11/2025

Just published 🔥

𝗥𝗲𝗰𝗼𝘃𝗲𝗿𝘆 𝗦𝘁𝗮𝗴𝗲𝘀 𝗔𝗳𝘁𝗲𝗿 𝗔𝗻𝘁𝗲𝗿𝗶𝗼𝗿 𝗖𝗿𝘂𝗰𝘂𝗶𝗮𝘁𝗲 𝗟𝗶𝗴𝗮𝗺𝗲𝗻𝘁 𝗥𝗲𝗰𝗼𝗻𝘀𝘁𝗿𝘂𝗰𝘁𝗶𝗼𝗻 🦵

📘 https://pubmed.ncbi.nlm.nih.gov/41314701/

Postoperative rehabilitation after an anterior cruciate ligament (ACL) reconstruction is critical for restoring strength, function, and confidence while reducing the risk of reinjury. Recovery generally takes 9 to 12 months and follows a phased, time- and criterion-based progression that guides safe advancement through rehabilitation (https://pubmed.ncbi.nlm.nih.gov/27539507/).

𝗘𝗮𝗿𝗹𝘆 𝗣𝗵𝗮𝘀𝗲 (𝗪𝗲𝗲𝗸𝘀 0–6)
This phase focuses on reducing pain and swelling, restoring knee range of motion (ROM), and reactivating the quadriceps—aiming for a quadriceps limb symmetry index (LSI) ≥60%. Modalities such as neuromuscular electrical stimulation and blood flow restriction (BFR, https://pubmed.ncbi.nlm.nih.gov/38889851/) training may support early strength gains. Open kinetic chain exercises can be gradually incorporated to strengthen the quadriceps without overloading the graft (safe start after 4 weeks within a restricted range of motion (ROM) of 90-45°, https://pubmed.ncbi.nlm.nih.gov/39985872/)

𝗜𝗻𝘁𝗲𝗿𝗺𝗲𝗱𝗶𝗮𝘁𝗲 𝗣𝗵𝗮𝘀𝗲 (𝗪𝗲𝗲𝗸𝘀 7–9)
Entry into this phase requires achieving 0°–115° of ROM, ≤1+ effusion, and a normalized gait. Rehabilitation emphasizes balance work, neuromuscular re-education, and aerobic conditioning. The major goals are full, symmetrical ROM and quadriceps strength reaching an LSI of at least 70%, typically achieved through progressive overload strength training.

𝗟𝗮𝘁𝗲 𝗣𝗵𝗮𝘀𝗲 (𝗪𝗲𝗲𝗸𝘀 10–16)
Running is introduced once quadriceps strength (and hop tests) reaches an LSI ≥70-80%, no or minimal pain (

29/11/2025

28/11/2025

Cancer deaths expected to rise to over 18 million in 2050—an increase of nearly 75% from 2024, study forecasts.

Over 40% of cancer deaths globally are linked to 44 modifiable risk factors including to***co use, an unhealthy diet, and high blood sugar—presenting an opportunity for prevention.

Explore the latest data, link in comments below 👇

📊 Figure: Global age-specific cancer (A) incidence and (B) mortality in 2023 for all sexes combined.

23/11/2025

23/11/2025

is a common disease among older adults that weakens bones and increases the likelihood of fractures.

Worldwide, 1 in 3 women and 1 in 5 men older than 50 years have a bone fracture due to osteoporosis during their lifetime.

This JAMA Patient Page describes osteoporosis risk factors, symptoms, screening, diagnosis, and treatment. https://ja.ma/481nFIs

22/11/2025

🟦 Cervicogenic Dizziness (CGD): Exploring a Debated Clinical Entity Linking Neck Pain and Balance

👉Cervicogenic dizziness (CGD) is a significant clinical concern, recognized as a potential cause of dizziness and vertigo, which affects up to 15 to 20% of adults annually.

While commonly recognized in clinical settings, CGD remains a debated clinical entity.
This perspective explores the complex nature of CGD, focusing on its proposed pathophysiology, the persistent diagnostic challenges, and promising therapeutic strategies.

👇

🟦 Defining Cervicogenic Dizziness

👉Cervicogenic dizziness is characterized as a non-rotatory dizziness associated with cervical pain or dysfunction, resulting from altered proprioceptive input from the cervical spine.
Patients typically describe sensations of light-headedness, giddiness, unsteadiness, or a feeling of imbalance, rather than true vertigo.
The dizziness is usually provoked by cervical movements or positions, specifically head movements relative to the torso.
A crucial aspect of CGD is the coincidence of neck pain and dizziness.
43% of patients with long-lasting neck pain report dizziness, a prevalence higher than the general population.
In the narrow definition of CGD, the condition is linked to a sensory mismatch hypothesis caused by cervical proprioceptive impairment.

🟦 Pathophysiology: The Sensory Mismatch Theory

👉Balance maintenance relies on the integration and interpretation of input from the visual, vestibular, and somatosensory systems, including cervical proprioception.
In CGD, disrupted cervical proprioception interacts maladaptively with the vestibular and visual systems, leading to postural instability and dizziness.

▪ Proprioceptive Impairment

Altered proprioceptive inputs often originate from mechanoreceptors and muscle spindles in the deep cervical muscles, joints, discs, and ligaments.
Dysfunctional joints can alter afferent input, and this aberrant information interacting with the vestibular nuclei may cause dizziness.

▪ The Role of Pain

Neck pain is a major factor in disrupting proprioceptive signals.
Acute conditions like whiplash injuries can damage these receptors.
Subjects with cervical pain exhibit decreased sensorimotor control, supporting the idea that pain fosters a sensory mismatch.
Experimentally induced deep cervical muscle pain has been shown to distort head-on-trunk orientation in humans.

▪ Central Maladaptation

Cervical proprioceptive signals converge with vestibular and visual inputs at multiple levels of the central nervous system, including the vestibular nuclei, thalamus, and cerebral cortex.
When chronic cervical dysfunction is present, compensatory mechanisms may become maladaptive.
This results in abnormal interactions between sensory cortices, leading to maladaptive sensory reweighting.
This maladaptive process may contribute to the visual dependence observed in patients with neck pain and CGD.

▪ Autonomic Symptoms

CGD can involve autonomic symptoms like nausea and palpitations, possibly due to connections between the spinal cord/vestibular nuclei and the reticular formation/parabrachial nucleus, causing abnormal sympathetic outflow.

🟦 Diagnostic Challenges and Assessment

👉Diagnosis is complicated by the absence of specific diagnostic criteria or gold-standard tests.
Therefore, CGD remains a diagnosis of exclusion, requiring clinicians to rule out other potential causes of dizziness such as vestibular, cardiovascular, or central nervous system disorders.

▪ History Taking

Clinicians focus on symptoms of imbalance or unsteadiness, the presence of neck pain or stiffness, and a temporal relationship where neck pain precedes dizziness.

▪ Physical Examination

This focuses on the upper cervical spine, combined with oculomotor and balance testing.

▪ Cervical Mobility and Pain

Assessment of active cervical movements may reveal reduced range of motion, and palpation often reveals local muscle tenderness or tightness.
Reproduction of dizziness or pain during these tests is considered consistent with CGD.

▪ Joint Position Error (JPE)

This test assesses proprioceptive input by measuring the accuracy of returning the head to a predefined position.
Patients with CGD demonstrate greater JPE compared to those with benign positional vertigo.
However, these deficits are not unique to CGD.

▪ Oculomotor Testing

The Cervical Rotation Torsion Test rotates the body beneath a stationary head to isolate cervical afferents and shows diagnostic utility.
CGD patients more frequently exhibit nystagmus during this test.
The Smooth Pursuit Neck Torsion Test is another proposed tool but has limited specificity.

▪ Balance Testing

Posturography shows distinctive patterns of altered postural control in patients with suspected CGD.
These patients also demonstrate reduced neck mobility compared to controls.

✨

🟦 Therapeutic Implications

There is moderate evidence that treatment targeting the neck reduces CGD symptoms.
Management should address both cervical and vestibular components.

▪ Manual Therapy

Manual therapy combined with specific movement exercises aims to restore cervical joint function and reduce pain.
These interventions may normalize proprioceptive input by restoring normal movement.
Systematic reviews support the use of cervical manual therapy for CGD.

▪ Sensorimotor Exercises

A tailored sensorimotor control program addressing head and eye movement control and balance can reduce symptoms and help prevent recurrence.

▪ Integrated Care

Given the complexity of central maladaptation, treatment should not focus solely on one system.
Integrated care including vestibular rehabilitation alongside cervical-focused interventions is recommended.

📝

🟦 Future Research Directions

▪ Standardized Diagnosis

There is a need for validated diagnostic criteria with adequate sensitivity and specificity.
Current tests provide insights but lack diagnostic precision.

▪ Central Mechanisms

Further investigation is needed to understand how chronic cervical dysfunction affects sensory processing and why only some individuals with neck pain develop CGD.

▪ Proprioceptive Training

There is a lack of studies evaluating specific proprioceptive training in treatment protocols despite its clear relevance.

A comprehensive framework for diagnosis and management is required to better serve patients with persistent dizziness and cervical involvement.

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⚠️Disclaimer: Sharing a study or a part of it is NOT an endorsement. Please read the original article and evaluate critically.⚠️

Link to Article 👇

20/11/2025

📌Effects of physical exercise on neuromuscular junction degeneration during ageing: A systematic review

👉Physical exercise (or physical training) serves as a therapeutic strategy aimed at decelerating or potentially reversing age-related neuromuscular junction (NMJ) degeneration.
In brief, the effects of physical exercise on the NMJ, particularly in aged animals and humans, include:

🧩 General and Structural Remodeling

▪️ 🏋️ Exercise promotes NMJ hypertrophy and accelerates the remodeling process in the elderly, which may mitigate NMJ degradation and alleviate the progression of neuromuscular degeneration.

▪️ 🔄 Physical exercise can result in a partial reversal of structural alterations that have already occurred due to aging.

▪️ 🚴 Endurance training demonstrated a more pronounced effect on NMJ structural remodeling compared to resistance and voluntary exercise regimens, especially in fast twitch muscle fibers.

▪️ 💪 The adaptations of NMJ to resistance exercise appear to be independent of changes in muscle fiber profile.

👇

🧠 Presynaptic Compartment

▪️ 🔬 Some studies reported significantly smaller and more homogeneous nerve terminals in old animals following exercise.

▪️ 🌿 Exercise may lead to a greater number of nerve terminal branches and total branch length in young animals, although this effect was less observed in older animals.

▪️ 📌 Exercise training affects presynaptic proteins, such as Bassoon, which anchors active zones for presynaptic ACh vesicles.

▪️ 🦵 In one study, all physiological age-related changes were prevented in the extensor digitorum longus (EDL) NMJs by exercise, but not in the soleus NMJs.

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🎯 Postsynaptic Compartment (AChRs)

▪️ ✨ Exercise helps promote the formation and maintenance of acetylcholine receptor (AChR) clusters.

▪️ 🧩 It reduces postsynaptic receptor fragmentation.

▪️ 📐 Exercise improved the AChR perimeters and the overlap area of the NMJ in aged animals.

▪️ 📈 Resistance exercise has been shown to result in a 2-fold increase in the number of AChRs per field.

👇

🔬 Molecular and Functional Changes

▪️ 🛡️ Exercise stabilizes key regulatory proteins: Physical exercise promotes AChR cluster formation and maintenance by increasing recombinant docking protein 7 (Dok7) expression and stabilizing Agrin and lipoprotein receptor-related protein 4 (LRP4). Dok7 protein expression was found to be significantly higher in the exercise group than in sedentary mice.

▪️ ⚡ NMJ Transmission: Voluntary wheel running resulted in a significant improvement in NMJ transmission.

▪️ 🧬 Exercise influences gene expression: There is a significant upregulation of AChR α1 mRNA in the exercised leg in both elderly and young women. Genes encoding transporters and receptor components of glutaminergic transmission were significantly upregulated in exercised muscles in aged rodent models.

▪️ 💠 Physical exercise has been shown to improve the proportion of Type IIB muscle fibers and decrease Type IIA fibers in the gastrocnemius muscle of aged mice.

▪️ 🔋 Exercise may counteract age-related mitochondrial oxidative stress, which is implicated in metabolic impairment of NMJs. Physical exercise induces mitochondrial morphological adaptations and increases the capacity to produce ATP.

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⚠️Disclaimer: Sharing a study or a part of it is NOT an endorsement. Please read the original article and evaluate critically.⚠️

Link to Article 👇

12/11/2025

09/11/2025

ANATOMY OF TRIGEMINAL NERVE ✍️.

✅ The trigeminal nerve (CN V) is the fifth cranial nerve, originating in the brainstem from four nuclei (three sensory and one motor). It forms a sensory root and a motor root that merge before giving rise to the trigeminal ganglion, a cluster of nerve bodies. From the ganglion, it branches into three divisions: the purely sensory ophthalmic (V1), maxillary (V2), and mandibular (V3) nerves, with V3 also carrying the motor fibers.

✅ Core components
Nuclei: The nerve's nuclei are located in the brainstem (midbrain to medulla) and include:
Sensory nuclei: Mesencephalic, principal sensory, and spinal.
Motor nucleus: Controls chewing muscles.
Roots: The sensory and motor nuclei form the sensory and motor roots, respectively, which emerge from the pons.
Trigeminal Ganglion: Located in a dural cave in the middle cranial fossa, this is where the sensory neuron cell bodies reside. The motor root runs beneath the sensory root.

✅ The three branches
Ophthalmic (V1) (Sensory): Supplies the scalp, forehead, upper eyelid, and nose.
Maxillary (V2) (Sensory): Supplies the lower eyelid, cheeks, upper lip, and nasal cavity.
Mandibular (V3) (Mixed): Carries sensation from the lower lip, jaw, and chin, and is the only branch to contain motor fibers, which control the muscles of mastication (chewing).

09/11/2025

Just pubished 🔥

𝗔𝗲𝗿𝗼𝗯𝗶𝗰 𝗘𝘅𝗲𝗿𝗰𝗶𝘀𝗲 🚴‍♀️ 𝗮𝘀 𝗮 𝗧𝗵𝗲𝗿𝗮𝗽𝗲𝘂𝘁𝗶𝗰 𝗢𝗽𝘁𝗶𝗼𝗻 𝗳𝗼𝗿 𝗖𝗵𝗿𝗼𝗻𝗶𝗰 𝗟𝘂𝗺𝗯𝗮𝗿 𝗥𝗮𝗱𝗶𝗰𝘂𝗹𝗮𝗿 𝗣𝗮𝗶𝗻. 𝗔 𝗖𝗮𝘀𝗲 𝗦𝗲𝗿𝗶𝗲𝘀

Lumbar radicular pain (LRP), often termed sciatica, is a prevalent musculoskeletal condition with a lifetime incidence of up to 43% (https://pubmed.ncbi.nlm.nih.gov/18923325/). Patients with LRP typically experience more severe pain and disability compared to those with nonspecific low back pain (https://pubmed.ncbi.nlm.nih.gov/21358478/; https://pubmed.ncbi.nlm.nih.gov/23328336/). Conventional conservative management—including manual therapy, motor control training, or neurodynamic techniques—offers only modest benefits (https://pubmed.ncbi.nlm.nih.gov/36580149/).

🚴 Emerging preclinical evidence has highlighted the potential neuroprotective and analgesic benefits of aerobic exercise (AE) in animal models of sciatic nerve injury, showing reductions in hypersensitivity and neuroinflammation (https://pubmed.ncbi.nlm.nih.gov/36690283/; https://pubmed.ncbi.nlm.nih.gov/38137395/). Despite these promising findings, there is a substantial translational gap, as AE has been scarcely examined in clinical populations with radiculopathy (https://pubmed.ncbi.nlm.nih.gov/33490836/).

📘 In a brand-new study, Esposto, Arca, and Schmid (2025,👉 https://www.jospt.org/doi/10.2519/josptcases.2025.0171) conducted a case series to investigate whether aerobic exercise could be safely and feasibly integrated into a tele-rehabilitation program for patients with chronic lumbar radicular pain, and whether it may improve pain and functional outcomes.

✏️ This retrospective case series followed CARE guidelines (https://pubmed.ncbi.nlm.nih.gov/28529185/) and included five adult patients (aged 25–49 years) presenting with chronic lumbar radicular pain with or without radiculopathy treated in a telemedicine rehabilitation setting.

📋 The criteria for diagnosing lumbar radicular pain with or without radiculopathy followed published clinical recommendations: pins and needles or numbness in the involved lower limb; leg pain more severe than back pain; leg pain spreading below the knee; motor, sensory, or reflex deficits upon neurological examination; positive neurodynamic test (eg, straight-leg raise [SLR] or crossed SLR). The presence of a minimum sum score of 6 out of 10, representing 93% probability of sciatica according to Stynes et al. (https://pmc.ncbi.nlm.nih.gov/articles/PMC5886387/), was required for inclusion.

🚴 Intervention

Participants underwent a multicomponent tele-rehabilitation program combining:

💬 Patient education about pain mechanisms and active recovery. The aim was to help patients understand the difference between acute and persistent pain, the specifics of nerve pain, and the role of active recovery strategies such as AE.

💪 Graded strengthening to address strength deficits identified during the initial examination As patients’ tolerance and confidence improved, the program progressed to include more complex movements as well as specific activities that patients wanted to be able to perform again) and

💁‍♂️ neurodynamic exercises (eg, nerve sliders, performed daily within a pain-free range of motion).

🚴 Aerobic exercise (AE) was performed 3–5 times per week (cycling, walking, or interval running) with a duration of 20 to 30 minutes per session. AE was prescribed at 60–70% of maximum heart rate (HRmax), estimated by Fox’s formula (HRmax = 220 – age, https://pmc.ncbi.nlm.nih.gov/articles/PMC7523886/). Exercise intensity and duration were progressively adjusted based on tolerance. The specific modality was chosen based on the patient’s preference and symptoms tolerance, utilizing either a stationary bike, walking, or a combination of walking and running. For patients who chose running, a graded interval-based approach was used, starting with short running intervals (eg, 1 minute) alternating with longer walking periods (eg, 3 minutes).

📊 Outcome Measures

Primary outcomes were:

▶️ Pain intensity, measured by the Numeric Pain Rating Scale (NPRS)
▶️ Function, assessed by the Patient-Specific Functional Scale (PSFS)

Outcomes were measured monthly for 3–6 months. Adherence and adverse events were recorded at each session.

📊 Results

All five patients showed large, clinically meaningful improvements in both pain and disability:

✅ Mean leg pain decreased by 4–8 points on the NPRS.

✅ Functional scores on the PSFS improved by 3–6 points, surpassing minimal clinically important differences (https://pubmed.ncbi.nlm.nih.gov/24828475/).

✅ Average adherence was 87.6% for the full program and 86.2% for AE specifically.

✅ No major adverse events occurred; there were four minor and two moderate self-limiting flare-ups.

✅Notably, four patients reported immediate post-exercise hypoalgesia, consistent with the phenomenon of exercise-induced hypoalgesia described in pain research (https://pubmed.ncbi.nlm.nih.gov/30904519/; https://pubmed.ncbi.nlm.nih.gov/33062901/).

💡 Discussion

Aerobic exercise might be a feasible, safe, and potentially effective adjunct for patients with chronic lumbar radicular pain. These results provide preliminary clinical support for preclinical findings showing AE’s role in modulating neuroinflammation and promoting neural recovery (https://pubmed.ncbi.nlm.nih.gov/36690283/; https://pubmed.ncbi.nlm.nih.gov/38137395/).

While the multimodal design precludes causal attribution to AE alone, consistent improvement across all cases strengthens the hypothesis that AE contributes meaningfully to symptom relief and functional recovery. Moreover, the tele-rehabilitation approach demonstrated strong feasibility and adherence.

⭕ Key limitations include:

☑️ Small sample size (n=5) and lack of a control group
☑️ Retrospective design and absence of long-term follow-up
☑️ Possible inaccuracy in AE intensity estimation via HRmax formula

Illustration of SLR: https://www.magonlinelibrary.com/doi/abs/10.12968/pnur.2023.34.11.400?journalCode=pnur