Centro Fisioterapia e Osteopatia Martinelli Gianluca

07/01/2026

Exercise enhances hormone shuttling across blood brain barrier

Researchers have discovered that tiny particles in the blood, called extracellular vesicles (EVs), are a major player in how a group of hormones are shuttled through the body. Physical exercise can stimulate this process. The findings, published in the journal Proceedings of the National Academy of Sciences (PNAS), open the door to deeper understanding of hormone circulation and access to the brain, how exercise may trigger changes in energy balance, mental health, and immune function, and circulation of certain drugs.

Scientists have known that EVs play key roles, from the immune response to cancer progression, but much less is known about how they might interact with hormones.

The researchers focused on a hormone precursor called proopiomelanocortin (POMC), which transforms into a range of hormones including endorphins (responsible for the runner’s high) and adrenocorticotropic hormone (ACTH), which manages the body’s stress response. Because exercise has been previously associated with these hormones, the researchers used exercise to provoke changes to shed light on interactions between POMC and EVs.

The study found that vigorous exercise causes four times more POMC to hitch a ride on the EVs.

The study also found that in the lab, EV-bound POMC can cross human blood vessel barriers, including the blood-brain barrier, more efficiently than POMC alone.

Since POMC must be processed into so-called “mature” hormones to initiate a response in the notoriously difficult-to-access brain, more work is required to understand how the exercise-induced rise in POMC affects the brain.

https://sciencemission.com/Exercise-enhances-hormone-shuttling-across-BBB

05/01/2026

How much oxygen your body can use is one of the best predictors of long-term health

This figure shows how cardiorespiratory fitness (VO₂max) - the body’s ability to use oxygen during exercise predicts health, longevity, and physical capacity across life. VO₂max reflects how efficiently the lungs, heart, blood, and muscles work together to deliver and use oxygen.

🟡 Panel A: VO₂max levels across populations
Elite endurance athletes reach 70–90 mL/kg/min, while sedentary adults average below 45. Values under 17.5 mark the aerobic frailty threshold, and below 10.5 approach the mortality threshold where daily function and survival are compromised.
➡️ Training can raise VO₂max by 10–20%, while aging lowers it about 7–10% per decade.

🟡 Panel B: Fitness decline and mortality risk
VO₂max steadily declines with age but staying in higher fitness percentiles dramatically reduces all-cause mortality.
➡️ People in the “exceptional” fitness range have about five times lower risk of death compared to those in the lowest fitness group. Even being “above average” lowers mortality by over 40%.

🟡 Panel C: The physiology behind VO₂max
Every system contributes to oxygen delivery and energy use:

Lungs and respiratory muscles draw in oxygen

Red blood cells carry it through the bloodstream

The heart pumps oxygenated blood to tissues

Vessels distribute oxygen efficiently

Muscles extract and convert it into ATP for movement

💡 The bigger picture
VO₂max is one of the strongest predictors of overall health and lifespan—more powerful than blood pressure or cholesterol. Improving it through regular aerobic exercise strengthens every component of the oxygen delivery chain, protecting against disease and functional decline with age.

DOI: 10.1152/physrev.00045.2024

04/01/2026

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.⚠️

Link to Article 👇

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.⚠️

Link to Article 👇