Motor Learning for Hypermobility: How Your Nervous System Actually Builds Reliable Movement

Last week we covered why your hypermobile muscles can feel both tight and weak at the same time. The short version: it’s a nervous system problem dressed up as a muscle problem. The longer version sits over here: why your hypermobile muscles feel tight and weak at the same time.

This week we pick up where that one finished. If the body map and the readiness tone are what you’re trying to build, the next obvious question is, well, how does the nervous system actually build them. What does it need from you? In what order? And why does so much standard advice end up missing the mark for those with hypermobility?

That’s a motor learning question. And motor learning, as a field, has a fairly mature body of evidence behind it that almost nobody applies properly to chronic pain or hypermobility. Standard gym programming was built for healthy nervous systems running on accurate signals. Yours probably isn’t, not yet, and the way you train has to reflect that.

This post walks through the actual stages your brain runs through when it learns a movement, the bits of the science that are well evidenced, the bits that are weaker than people pretend, and what all of that means for how you train.

What this post does not cover: the specific sets, reps, exercises, and progression rules. We’ve put those in a dedicated programming guide for the people who want the prescriptive layer. This piece is about the why, the framework, and the principles. Once you’ve got the why, the prescriptive layer makes sense in a way it never can if it’s just numbers on a page.

So, if you’ve ever wondered why the same thing works for one person and stalls for another, why two months on a programme can feel like nothing’s happening even though it is, or why you can lift more than your physio expected and still feel like your body’s about to fold, this is for you.

Training Is A Motor Learning Task First

There’s one frame that, if you take nothing else from this whole piece, is worth holding onto. When you’re rebuilding from chronic pain or hypermobility, training is a motor learning task before it’s a strength task. You are teaching your nervous system how to do a movement carefully, with attention, until it becomes automatic. The strength bit will come. But it comes downstream of the learning bit, not in place of it.

That isn’t fluff. The motor learning literature has been clear on this for decades, and it has a specific shape that informs every decision a sensible rehab programme makes. Most online gym writing skips that shape entirely, because, when it comes to chronic pain and hypermobility, most gym writing is for people whose nervous systems already trust their joints. Yours probably doesn’t. Not yet.

Scheper and colleagues, in 2017, made the point in plain academic English [1]. They studied 24 adults with the hypermobile type of Ehlers Danlos syndrome and 24 healthy controls. They measured muscle strength, they measured proprioception, they measured how those two things related to actual everyday function. What they found was that the relationship between strength and function in EDS-HT was confounded by proprioception. Translation: how strong you can pull on a dynamometer matters less, in real life, than how good your sense of where the joint is. The nervous system needs to trust the information coming from the joint before adding load to it makes much sense.

That single finding rewrites how you’d plan a programme. If you take it seriously, you don’t start with load. You start with signal.

Bernstein And The Three Stages

Right, let’s actually walk through what motor learning looks like.

Nikolai Bernstein was a Soviet neurophysiologist who, decades ago, asked a question that sounds basic but isn’t. The human body has so many joints and hundreds of muscles. How does the brain coordinate all of that into a single smooth movement? He called it the degrees of freedom problem.

His answer described three rough phases of motor skill development, and the framework still holds up.

In the first phase, which he called freezing, the learner locks down as many joints as possible and moves as a single stiff unit. Picture someone learning to ski for the first time. Rigid from the knees up, arms braced, getting down the hill on sheer tension and a prayer. The brain is solving the problem by reducing the number of variables it has to manage. It’s an inefficient strategy, but it’s the safest one available when the motor system has no good model yet of how to handle all those moving parts.

Now here’s the wrinkle that matters for those with hypermobility. Many people arrive at training already in a chronic freezing pattern. Gripping at the hips. Clenching the jaw. Holding the shoulders tight. That’s not real motor control. That’s survival mode, a long-term coping strategy for joint instability. The first job of any sensible rehab programme is to recognise the difference between the freezing that’s part of skill acquisition and the freezing that’s been baked in as a default coping pattern. Different problems, different solutions.

In the second phase, freeing, adjacent joints and segments start to work together more fluidly. The movement becomes less rigid, smoother, more coordinated. Things might actually feel a bit wobbly at first, weirdly. That’s not regression. That’s the white-knuckling being released. Underneath the brace, the real pattern is starting to form. It can feel like a step backwards because you’ve been used to the rigid version feeling like control, when it was really just stiffness pretending to be control.

In the third phase, exploiting, the learner starts to use reactive forces, passive tissue dynamics, and the body’s own mechanics to make movement more efficient. This is skilled movement. The body cooperates with its own physics rather than fighting it. For those with hypermobility, this is the actual destination: a system that can use its range without fearing it, and adapt on the fly when something unexpected happens.

So, if you’re somewhere in the messy middle of all that, gripping on Monday, looser by Wednesday, wobbling Thursday, you’re not failing. You’re moving through a process that, when it comes to skill acquisition, has been described in the motor learning literature for almost eighty years.

Fitts And Posner: The Same Story, Felt From The Inside

Bernstein’s stages describe what’s happening mechanically. In 1967, two American researchers called Paul Fitts and Michael Posner published a model that mapped onto Bernstein’s stages but described them from the learner’s perspective. Their model has held up remarkably well across nearly six decades, and it remains one of the most widely used frameworks in physical therapy and motor learning teaching today.

In the cognitive stage, every step needs thinking. The movement is clunky, errors are frequent, things feel slow and effortful. You need instruction and clear cues. This is where most rehab programmes do their work, because this is where conscious attention is doing most of the heavy lifting. The cognitive stage is supposed to be uncomfortable. If it isn’t, you’re either past it or you’re not really paying attention to what your body is doing.

In the associative stage, the movement starts to make sense. Errors get smaller. You can self correct a bit. Things still feel deliberate but a lot less draining. This is where honest progress happens. Most of the people we work with spend more time here than they expect to, and that’s fine. Camping in the cognitive stage, coincidentally, is one of the more common mistakes in rehab. People stay in heavy cueing mode forever because it feels safe, and they never let the nervous system take the wheel.

In the autonomous stage, the movement is automatic. You can do it tired. You can do it whilst chatting. You can do it under unexpected conditions and the form holds. It feels yours. That last word matters. Owned movement is a real thing, and it’s the marker we look for before adding load or complexity.

There’s no fixed timeline through those stages. Some movements click in a single session. Others, particularly in chronic pain populations or people with significant proprioceptive deficits, take weeks in the cognitive stage. Both are normal. The mistake is rushing. The other mistake, equally common, is staying in the learner zone forever because progressing feels risky. Neither is the goal.

Schema Theory: Why You Have To Vary The Conditions

Richard Schmidt’s 1975 schema theory is, in our view, one of the most practically underused ideas in rehab. It argued that the brain doesn’t store every movement as a separate fixed programme. Instead, it builds a generalised rule, a schema, that lets it produce related movements it has never specifically performed before. The way you build a richer, more flexible schema is through variable practice. Doing the same movement in slightly different ways, at slightly different speeds, with slightly different loads or surfaces.

The practical implication is huge, and it’s the part most people get wrong. If you do the exact same exercise, the same way, at the same speed, on the same surface, every single session, you are teaching the nervous system one very narrow thing. You are not building an adaptable movement skill. You are building a rote response to a specific set of conditions, which then collapses the moment real life serves you something slightly different.

Shea and Morgan demonstrated this experimentally back in 1979, in what’s known as the contextual interference effect. Interleaving different tasks in practice produces better long-term retention than blocked, repetitive practice, even though the interleaved version feels harder and messier in the session. The brain learns more from messy variation than from neat repetition. That feels counter-intuitive when you’re in it. It’s also one of the more reliable findings in the field.

For those of us managing symptoms, this principle gets squashed by a different instinct. When you’re coping with pain or fatigue, the natural move is to find something that works, then repeat that exactly. Same exercise, same room, same time of day, same shoes. It feels safe. The problem is that the nervous system needs variety to build something that holds up outside that exact set of conditions. So your training has to have some variation built into it, even when the symptoms are pushing you towards rote repetition.

We’ll come back to what variation looks like in practice further down. But the principle, if you remember nothing else, is this. Variety beats repetition for building anything that transfers to real life.

External Focus: The Most Boringly-Solid Bit Of Motor Learning

Two researchers, Gabriele Wulf and Rebecca Lewthwaite, published what they called the OPTIMAL theory of motor learning in 2016 [2]. It bundles together three ideas. External focus of attention, which means focusing on the effect of the movement, not the muscles producing it. Enhanced expectancies, meaning you learn better when you expect to do well. And autonomy support, which means having some say in how you train.

Of those three, external focus has by some distance the strongest, most consistent evidence behind it.

Chua and colleagues, in 2021, published a meta-analysis of seventy three studies covering 1,824 participants, looking at external versus internal focus of attention on motor performance and learning [3]. The effect on retention was a Hedges’ g of 0.583 (95% CI 0.425 to 0.741). On transfer, the effect was very similar at 0.584 (95% CI 0.325 to 0.842). Even on direct EMG measures of muscular efficiency, external focus produced more efficient neuromuscular activity, with an effect size of 0.833 (95% CI 0.453 to 1.213). The effect held across ages, across health conditions, and across skill levels. That’s about as consistent as motor learning research gets.

The practical takeaway is unglamorous but useful. Aim at the floor. Push the wall. Reach toward the target. Don’t fixate on whether your glute is firing or whether your transverse abdominis is engaged. Trust that the external focus will get the muscles involved. In most cases, it does, and the movement comes out cleaner because, when it comes to attention, parking it on the goal works better than trying to micromanage a body part.

There’s a wrinkle worth telling you about, though. The other two pillars of OPTIMAL theory, enhanced expectancies and autonomy support, have had a rougher time in the literature than the original 2016 paper suggested. McKay and colleagues, in a more recent meta-analysis [4], found that after correcting for reporting bias and underpowered study designs, the effects of self-controlled practice and enhanced expectancies were considerably smaller than originally claimed. That doesn’t mean having some choice in your programme is useless. It probably matters. But the science isn’t as tidy as the early version suggested, and we’d rather you knew that than be sold a story that won’t quite hold up. External focus is the part of OPTIMAL theory you can lean on.

Distributed Practice: Short And Often Beats Long And Occasional

The motor learning literature is also fairly consistent on this one. Distributed practice (shorter sessions spread more frequently across the week) produces better skill retention than massed practice (fewer, longer sessions covering the same total volume). A related example sits in chronic pain rehab. Lorimer Moseley’s graded motor imagery work for complex regional pain syndrome used a structured programme built around short, repeated daily practice rather than infrequent long blocks, and it produced meaningful improvements in pain and function [5]. The session structure in that work wasn’t framed as a test of distributed practice as a mechanism, but the principle, that the nervous system consolidates learning in the gaps between sessions and not in the duration of any one session, sits underneath it.

For practical purposes: twenty minutes of focused, attentive practice four times a week will generally outperform one ninety minute session done once. That isn’t an opinion, and it isn’t because the longer session is “too much.” It’s that motor consolidation needs the breaks. The work done in the gaps is real work, even if you can’t see it.

Twenty focused minutes is also a much more achievable target on a difficult day than ninety. So the literature happens to align with the lifestyle realities of people managing chronic conditions, which is a happy coincidence.

Why The First Two Months Look Like Nothing’s Happening

When you start a new programme, the first changes are not in the muscles. They are in the nervous system.

Sale, in a 1988 review that’s still a useful reference point in the field [6], laid out the mechanisms. Early strength gains come from the nervous system getting better at recruiting the muscle fibres you already have, reducing wasteful antagonist co-activation, and improving the synchronisation between muscles that work together. The muscles aren’t getting bigger yet. They’re being run more efficiently.

Folland and Williams, in their 2007 review, established that detectable structural changes in muscle volume only appear later in a training programme [7]. So for the first stretch of any new programme, you might notice that you’re moving better, that things feel easier, that your coordination has improved, but you might not see anything in the mirror. Both of those things are normal. The strength changes are happening through the nervous system first, and the visible muscle changes come later.

This explains a few things at once. Why early gains feel real but look invisible (they are real). Why changing programmes every two or three weeks is such a mistake (you never let the nervous system consolidate what it’s just learning, so you sit in the cognitive stage forever). And why the right question in the early phase of any new exercise is not “am I getting stronger?” but “is my movement quality improving? Is the pattern getting cleaner? Does it feel more mine than it did?”

For those with hypermobility, this matters extra. When it comes to long-term progress, the neural foundation is the foundation. If you skip past it and load up too fast, you’re loading a system that hasn’t yet learned what good looks like. The strength might come, briefly. The pattern won’t hold under pressure.

When The System Goes Quiet: Arthrogenic Muscle Inhibition

Now here’s a finding that should be on the wall of every gym that takes rehab seriously, and almost never is.

Rice and McNair, in their 2010 review [8], described a phenomenon called arthrogenic muscle inhibition, AMI for short. It’s the reflexive shutting-down of muscles surrounding a joint, caused by abnormal sensory input from that joint when it’s swollen, inflamed, or structurally disrupted. It is not voluntary. It is not a confidence problem. It cannot be overcome by trying harder. It is a spinal reflex.

That last bit matters. When a joint is in that state, the nervous system simply will not allow full motor unit recruitment in the muscles around it. Pressing the accelerator while the handbrake is on, mechanically. The biology stops you, no matter how committed you are.

This is especially relevant for hypermobile bodies, because low-grade joint irritation after activity is common. A joint doesn’t have to be visibly swollen to be in a state of mild effusion that’s quietly inhibiting the muscles around it. Rice and McNair also note that joint laxity itself may chronically alter how the joint’s mechanoreceptors fire, contributing to baseline neuromuscular inhibition even without frank swelling.

Read that again. Even without obvious swelling, a chronically lax joint may be sending altered sensory signals that suppress the muscles around it. Which is, when it comes to building stable hypermobile bodies, exactly the problem you’d want to know about.

The practical upshot is that strengthening exercises prescribed to a freshly irritated joint are not going to do what people expect them to. The biology gets in the way. You need to settle the joint first, restore the input the brain is reading, and then reload. Not the other way round.

When The Map Smudges: Cortical Reorganisation In Chronic Pain

Beyond the spinal-reflex level, there’s a cortical picture. Tsao, Galea and Hodges in 2008 [9], and Tsao, Danneels and Hodges in 2011 [10], studied the motor cortex maps of people with recurrent low back pain. The brain’s map of the affected area becomes less precise. Less clearly defined.

The 2011 paper described it as smudging the motor brain. The map for one muscle starts overlapping with the map for the muscle next to it. The fine-grained ability to fire one without firing the other gets lost. Practically, that means a person in chronic pain often can’t activate the muscles around the painful area in a discrete way. Everything switches on together, because the brain has lost the ability to drive them separately.

Those studies were on low back pain, not hypermobility specifically. But the mechanism is general. Whenever a body region has been giving the brain unreliable signals for long enough, the cortical map of that region starts to lose definition. The nervous system can only build a precise map from precise input. Give it noisy input over years, and the map gets fuzzy.

This is why returning from injury or a flare is rarely just a strength problem. It’s a re-mapping problem. When it comes to coming back from a setback, the pattern needs to be re-learned, not just reloaded. Tactile cues, deliberate slow movement, attention paid to where the joint actually is in space, all of those are doing the cortical work that strength training alone won’t touch.

When The System Says Stop: Sickness Behaviour

One more finding worth knowing, because it explains something a lot of people with chronic conditions experience and rarely get a clean explanation for.

Dantzer and Kelley, in a 2007 review covering twenty years of research on this [11], laid out what’s called sickness behaviour. When the body is fighting infection or managing an inflammatory process, pro-inflammatory cytokines circulate in the bloodstream and act directly on the brain. The result is fatigue, pain amplification, reduced motivation, and cognitive sluggishness. Not because you’re weak. Not because you’re failing to push through. Because the nervous system is reducing motor output as part of a coordinated biological response to immune challenge.

You can’t override that with willpower, and you shouldn’t try. When you’re in a sickness or inflammatory state, the signal quality between your brain and your body has degraded for biological reasons. Training through it doesn’t produce the adaptations training is meant to produce. It produces fatigue, sometimes flares, and rehearsal of poor patterns.

That isn’t permission to stop training forever, by the way. It’s permission to stop pretending that all sessions are the same. Some days the system is online and ready to learn. Some days it’s offline doing other work. Respecting that is the boring part of long-term progress.

What This Looks Like In Practice

Pull all of that together and a fair amount of it translates into things you can actually use today. We’re not going to hand over the full prescriptive system here, that lives in a dedicated guide and inside the courses for a reason, but plenty of what we use day to day is general motor-learning principle, and there’s no good reason to hide that.

Signal before load, every single time

When it comes to programming for hypermobility or chronic pain, the question to ask at every stage is not “how much load?” The question is “how good is the signal?” Load can come later. It stays later for a reason. If the signal coming back from the joint is poor and you load anyway, all you’re doing is amplifying the existing pattern, including the bracing and the compensations. That’s not progress. That’s rehearsal of the wrong thing under more weight.

In practice this means there’s no rush to add weight. The early phase of any new exercise is about cleaning the pattern, not loading it. If you’re still in the cognitive stage on a movement, more reps of clean ones will outperform added load every time.

Twenty sharp minutes beats forty foggy ones

For those of us managing chronic pain, fatigue, or dysautonomia, attention is a finite resource that runs out faster than the textbook assumes. Attention is the rate-limiter for motor learning. Twenty focused, attentive minutes will do more for your nervous system than an hour grinding through movements with attention checked out at minute fifteen.

A practical rule of thumb that holds up well: if the last few reps of a set look nothing like the first few, you’ve done too many. Stop the set. Take an honest rest. Come back next session with fewer. You’ll learn more from fifteen sharp reps than from twenty-five degraded ones.

Short and frequent beats long and occasional, too. Twenty minutes four times a week will generally outperform one ninety-minute session done once. The motor learning literature is fairly consistent on that, and it’s also a much more achievable target on a difficult day.

Vary the conditions, don’t switch the exercises

This is the bit most people get backwards. They feel like they need fresh exercises every couple of weeks to keep things interesting, when what they actually need is variation inside the exercises they’re already learning.

The variation menu is small and not complicated. Pick one or two parameters at a time:

– Speed: some reps slow, some at a normal pace. Slow reps give the nervous system more positional information. Faster reps train the reactive system. Alternating between them builds both. – Range: sometimes work the full available range. Sometimes work a shorter arc with more precision. Both have value, and swapping between them is a form of variation. – Focus: one session you might focus on what the foot is doing. Another session, focus on the target you’re reaching towards. Some sessions, eyes open. Other sessions, when it’s safe, eyes closed for a portion of the work. Different sensory conditions, same movement. – Surface or context: sitting versus standing versions of the same drill. A firm floor versus a folded towel underfoot. Small changes that ask the nervous system to adapt what it knows to a slightly new situation.

You’re not changing the exercise itself constantly. That’s programme hopping, which is a different problem. You’re varying the conditions inside exercises you already know. It’s the difference between learning one song in a few different rooms and starting a new song every week and never really knowing any of them.

And you don’t need to vary every parameter every time. Pick one or two. Keep the rest consistent so the nervous system has something to anchor to. Variety belongs around an anchor, not instead of one.

Felt quality is the metric, not the numbers

This one is hard for people coming from a gym background. The number on the bar isn’t a useful proxy for whether the work is doing what it’s meant to. The right question after a set is not “was that hard?” It’s “did that feel owned?” Owned. Controllable. Reliable. Yours.

A few things to scan for during the actual movement, because they tell you a lot about whether the pattern is clean:

– Is your breath holding? Real motor control runs on a relaxed diaphragm. If you’ve been holding your breath through reps, you’re bracing harder than the movement actually needs.

– Is your jaw clenching? Same story. The jaw is one of the most reliable tells that the nervous system is gripping when it doesn’t need to.

– Is the neck rope showing? You’ll see the sternocleidomastoid standing out at the side of the neck if you’re recruiting it to hold your head still. That’s compensation, not control.

– Are other body parts drifting in to help? If you’re meant to be doing a hip hinge and the lower back is doing the work, the pattern has shifted.

– Is there a pain spike during the set or in the 24 hours after? That’s information. Don’t ignore it.

If those five are clean across two sessions running, that’s the moment to consider adding a layer. More reps. Then a variation. Then, eventually, load. In that order. Not before. When it comes to self-directed rehab, skipping the order is one of the most common failure modes. We see it constantly. People feel a bit better, jump straight to load, lose the pattern, get hurt or discouraged, and start over from a worse baseline.

Sets and reps look different in rehab to the gym

In standard gym programming, reps are about creating mechanical and metabolic stress on a muscle until it adapts by getting bigger or stronger. The numbers there are tuned for hypertrophy or maximal strength, and they assume the nervous system is already running cleanly.

What we’re doing is different. Reps are practice trials for a new motor skill. The goal of every set is repetitions of a clean pattern, not muscle exhaustion. That changes the maths considerably. Skill consolidation in the motor learning literature consistently shows that what matters is not the load you used or how close to failure you got, it’s how many high-quality repetitions of the target pattern your nervous system has logged. Hundreds of clean reps spread over weeks build the schema. Twenty grindy reps to failure build muscular fatigue and reinforce a sloppy pattern.

In practical terms, that means most rehab work sits at higher rep ranges than a strength programme would, with light load. The reps are there for the practice volume. The load stays light because we’re protecting the joints from poorly-controlled stress while the pattern is still being learned.

Tactile cues are not training wheels

Tactile cues, by which we mean physical contact at or near the relevant body part to help the brain understand position and movement, are not for beginners only. There’s a tendency to treat them as something you graduate out of, and that’s not how they work. They’re a tool for re-anchoring the brain when the system is noisy. The system gets noisy for all sorts of reasons.

Dial them up: returning from illness, in the days after a flare, after a break of more than a week or two, when introducing a new exercise even if you’re experienced, on brain fog days, on a high symptom cycle day, when sleep has been broken.

Dial them down: when the movement is genuinely owned across the felt-quality criteria above, when proprioception is sharp, on good days with low symptom load.

They never disappear from the toolkit. They drift in and out based on what the system needs. There is no moment at which you’ve moved past tactile cues. You’re just using them less frequently because the system is more reliable more often. The moment the system gets less reliable again, they come back in. That’s not regression. That’s appropriate calibration.

How to know when to hold, and when to step back

Progress isn’t a calendar. It’s a quality threshold. When the pattern is owned across two sessions, you can move up. When it isn’t, you hold where you are. Same numbers, same level, no change. Sitting at the same level for several sessions isn’t failure. It’s honest calibration. The progression will come. Rushing past it usually means rebuilding from a lower point a few weeks later, which costs more time overall.

Regression is also part of the toolkit, not a punishment. If there’s been a pain flare, a fear flare, an illness, a significant life stressor, or a break of more than a week from training, drop a layer. That might mean dropping a variation you’d added and going back to the base movement. It might mean returning to tactile cues on movements you’d been doing without them. The principle is simple: if something has changed in the system, you’re now in a different starting state than you were before. Don’t pretend otherwise. Start from where you actually are.

Frequency: starting and building

If you’re starting out or returning after an extended break, twice a week is the appropriate dose. Two sessions, ideally split between something more upper-body or core focused and something more lower-body focused. The goal at this stage is establishing a consistent practice and building a habit. Two sessions a week, every week, will produce meaningful adaptation over a six to eight week stretch.

Once things are consistent and the programme is well established, three to four sessions a week is the building point. Beyond four, for most people in this population, returns diminish sharply and accumulated fatigue starts to compromise the quality of what you’re doing. More is not better. Better is better.

What we’re not covering here

There is a layer of specificity beyond what we’ve covered, and it sits in our Programming, Sets and Reps guide, found in the hypermobility 101 course. The guide gets into specific exercise prescriptions, the actual rep ranges across categories of exercise, the templates that build a week of training around different stages of capacity, and the bits where the picture gets more complicated for specific groups. The cycle and hormones conversation, which is more nuanced and less neat than the popular version on social media. The postpartum return, where joint architecture continues to change well beyond the standard six week clearance and that clearance often doesn’t really apply to hypermobile bodies. Menopause and resistance training, which is one of the few places where the case for doing more strength work, not less, gets surprisingly strong. The wound healing section, which matters if you’ve had surgery and is routinely misrepresented in patient-facing content.

Those are the bits that change depending on the person, and they need to live somewhere proper rather than in a single blog post. The principles in this post will get you a long way on their own. The guide is the next layer down for the people who want it.

We’ve covered a lot of the supporting territory in other posts on the blog if you want to keep reading. Why your hypermobile muscles feel tight and weak at the same time sets up the muscle tone story this post builds on. Hypermobility core exercises that actually work and hypermobility knee instability exercises give a flavour of what variation-rich training looks like at specific joints. Fear of movement in hypermobility and EDS sits alongside this one for anyone whose nervous system is doing more guarding than learning. Hypermobile flat feet and hypermobility rib subluxation extend the same principles into specific regions. KT tape for hypermobility and Ehlers-Danlos syndrome covers tactile cueing in detail. And the broader hypermobility and exercise: part 1 walks through how this framework sits alongside more conventional gym thinking.

— The Fibro Guy Team —

Frequently Asked Questions

References

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[2] Wulf G, Lewthwaite R. (2016) Optimizing performance through intrinsic motivation and attention for learning: The OPTIMAL theory of motor learning. Psychonomic Bulletin & Review 23(5):1382-1414. doi: 10.3758/s13423-015-0999-9

[3] Chua LK, Jimenez-Diaz J, Lewthwaite R, Kim T, Wulf G. (2021) Superiority of external attentional focus for motor performance and learning: Systematic reviews and meta-analyses. Psychological Bulletin 147(6):618-645. doi: 10.1037/bul0000335

[4] McKay B, Bacelar MFB, Parma JO, Miller MW, Carter MJ. (2025) The combination of reporting bias and underpowered study designs has substantially exaggerated the motor learning benefits of self-controlled practice and enhanced expectancies: a meta-analysis. International Review of Sport and Exercise Psychology 18(1):242-262. doi: 10.1080/1750984X.2023.2207255

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[7] Folland JP, Williams AG. (2007) The adaptations to strength training: morphological and neurological contributions to increased strength. Sports Medicine 37(2):145-168. doi: 10.2165/00007256-200737020-00004

[8] Rice DA, McNair PJ. (2010) Quadriceps arthrogenic muscle inhibition: neural mechanisms and treatment perspectives. Seminars in Arthritis and Rheumatism 40(3):250-266. doi: 10.1016/j.semarthrit.2009.10.001

[9] Tsao H, Galea MP, Hodges PW. (2008) Reorganization of the motor cortex is associated with postural control deficits in recurrent low back pain. Brain 131(8):2161-2171. doi: 10.1093/brain/awn154

[10] Tsao H, Danneels LA, Hodges PW. (2011) ISSLS prize winner: Smudging the motor brain in young adults with recurrent low back pain. Spine 36(21):1721-1727. doi: 10.1097/BRS.0b013e31821c4267

[11] Dantzer R, Kelley KW. (2007) Twenty years of research on cytokine-induced sickness behavior. Brain, Behavior, and Immunity 21(2):153-160. doi: 10.1016/j.bbi.2006.09.006