Centre de formation et physiothérapie de Lutry

Centre de formation et physiothérapie de Lutry Centre de formation et physiothérapie

09/11/2025

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/).

📘 Esposto, Arca, and Schmid (2025, https://www.jospt.org/doi/10.2519/josptcases.2025.0171) conducted a case series to investigate whether AE 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. Patients were treated between October 2024 and April 2025 in a private 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
☑️ High variability in individual exercise regimens

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

01/11/2025

𝗛𝗼𝘄 𝗺𝘂𝗰𝗵 𝗮𝗲𝗿𝗼𝗯𝗶𝗰 𝗲𝘅𝗲𝗿𝗰𝗶𝘀𝗲 𝗶𝘀 𝗻𝗲𝗲𝗱𝗲𝗱 𝘁𝗼 𝗿𝗲𝗱𝘂𝗰𝗲 𝗺𝗶𝗴𝗿𝗮𝗶𝗻𝗲?

🤕 Migraine, a leading cause of disability affecting over 1.16 billion people worldwide (GBD Collaborators, 2024; Woldeamanuel & Cowan, 2017), contributes to an estimated $1.9 trillion economic burden in 2025 (Woldeamanuel et al., 2025). Given the limitations of pharmacologic therapy and access disparities in headache care (Bentivegna et al., 2023; Lanteri-Minet et al., 2024), scalable interventions like exercise are urgently needed.

📘 A brand-new dose-response meta-analysis by Ogrezeanu et al. (2025, https://pubmed.ncbi.nlm.nih.gov/41085000/) quantified, for the first time, a therapeutic dose of aerobic exercise for migraine and revealed a U-shaped dose–response curve.

🏃‍♀️Aerobic training significantly reduced both:

⬇️ Migraine pain intensity (SMD = –1.10),

⬇️ Attack frequency (SMD = –0.79),

✅ with optimal benefits achieved at 900–950 cumulative minutes of moderate-intensity aerobic exercise delivered over 10–11 weeks (equivalent to ~30 minutes, three sessions per week at 50–70% VO₂peak, infographic below).

👉 These findings build on earlier reviews supporting exercise efficacy (La Touche et al., 2020; Varangot-Reille et al., 2022; Reina-Varona et al., 2024) but are the first to define specific exercise dosing guidelines.

👉 Subgroup analyses suggest s*x differences and migraine chronicity modify treatment response:

▶️ Greater effects in episodic migraine than in chronic migraine (Ogrezeanu et al., 2025),

▶️ Larger reductions in attack frequency among women, consistent with s*x-based pain sensitivity and hormonal influences (Amin et al., 2018).

🏃‍♂️‍➡️ In an editorial, Woldeamanuel emphasizes a precision medicine approach, advocating graded exercise pacing to prevent overexertion cycles common in migraine patients (Andrews et al., 2012; Nielson et al., 2014). For sedentary individuals or those with kinesiophobia (fear of movement) (Benatto et al., 2019), exercise initiation at low intensity (40–50% VO₂peak) using time-contingent progression strategies is recommended (La Touche et al., 2023).

Importantly, exercise efficacy may be enhanced by addressing sleep and circadian regulation, as morning light exposure combined with exercise improves migraine stability (Youngstedt et al., 2016; Ong et al., 2018; Woldeamanuel et al., 2023).

💡 Practical tips:

☀️ Circadian Alignment: Encourage morning exercise with outdoor light exposure to stabilize sleep wake cycles.

😴 Lifestyle Integration: Advise consistent sleep (7-8 hoursnightly), strict meals at fixed daytimes, and hydration tracking.

⬆️ For complex cases with comorbid disorders—such as vestibular migraine, postural orthostatic tachycardia syndrome (POTS), or exercise intolerance—modifications including recumbent cycling, hydration strategies, compression garments, vestibular rehabilitation (gaze stabilization or balance training), and neck strengthening (Sun et al., 2022; Benatto et al., 2022) may improve tolerance.

🏋️‍♀️ Although promising, the review evidence is rated low to very low certainty due to heterogeneity and small sample sizes. In future studies, a comparison of aerobic vs. strength training is mandatory, as resistance training may be equally or more effective (Woldeamanuel & Oliveira, 2022; Wang et al., 2025; Sari Aslani et al., 2022).

✅ Conclusion

Exercise is positioned as a first-line behavioral intervention for migraine prevention. A personalized prescription of 900–950 cumulative minutes of moderate-intensity aerobic exercise over 10–11 weeks is supported by current evidence. Pharmacologic therapies should be used as bridge therapies to enable long-term lifestyle interventions that improve self-efficacy and disease control (Irby et al., 2016).

📚 References

Amin FM, Aristeidou S, Baraldi C, et al. (2018). J Headache Pain, 19:83.

Andrews NE, Strong J, Meredith PJ. (2012). Arch Phys Med Rehabil, 93:2109–2121.

Benatto MT, Bevilaqua-Grossi D, Carvalho GF, et al. (2019). Pain Med, 20:846–851.

Benatto MT, Florencio LL, Bragatto MM, et al. (2022). BMC Neurol, 22:126.

Bentivegna E, Onan D, Martelletti P. (2023). Neurol Ther, 12:337–342.

GBD 2021 Diseases and Injuries Collaborators. (2024). Lancet, 403:2133–2161.

Irby MB, Bond DS, Lipton RB, et al. (2016). Headache, 56:357–369.

La Touche R, Fernández Pérez JJ, Proy Acosta A, et al. (2020). Scand J Med Sci Sports, 30:965–982.

La Touche R, Fierro-Marrero J, Sánchez-Ruiz I, et al. (2023). J Headache Pain, 24:68.

Lanteri-Minet M, Leroux E, Katsarava Z, et al. (2024). J Headache Pain, 25:134.

Nielson WR, Jensen MP, Karsdorp PA, Vlaeyen JWS. (2014). Clin J Pain, 30:639–645.

Ogrezeanu DC, Núñez-Cortés R, Salazar-Méndez J, et al. (2025). Headache.

Ong JC, Taylor HL, Park M, et al. (2018). Headache, 58:1040–1051.

Reina-Varona Á, Madroñero-Miguel B, Fierro-Marrero J, et al. (2024). Headache, 64:873–900.

Sari Aslani P, Hassanpour M, Razi O, et al. (2022). Sport Sci Health, 18:433–443.

Sun L, Li G, Liu F, et al. (2022). Rev Neurol (Paris), 178:370–376.

Varangot-Reille C, Suso-Martí L, Romero-Palau M, et al. (2022). J Pain, 23:1099–1122.

Wang Y, Zhu X, Liang Y. (2025). Am J Lifestyle Med.

Woldeamanuel YW, Cowan RP. (2017). J Neurol Sci, 372:307–315.

Woldeamanuel YW, Oliveira ABD. (2022). J Headache Pain, 23:134.

Woldeamanuel YW, Palesh O, Cowan RP. (2023). Ann Neurol, 94:S152.

Woldeamanuel YW, Fani M, Javaheri E, et al. (2025). Ann Neurol, 98:S205.

Woldeamanuel YW. (2025). Headache, 00:1–4.

Youngstedt SD, Kline CE, Elliott JA, et al. (2016). J Circadian Rhythms, 14:2.

26/10/2025
La douleur est une illusion qui trompe énormément…
23/10/2025

La douleur est une illusion qui trompe énormément…

18/10/2025
18/10/2025

💊 Take Your Polypill! The Exerkine Network Behind Exercise-Induced Health

Engaging in physical exercise initiates the release of numerous signaling molecules from muscles and other organs. Collectively, these exercise-responsive factors are known as exerkines—humoral signaling molecules secreted in response to both acute and chronic physical activity. Exerkines exert their effects through endocrine, paracrine, and autocrine pathways (https://www.nature.com/articles/s41574-022-00641-2). A wide array of tissues contributes to exerkine production; for example, skeletal muscle releases myokines, while adipose tissue secretes adipokines, among others. Importantly, skeletal muscle is now recognized as a secretory organ. During contraction, it stimulates the release of myokines such as interleukin-6 (IL-6), brain-derived neurotrophic factor (BDNF), irisin, and others (https://pubmed.ncbi.nlm.nih.gov/27765498/; https://pubmed.ncbi.nlm.nih.gov/39456138/). These molecules play a pivotal role in communication between muscles and distant organs and are thought to be central mediators of the systemic health benefits associated with regular exercise.

The figure below gives an overview of the major exocrine-producing tissues and representative factors released in response
to exercise (https://pubmed.ncbi.nlm.nih.gov/41038351/):

💪 Skeletal Muscle (Myokines)

• IL-6: promotes glucose uptake and fat oxidation and reduces inflammation

• IL-15: supports muscle–fat crosstalk and mitochondrial biogenesis

• Irisin: cleaved from FNDC5, drives browning of white adipose tissue

• Myonectin (CTRP15): enhances lipid uptake in liver and adipose tissue

• Myostatin (GDF-8): negative regulator of muscle growth, downregulated by exercise

🧈 Adipose Tissue (Adipokines)

• Adiponectin: improves insulin sensitivity and anti-inflammatory signaling

• Leptin: regulates appetite and energy expenditure

• Resistin: links obesity to insulin resistance and inflammatory pathways

• Apelin: modulates cardiovascular function and glucose homeostasis

🧬 Liver (Hepatokines)

• FGF21: augments fatty-acid oxidation and ketogenesis

• Fetuin-A: influences insulin receptor signaling and inflammation

• ANGPTL4: regulates lipoprotein lipase and plasma triglycerides

❤️ Heart (Cardiokines)

• ANP (atrial natriuretic peptide): promotes vasodilation and lipolysis

• BNP (B-type natriuretic peptide): modulates blood pressure and natriuresis

🧠 Brain and Peripheral Nerves (Neurokines)

• BDNF (brain-derived neurotrophic factor): enhances synaptic plasticity and mood

• NGF (nerve growth factor): supports neuronal survival and repair

📦 Extracellular Vesicles & Nucleic Acids

• Exosomes carrying microRNAs (e.g., miR-21, miR-126): modulate gene expression in distant tissues

• Circulating mitochondrial DNA fragments: act as damage-associated molecular patterns

🌿 Vascular-Derived Factors (Angiokines)

• VEGF (vascular endothelial growth factor): stimulates angiogenesis and vascular remodeling

• Angiopoietins: regulate vascular stability and permeability

🦴 Bone-Derived Factors (Osteokines)

• Osteocalcin: influences energy metabolism and cognition

• Sclerostin: binds LRP5/6 co-receptors to antagonize Wnt/β-catenin signaling and fine-tune bone formation and remodeling

• FGF23: may dampen phosphate-driven microglial activation and the release of pro-inflammatory cytokines

🍽️ Gastrointestinal Tract-Derived Factors (Gastrokines)

• GLP-1 (glucagon-like peptide-1): contributes to improved glucose homeostasis and insulin sensitivity in skeletal muscle and adipose tissue

• Ghrelin: helps explain the transient appetite-suppressant (“anorexigenic”) window seen post-workout and contributes to exercise-induced improvements in energy balance

⚙️ Summary Insight

Exerkines form an integrated signaling network linking muscle activity to systemic adaptations — spanning metabolism, cardiovascular health, neuroplasticity, and immune regulation. Understanding these pathways provides insight into how exercise acts as a “polypill” for preventing and treating metabolic and chronic diseases.

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