Centro Fisioterapia e Osteopatia Martinelli Gianluca

31/12/2025

31/12/2025

🧩 𝐓𝐡𝐞 𝐌𝐲𝐬𝐭𝐞𝐫𝐲 𝐨𝐟 𝐭𝐡𝐞 𝐒𝐭𝐫𝐞𝐭𝐜𝐡-𝐒𝐡𝐨𝐫𝐭𝐞𝐧𝐢𝐧𝐠 𝐂𝐲𝐜𝐥𝐞: 𝐌𝐞𝐜𝐡𝐚𝐧𝐢𝐜𝐚𝐥 𝐨𝐫 𝐍𝐞𝐮𝐫𝐚𝐥?

■ In human movement, muscles often perform better when they are actively stretched immediately before they shorten. This phenomenon is known as the Stretch-Shortening Cycle (SSC).

■ A common example is the way we naturally dip down (stretch) before jumping up (shorten).
■ This sequence produces higher force, work, and power compared to a shortening movement that starts from a standstill—a boost known as the SSC effect.
■ While the existence of the SSC effect is well-documented, the exact physiological reasons behind it are debated.

■ Scientists generally group the causes into two categories:

■ ⚙️ Mechanical factors: Changes within the muscle fibers themselves, such as elastic energy return or the engagement of the protein titin.
■ 🧠 Neural factors: Changes in the nervous system, such as reflexes or increased excitability in the spinal cord and motor cortex.

■ A 2025 study by Rissmann et al. sought to determine if the brain and spinal cord modulate their excitability during the shortening phase of the SSC to contribute to this performance boost.

🔬 The Study Design

■ The researchers studied the plantar flexor muscles (calf muscles) of 18 healthy adults.
■ Participants performed two types of movements on a dynamometer, carefully matched to have the same level of muscle activity (EMG):
■ ➡️ Pure Shortening (SHO): The muscle shortened without a prior stretch.
■ 🔁 Stretch-Shortening Cycle (SSC): The muscle was actively stretched immediately before shortening.
■ To measure neural excitability during these movements, the researchers used advanced stimulation techniques:
■ 🧠 Transcranial Magnetic Stimulation (TMS): To measure cortical excitability (how responsive the motor cortex in the brain is).
■ 🧠 Cervicomedullary Electrical Stimulation (CES): To measure spinal excitability (how responsive the spinal cord is).
■ 📈 Electromyography (EMG): To detect stretch reflexes.

📊 Key Findings

■ 1. The SSC Effect is Real but Not Neural
■ As expected, the participants produced significantly more torque (about 12% more) during the SSC contractions compared to the pure shortening contractions.
■ However, when the researchers looked at the nervous system, they found no corresponding boost:
■ 🚫 No Cortical Change: There was no difference in cortical excitability between the SSC and pure shortening conditions.
■ 🚫 No Spinal Change: Similarly, spinal excitability remained unaltered during the shortening phase of the SSC.
■ 🚫 Absent Reflexes: The researchers found almost no stretch reflex activity during the active stretch phase (observed in only 1 out of 15 participants).

■ 2. The Mechanism is Mechanical
■ Because the performance increased (the 12% boost) while the neural drive from the brain and spine remained constant, the authors concluded that the SSC effect in this context is driven by mechanical mechanisms rather than neural ones.
■ This supports the theory that intrinsic properties of the muscle sarcomeres—such as "residual force enhancement" (rFE) and altered cross-bridge kinetics—are responsible for the extra power.

■ 3. Residual Force Depression (rFD)
■ The study also examined what happened after the movement, during a steady isometric hold.
■ Muscles typically produce less force after shortening, a phenomenon called Residual Force Depression (rFD).
■ The study found that steady-state torque was significantly lower following the SSC compared to the reference contractions.
■ Interestingly, just like the shortening phase, this depression in force was not correlated with any changes in cortical or spinal excitability.

🧠 Conclusion

■ The results of this study indicate that the performance benefits of the stretch-shortening cycle—at least during submaximal, controlled movements—are not associated with modulations in cortical or spinal excitability.
■ The nervous system does not appear to "ramp up" its responsiveness to facilitate the movement.
■ Instead, the boost is derived from mechanical factors triggered during the active stretch, which persist to enhance force during the subsequent shortening phase.

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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.⚠️

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29/12/2025

How exercise may control diabetes via gut microbiome-adipose crosstalk

There is a wide interpersonal variability in prevention and management of diabetes via exercise.

The researchers identify soluble interleukin-6 receptor (sIL-6R) as a key exerkine determining the efficacy of exercise in diabetes prevention.

Mechanistically, the authors show that elevated gut microbiome-mediated leucine in non-responders acts on white adipocytes to promote disintegrin and metalloproteinase 17 (ADAM17)-mediated sIL-6R production via the mammalian target of rapamycin (mTOR)-hypoxia-inducible factor 1α (HIF1α) pathway.

This in turn impairs the metabolic benefits of exercise through interleukin (IL)-6 trans-signaling-induced adipose inflammation. which is modulated by microbiome-dependent leucine through a gut-adipose tissue axis.

Pharmacological or dietary interventions targeting adipocyte-secreted sIL-6R may help to improve the metabolic outcomes in those exercise non-responders.

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(25)00473-5
https://sciencemission.com/Gut-microbiome-adipose-crosstalk

27/12/2025

26/12/2025

26/12/2025

𝗦𝘁𝗿𝗼𝗻𝗴 𝗠𝘂𝘀𝗰𝗹𝗲𝘀, 𝗥𝗲𝘀𝗶𝗹𝗶𝗲𝗻𝘁 𝗕𝗿𝗮𝗶𝗻: 𝗛𝗼𝘄 𝗥𝗲𝘀𝗶𝘀𝘁𝗮𝗻𝗰𝗲 𝗧𝗿𝗮𝗶𝗻𝗶𝗻𝗴 𝗣𝗿𝗼𝘁𝗲𝗰𝘁𝘀 𝗔𝗴𝗮𝗶𝗻𝘀𝘁 𝗡𝗲𝘂𝗿𝗼𝗱𝗲𝗴𝗲𝗻𝗲𝗿𝗮𝘁𝗶𝗼𝗻

⬜ While aerobic exercise is often praised for its cardiovascular benefits, growing evidence highlights resistance training (RT) as a distinct and powerful intervention for preserving brain health and reducing the risk of Alzheimer’s Disease and related dementias. Reduced cerebral blood flow and vascular dysfunction frequently appear long before memory loss, and RT directly targets these early changes, helping the brain “resist” cognitive decline.

⬜ Unlike the steady, continuous demands of aerobic exercise, resistance training produces rapid, high-magnitude oscillations in blood pressure. This unique hemodynamic stress may condition cerebral arteries to regulate blood flow more effectively and dampen pressure surges, thereby protecting fragile brain microvasculature from long-term damage.

⬜ Beyond vascular effects, habitual resistance training lowers oxidative stress and systemic inflammation, including key inflammatory markers such as IL-6 and TNF-α, which are known drivers of neurodegeneration. At the same time, RT stimulates the release of neurotrophic factors such as BDNF and IGF-1, supporting neuron survival, synaptic plasticity, and overall brain resilience. These adaptations appear to protect the hippocampus from atrophy and may enhance blood–brain barrier integrity, improving the clearance of toxic amyloid-beta proteins.

⬜ Importantly, gains in muscle strength are consistently linked to better executive function and memory performance. High-intensity resistance training, in particular, has demonstrated lasting benefits for memory retention, reinforcing the idea that stronger muscles support a healthier brain.

⬜ To maximize these cognitive benefits, resistance training programs should emphasize progressive overload while prioritizing safety through proper supervision and breathing techniques, avoiding the Valsalva maneuver. Even for older adults, machine-based or resistance-band exercises can improve cognitive outcomes and sleep quality, further supporting the brain’s ability to clear metabolic waste.

⬜ Think of cerebral arteries as the shock absorbers of the brain. Just as controlled speed bumps strengthen a car’s suspension, the pressure fluctuations during resistance training condition brain vessels to better absorb stress, ensuring a smoother, more protected environment for neural circuits as we age.

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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.⚠️

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11/12/2025

🧠 𝐔𝐧𝐝𝐞𝐫𝐬𝐭𝐚𝐧𝐝𝐢𝐧𝐠 𝐂𝐞𝐧𝐭𝐫𝐚𝐥 𝐍𝐞𝐫𝐯𝐨𝐮𝐬 𝐒𝐲𝐬𝐭𝐞𝐦 𝐅𝐚𝐭𝐢𝐠𝐮𝐞 𝐢𝐧 𝐒𝐩𝐞𝐞𝐝 𝐚𝐧𝐝 𝐏𝐨𝐰𝐞𝐫 𝐀𝐭𝐡𝐥𝐞𝐭𝐞𝐬

▪️ For coaches and athletes focused on speed and power, Central Nervous System (CNS) fatigue is a concept frequently discussed but often misunderstood. While the term is commonplace in training rooms and coaching forums, scientific literature on how it specifically affects high-intensity athletes—rather than endurance athletes—remains somewhat elusive.

▪️ Based on the insights provided by strength and conditioning coach Carmen Bott, here is a thorough breakdown of what CNS fatigue is, how it manifests in power athletes, and the biological mechanisms behind it.

⚡ What is CNS Fatigue?

▪️ At its core, fatigue is the inability to maintain a given exercise intensity.

▪️ However, CNS fatigue is distinct from the fatigue experienced strictly within the muscle cells (peripheral fatigue).

▪️ It is defined as a failure to maintain the expected power or force output that cannot be explained by dysfunction in the muscle itself.

▪️ Essentially, the muscle might be physically capable of performing, but the central drive sending signals to that muscle is compromised.

▪️ When the CNS is fatigued, it requires more stimulation (input) to produce a desired level of muscular contraction (output).

🏃‍♂️ 𝐏𝐫𝐚𝐜𝐭𝐢𝐜𝐚𝐥 𝐓𝐫𝐢𝐠𝐠𝐞𝐫𝐬: 𝐓𝐡𝐞 𝐂𝐡𝐚𝐫𝐥𝐢𝐞 𝐅𝐫𝐚𝐧𝐜𝐢𝐬 𝐀𝐩𝐩𝐫𝐨𝐚𝐜𝐡

▪️ Renowned sprint coach Charlie Francis provided a practical framework for understanding optimal CNS function, describing it as the efficient routing of motor signals.

▪️ According to Francis, CNS fatigue occurs when the by-products of high-intensity exercise accumulate to a point where this signal transmission is impaired.

🔸 Common causes of CNS fatigue include:

▪️ High Frequency: Performing high-intensity work too frequently in a training cycle.
▪️ Excessive Volume: Too much high-intensity volume in a single session.
▪️ Premature Intensity: Introducing high-intensity training before residual fatigue has cleared.

🔸 Specific activities that tax the CNS include:

▪️ Sprints at maximum speed (100% intensity) for 30–120 meters.
▪️ Heavy weightlifting in the 2–5 repetition range.
▪️ Explosive jumping and bounding (plyometrics).

🔁 The Recovery Curve

▪️ One of the most critical aspects of managing CNS fatigue is respecting the recovery timeline.

▪️ While low-intensity workouts (65–80% of 1RM) leave the CNS relatively intact, high-intensity work requires significant recovery.

▪️ Francis noted that recovery demands increase disproportionately with intensity.

▪️ For example, a 95% effort might require 48 hours of recovery, whereas a personal record (100% effort) could necessitate up to 10 days of recovery.

▪️ This suggests that there is a massive difference in the biological toll taken between near-maximal and maximal efforts.

🔬 𝐓𝐡𝐞 𝐁𝐢𝐨𝐥𝐨𝐠𝐢𝐜𝐚𝐥 𝐌𝐞𝐜𝐡𝐚𝐧𝐢𝐬𝐦𝐬: 𝐖𝐡𝐚𝐭 𝐢𝐬 𝐇𝐚𝐩𝐩𝐞𝐧𝐢𝐧𝐠 𝐈𝐧 𝐬 𝐯 𝐢𝐝𝐞?

▪️ While much of the science is drawn from endurance models or chronic fatigue syndrome, researchers suggest similar markers apply to power athletes.

▪️ The mechanisms can be divided into electrophysiological and biochemical categories.

⚡ 1. Electrophysiological Factors

▪️ CNS fatigue involves a reduction in the neural drive to the motor neurons.

▪️ This happens through:

▪️ Reduced Impulses: A decrease in the descending impulses (signals) traveling from the brain to the spinal cord.

▪️ Afferent Feedback Inhibition: Sensory receptors in the muscles (mechanoreceptors and free nerve endings) detect pain and metabolic by-products.

▪️ These receptors send feedback to the brain, which effectively inhibits motor neuron excitability.

▪️ This is likely a protective reflex.

🔷 2. The Role of Neurotransmitters

▪️ Neurotransmitters are chemical messengers that transmit signals across synapses.

▪️ In the context of fatigue, a tug-of-war between specific neurotransmitters plays a major role:

▪️ Serotonin (The Fatigue Agent): Associated with lethargy and increased perception of effort. During prolonged work, serotonin synthesis increases, which can lead to a loss of motor drive.

▪️ Dopamine (The Performance Agent): Dopamine is crucial for movement, motivation, and neural drive. It helps delay fatigue by inhibiting serotonin synthesis and directly activating motor pathways. High dopamine levels are linked to an athlete's hunger to compete and train.

👉

🏁 Conclusion

▪️ CNS fatigue is not merely a feeling of tiredness; it is a complex physiological event where the body effectively throttles performance to protect itself.

▪️ For the speed and power athlete, this manifests as a decrease in the ability to drive high-quality movement, even if the muscles are fueled and ready.

▪️ Because the CNS may lessen exercise intensity to tolerable levels to protect the organism, coaches must be vigilant in monitoring loads.

▪️ Understanding that a true maximum effort requires significantly longer recovery than a sub-maximal effort is essential for preventing burnout and ensuring consistent high performance.

📃

🚗 Analogy

▪️ Think of your body as a high-performance sports car. Your muscles are the engine, and your CNS is the driver. Even if the engine has a full tank of gas and is mechanically perfect, the car won't go fast if the driver is falling asleep at the wheel or decides to ease off the gas pedal because the dashboard warning lights are flashing red.

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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.⚠️

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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 👇