Espace SOMA/Sutton

Keep this in mind, given your goals.

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Exercise guidance is written in minutes per week. Three minutes of sprinting moved a hundred times more blood protein than ninety minutes of cycling.

Working muscle does not only consume fuel. It secretes. Muscle, fat, liver and immune tissue release proteins and metabolites into circulation during and after exercise, collectively called exerkines, and these signals are the leading candidate for how a local activity in the legs produces effects in the brain, pancreas and blood vessels. The scale of that release is substantial. Profiling 4,163 plasma proteins in 75 middle-aged adults during a treadmill stress test found 765 of them changed at peak effort. What nobody had done was separate intensity from duration in the same people.

Manufacturing a protein and exporting it takes hours, yet the sprint response appeared immediately. The proposed route is that many of these proteins were never newly made. Pieces of proteins already anchored on cell surfaces are cut loose and released directly into circulation, a process requiring no new synthesis and therefore no delay. The team also mapped which tissues the regulated proteins likely came from and which they were heading toward, and found fat cells especially reactive: human adipocytes bathed in plasma drawn after sprinting underwent broad shifts in gene activity, including in how they handled fuel and sensed hormones.

Participants completed six all-out 30-second sprints, three minutes of genuine work, and separately performed 90 minutes of continuous moderate cycling. Of 2,884 plasma proteins measured, 714 changed immediately after the sprints, roughly one in four. Seven changed after the moderate session. Cross-referencing against a large population database, 32 of 33 proteins associated with lower metabolic disease risk were moved by sprinting, against three by moderate exercise. The response persisted after eight weeks of training.

These are small cohorts measured acutely, and a blood protein changing is not a health outcome. The disease associations come from an entirely separate population dataset layered on top, so they establish that these proteins track with lower risk in other people, not that moving them lowers anyone's risk. The comparison also confounds intensity with modality and duration at once, since sprints, cycling and running differ in more than how hard they are. Most importantly, the moderate session was not inert, it was slower: fatty acids and liver-derived proteins rose several hours afterward rather than immediately, which means a snapshot taken right after exercise is structurally biased toward whichever stimulus acts fastest. Reading the immediate window as the whole story would overstate the gap.

Twenty years ago, six sessions of sprint intervals over two weeks, totalling two and a half hours of training against ten and a half, with about 90 percent less total work performed, produced similar improvements in muscle oxidative capacity and time-trial performance to continuous endurance training. The molecular finding here sits underneath that older result rather than replacing it, and it offers a plausible reason why so little work produced so much adaptation.

What remains untested is whether a larger immediate protein response produces better long-term health, which would require a trial comparing intensities on actual outcomes rather than on blood. Nobody has run it. The closest real-world evidence comes from accelerometer data in 3,293 US adults who did no structured exercise at all, where brief vigorous bursts during ordinary daily life tracked with lower mortality in a dose-response pattern that flattened quickly.

Intensity is a lever most people are not pulling, and that it appears to be doing something chemically distinct rather than simply more of the same. That is not a case for abandoning moderate exercise, which carries the strongest outcome evidence and the lowest injury risk, and it is not a case for anyone with cardiovascular disease sprinting without medical guidance. It is a case for treating hard efforts as their own category rather than as an optional upgrade on volume.

Olsen et al., Cell Rep Med 2026;102988 · PMID 42594877
Mi et al., Mol Cell Proteomics 2023;22(8):100601 · PMID 37343698
Gibala et al., J Physiol 2006;575(Pt 3):901-11 · PMID 16825308
Koemel et al., Int J Behav Nutr Phys Act 2026;23(1) · PMID 41612409

Si vous avez la patience de "cliquer"...

Une collègue qui enseigne les ELDOAS au Liban. Que j'admire tellement. Sous les bombes, les menaces, le manque d'électricité. D'une résilience inouïe que j'admire avec humilité.

Parfois difficle d'expliquer la patience à la personne blessée.
Surtout quand la pratique sportive doit se faire attendre

You can't heal faster than your body!
Healing takes time, and a wee bit patience.
Sometimes a lot. 🙃
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Your muscle rebuilds in about three months. Your tendons and cartilage take roughly a year and a half. Your bone, up to two years. Adding 40 grams of whey daily for two weeks doesn't change any of those timelines.

That's the finding from a study published this month in the American Journal of Clinical Nutrition. The team measured rebuild rates across more than a dozen knee tissues in living older adults using a safe heavy-water tracer. Tissues sampled during routine knee replacement surgery. Half the participants kept their habitual diet. Half added 40 grams of whey daily for 14 days. At the end, the rebuild rates of every tissue were the same in both groups.

The hierarchy was dramatic.
Muscle rebuilt at about 1.2 percent per day. At that rate, your quadriceps theoretically turn over in roughly three months. Synovium, the membrane that lines the joint capsule, rebuilt at 0.8 percent per day. The fat pad behind your kneecap, about 0.5 percent. The cruciate ligaments deep in the knee, about 0.45 percent. The patellar tendon, the femoral cartilage, and the menisci all rebuilt at 0.18 to 0.21 percent per day, putting their full-pool turnover at roughly 1.3 to 1.5 years. Bone rebuilt at 0.12 to 0.21 percent per day across five sites, with the slowest taking up to 2.3 years for a complete cycle.

What this does and does not say.
It does not say protein doesn't build connective tissue. It does. Every tissue in your body depends on dietary amino acids as substrate, and the synthesis rates measured here confirm that all of these tissues are actively turning over. Bone is a living tissue that constantly remodels. Cartilage maintains itself, slowly. Tendons repair from training and from daily mechanical load, slowly.
What the study shows is that for these older adults on their normal diets, adding 40 grams of whey on top for two weeks did not accelerate the rebuild rate of any tissue measured. It is one trial. It is small and short. It cannot rule out effects in people with inadequate baseline intake, or effects that might appear with longer supplementation. What it does establish is that connective tissue synthesis rates are dramatically slower than muscle, and a two-week protein bump does not compress those rates.

That has direct implications for what protein supplementation is and isn't doing.
Protein supplementation is a tool for closing intake gaps and for hitting the per-meal threshold that maximizes muscle protein synthesis after training. It's effective at those goals. People who are not eating enough total protein, or who are not getting enough per meal to drive muscle protein synthesis in older muscle that has lost some sensitivity to amino acids, benefit from supplementation. That's well established and not in dispute.

Protein supplementation is not a connective tissue repair accelerator. Cartilage damage from running mileage, tendon overuse injuries, bone density loss in postmenopausal women, ACL rehabilitation timelines: none of these can be hurried with whey. The biology runs at its own clock speed regardless of how much you put in.

What this means in practice.
For training and recovery, the protein protocol that has actually been shown to work is unchanged. Roughly 1.6 grams per kilogram of body weight per day, spread across three or four meals, each meal hitting at least 0.4 grams per kilogram. Training stimulus and adequate sleep do the heavy lifting on muscle adaptation. Supplemental protein at the meal level helps people hit those thresholds, especially for older adults, vegetarians, and anyone with a small appetite.

For connective tissue, the levers are different. Mechanical load through progressive training is the dominant signal for tendon and ligament adaptation. Resistance training drives bone density gains. Cartilage health responds to weight management and joint loading more than to nutrition. Collagen and vitamin C combined before training has interesting data for tendon collagen synthesis, but the effect sizes are modest. None of these tissues respond meaningfully to a protein bolus in a two-week window the way muscle does after a single training session.

The bigger reframe.
We have been treating tissue protein synthesis like a single dial. The reality is that your body runs many tissue clocks at very different speeds. Muscle is the fast one. Most of what we call "tissue building" outside of muscle takes 1 to 2 years per cycle, not days. When you injure a tendon at 55, the rehab timeline is set by how fast that tendon can lay down new collagen. Mechanical load and time do the work. Adequate protein supports it but doesn't compress the timeline.

Muscle responds to protein on a short timescale. Everything else responds on a long one. The two are not interchangeable.

Houtvast et al., Am J Clin Nutr, 2026
Moore et al., J Gerontol A, 2015
Morton et al., Br J Sports Med, 2018
Bauer et al., J Am Med Dir Assoc, 2013
Shaw et al., Am J Clin Nutr, 2017

PARFOIS IL FAUT DEMANDER L'AVIS DES COLLÈGUES!
(ma demande auprès des Soma-thérapeutes/trainers)

CAS CLINIQUE: EMBUCHE FONCTIONNELLE!

Douleur aigüe sous mon pouce lorsque l'on tente EMF du droit fémoral, lequel est simplement impossible (bilatéral). Ma compréhension = le croisement de l'expansion de la bandelette et du tibialis antérieur est tendu au point où on ne peut cibler le droit fémoral.

Vous pensez quoi de mon hypothèse? Vous y voyez autre chose?

Le tibialis antérieur = très douloureux à la palpation tout le long du tibia.

Merci au cerveau collectif de vous tous!!👍🧠😊

The shoulder is no simple issue.
It is also the longest and most complex issue to resolve. For everyone.

You get rid of the tension and stabilize specific joints involved and reinforce the muscles that are not doing their job in the first place.

L'épaule n'est pas une question simple. C'est un complexe 5 dans 1. Elle demande temps et patience. Des traitements pour dénouer et des exercices pour stabiliser. Parfois un brin de renforcement auprès des muscles non-sollicités qui ont engendrés le déséquilibre au départ (quand une chute n'est pas la cause).

THE JOINTS OF SHOULDER REGION ✍️.

The shoulder is a complex, highly mobile, and often unstable structure composed of four joints—glenohumeralacromioclavicular (AC)sternoclavicular (SC), and scapulothoracic—that work together to provide a 360-degree range of motion. The primary, ball-and-socket glenohumeral joint connects the humerus to the scapula, while the others allow for scapular motion and attachment to the torso.

Je donne toujours des exercices après le traitement.
On appelle ce genre de résultat une normalisation.

This response is called a spontaneous adjustement in english.
A marvelous outcome on day 4 of Soma/ELDOA targeted exercise.

́rapie