Why Your Hypermobile Muscles Feel Tight and Weak at the Same Time: Understanding Muscle Tone

Adam Foster

This article is part of our comprehensive guide to exercise and rehabilitation for hypermobility.

Nearly everyone with hypermobility ends up holding two descriptions of their own body that flatly contradict each other. The first one arrives from a clinician, usually as the phrase low muscle tone, delivered in the voice that suggests the matter is now closed. Floppy, loose, not enough. The second one you worked out on your own, with nobody’s help at all, because your shoulders sit somewhere up near your ears, your jaw is already clenched when you wake up, and your back aches at the end of a day in which you genuinely did nothing.

Both of those are true at the same time, and the part nobody explains is why.

So the answer first, rather than making you scroll for it. Tone isn’t one thing, it’s at least two, and in symptomatic hypermobility the two tend to head in opposite directions. The resistance coming from your tissue often gives way earlier than average, which is the half your clinician was describing. The activity your nervous system adds on top often has to do more than average, as something has to hold that joint and the tissue isn’t managing all of it on its own. Loose underneath, gripping above it. Which feels like a contradiction, and is really just two different things sharing one word.

This article sits alongside our two part exercise guide. Part 1 went through why strength on its own doesn’t finish the job. Part 2 went through what your joints are actually reporting to your brain, and what’s gone slightly wrong with the reporting. Tone is where both of those show up in how your body feels by four in the afternoon, so it helps to have read them, and this piece stands up on its own if you haven’t.

One thing to flag before we start, as you may well have had it said to you with a great deal of confidence. The old explanation for all of this leaned on long term pain smudging the map of your body inside your brain, and that idea has not survived better scanners. We went through it properly in Part 2. Nothing in this article needs it, and nothing here rests on it.

What Tone Actually Means

Ask ten clinicians what muscle tone actually is and you’ll get a pause, then a sentence about resistance (we have tried this, and it’s remarkably consistent). That isn’t them being vague for the sake of it. The word genuinely is a mess, and the physiology literature says so out loud [1][2].

The clinical definition is the resistance somebody feels when they pick up your relaxed arm and move it. Which is a description of what the examiner feels, rather than of what’s producing it, and at least two quite different things are producing it [1].

The first is the tissue. Muscle, tendon, fascia and joint capsule all have physical properties, and those properties resist being stretched whether anybody is switched on or not. Think of an elastic band lying on a table. Nobody is pulling it, and it still has tension built into the material. That’s passive tone.

The second is your nervous system. There’s a low level of muscle activity running in the background all the time, keeping you upright and ready to do something, and it’s set by the brain and spinal cord rather than by the material [1][3]. That’s active tone, and you don’t choose any of it.

Now, those two get felt together and reported as one thing, which is where nearly all the confusion in this area comes from. A hand on a limb cannot tell you which of them it’s feeling, and the reviews are blunt about how poorly our usual measures separate them [2][3]. So when somebody tells you your tone is low, what they’ve assessed is the sum. You’ve been handed one word for two things that can run in opposite directions.

The Loose Half, And Who It Actually Applies To

Take the tissue first, as it’s the half that’s already been explained to you, just not very carefully.

In women with the hypermobile type of EDS, the resistance of the calf to being stretched came out lower than in controls, and the Achilles tendon was measurably less stiff [4]. Which is exactly what you’d predict. More compliant connective tissue stretches further before it pushes back, joints travel through bigger ranges, and the end of a range feels mushy rather than like a stop. Reviews of the tissue side land in the same place, with lower stiffness and more stretch under load turning up repeatedly, although a good deal of that work is still describing the material rather than showing what it does to your week [5]. Low tone as a clinical observation is common enough in the EDS family that it turns up in over half the cases in one review across subtypes [6].

Now, the caveat that almost never gets said, and it changes how you should read yourself. Measure resting muscle and tendon properties directly in hypermobile people who feel fine, and they come out the same as everybody else’s [7]. Same tone, same stiffness, same elasticity, at the muscle and at the tendon.

So lower passive tone isn’t a feature of being hypermobile. It’s something that shows up in the symptomatic group, which is the same split Part 2 kept running into. Being hypermobile on its own often produces nothing measurable at all. Being hypermobile with pain, instability, fatigue and years of a slightly different movement history behind you produces a great deal.

The Tight Half, And Why Your Brain Adds It

The gripping is the other half, and it’s the one you actually live with.

If the tissue isn’t holding the joint, something has to, and the only thing available is muscle. Your nervous system isn’t daft. It doesn’t let the joint flop about and hope for the best, it turns the muscle activity up to make up the difference. Which is a sensible response to the situation it’s in, and it’s also why you feel like a clenched fist by mid afternoon. It’s the same thing you do on a footbridge that moves under you. You grip, you shorten your stride, you hold your breath a bit, and you get across (nobody has ever crossed one of those casually). It works. It’s also exhausting, and it’s a terrible way to spend fifteen years.

That does turn up in the measurements. In pain free hypermobile adults doing nothing more demanding than standing still, the muscles on both sides of the knee were switched on together more than in the control group [8]. That’s called co contraction, and it’s what gripping a joint between two opposing muscles looks like on a readout. In hypermobile children landing from a jump, the calf took over a job the hamstring would normally do, and the muscles around the knee gripped harder in the moment before the foot hit the floor [9]. The landing itself looked completely normal. The organising of it didn’t, which is more or less the universal experience of being watched by somebody who then tells you it all looks fine.

In adults with EDS, walking involves muscles switching on late and staying on longer, with slower steps and shorter strides, while the visible shape of the movement stays close to normal [10]. In a small group on a treadmill, more co contraction and more muscle activity turned up in early stance, alongside a less stiff tendon and a higher energy cost for the same walk [11].

Now, the honest limit on all of that, as it gets overstated constantly, including by us in the past. This is not global bracing. Another walking study in hEDS found the amount of co contraction in the lower limb was much the same as controls, despite that group being considerably weaker [12]. Different tasks pull different strategies out of different people. So the accurate version is that the nervous system compensates in specific tasks, in ways that vary a fair bit from one person to the next, rather than every hypermobile body being braced everywhere all the time.

One more piece is worth having, as it points at where the extra effort is coming from. When quadriceps control was tested in hypermobile people, the line running from brain to muscle was easier to drive than in controls, while the reflex measures down at the spinal cord were unchanged [13]. So there isn’t a broken reflex sitting underneath this. It’s the level above, working harder to get the same job done.

And then the bit that isn’t muscle at all. Pressure that other people would call firm registers as painful in women with hEDS, and repeated pokes build up more than they should [14]. A muscle that’s sore to press and a muscle that’s genuinely short feel almost identical from the inside, and they are not the same problem. Some of what you’re calling tightness is compensation, some of it is a nervous system that has turned its sensitivity up, and the two arrive together. Telling them apart by feel isn’t really possible, which is a large part of why the stretching keeps not doing what you hoped. If you want the mechanism behind the sensitivity side, our piece on what causes chronic pain in fibromyalgia and hypermobility covers it in plain terms.

Readiness, And Why We Teach It That Way

We use a third idea in the studios and it’s worth being straight about what it is, as it isn’t standard physiology and we’re not going to dress it up as though it were.

Passive and active tone are the two the textbooks recognise [1][2]. The third one we teach is readiness, borrowed from Nikolai Bernstein, who described tone less as stiffness and more as a state of being prepared to move. Modern reviews of tone still cite that idea, it’s genuinely useful for getting your head around what’s going on, and nobody has validated it as a measurable category in hypermobility or anywhere else [1]. It’s a teaching tool. We use it because it gets people to the right answer quicker than the other two do, and that’s the whole of its claim on you.

What it means in practice is this: can you produce the right amount of force, in the right muscles, at the right moment, and then let go of it again. Think of a goalkeeper, who isn’t braced rigid, as she’d never get across the goal in time, and isn’t slumped either. Ready, is the word. Able to go from nothing to everything and back down again, in about a second.

That’s the thing most of those with hypermobility have lost, and it isn’t the same as being weak. It’s being stuck on one setting. The letting go is usually the harder half, and almost nothing in a standard programme trains it.

The Weakness That Isn’t About Muscle Size

Plenty of those with hypermobility notice genuine weakness. Grip gives out sooner than it should, legs go after not very much, and holding a position for any length of time turns into a whole project. The instinct, for you and usually for whoever is advising you, is that the muscles must be too small, so the answer must be to make them bigger.

That one has actually been measured properly, and it’s one of the better supported findings in this entire area. Women with the hypermobile type of EDS produced substantially less force at the knee than controls and fatigued sooner, while the amount of muscle on their legs came out much the same on a scan [15]. Followed up eight years later, the same pattern held, with strength still lower and no sign of the muscle wasting away faster than anybody else’s [16]. Later work looking at muscle mass and density in hEDS and HSD didn’t find a clear group difference either [17].

The muscle is there, it’s roughly the size it ought to be, and it isn’t producing what a muscle that size should produce.

Why that is, is genuinely unsettled, and anybody telling you otherwise is well ahead of the evidence. Force has to travel out of the muscle fibres, through the connective tissue around them and into the tendon, so if that tissue behaves differently, some of the force may not arrive where it was aimed [5]. Pain suppresses output. Years of doing less takes its own toll. And you can’t aim force well if you can’t tell precisely where the joint is, which is Part 2 in a single sentence. Our read is that it’s several of those at once, in a mix that differs from person to person, and that read is ours rather than a finding.

There’s one piece of work in here that changed how we assess people. Strength in the hypermobile type of EDS did relate to what somebody could actually manage in daily life, as you’d expect. For some of those tasks though, getting out of a chair over and over, and one of those daily living questionnaires with forty questions about opening jars, the relationship got muddled once the accuracy of joint position sense was taken into account [18]. Not for the six minute walk, which is worth saying, as the effect isn’t uniform. Still, for at least some of what makes a day hard, how well you can locate a joint changes what your strength is worth.

Force you can’t aim isn’t much use to you. Which is why you can have the strongest quads in the room and still have a knee that folds when you weren’t expecting it.

Why Everything Costs More Than It Should

Walking should be free. Standing should be free. Reaching for a mug should not require a committee meeting between your shoulder, your elbow and your wrist, and for a lot of those with hypermobility, that’s roughly what it feels like.

The likely explanation, and we’d mark this as our interpretation rather than as something anybody has demonstrated, is that you’re paying for the same movement twice. Once in muscle, the way everybody does. And once in attention, as a system running off an imprecise signal has to keep checking, and the checking comes out of the same budget you wanted for the rest of your day.

The cost itself is measurable, even if where exactly it comes from isn’t settled. Walking in hEDS and HSD takes more energy than it does in controls, and a less stiff tendon is part of that, as a tendon that gives way stores and returns less of the energy you put into each step [11]. Fatigue and quality of life track along with it [19]. And Part 2 covered the finding that performance falls further than average the moment somebody asks you to do a second thing at the same time, which is what it looks like when holding yourself together has stopped being automatic.

So you’re wrecked by seven in the evening having done, on paper, not very much. That isn’t a tolerance problem and it isn’t a fitness problem. It’s the bill for running a body on a signal that needs checking.

Where The Usual Advice Runs Out

Two things get recommended more than everything else put together, and neither is wrong exactly. They’re just aimed slightly to the left of the problem.

Stretching first. If your muscles feel tight, stretching them out is a perfectly reasonable thing to try, and for a specific tissue that genuinely has lost length it can help. What it doesn’t do much for is tension that’s being generated on purpose. If a muscle is switched on because the joint underneath it needs holding, lengthening the muscle doesn’t remove the reason, and the brain either puts the bracing back within a few days or it doesn’t and the joint takes the consequences. That’s our read of the mechanism rather than a tested prediction, and it’s why we don’t put stretching at the centre of anything for a joint that already travels too far. There’s a longer piece on that if you want the full version, our stretching and hypermobility guide goes through it properly.

Strength second, and we want to be careful here, as this is where our own older writing rather overshot. Getting stronger is genuinely worth doing, and the rehab literature in this population does support exercise and strength oriented work [20][21]. Part 1 goes through the studies where heavy, supervised, full range loading was tolerated perfectly well by people with symptomatic shoulders, and it carries the references for those. Nobody should read this article as a reason to stay away from weights.

What strength work doesn’t do on its own is teach a joint when to stiffen and when to let go. That’s timing and information rather than force. And how it gets delivered matters more than most programmes admit, as a self guided, non individualised resistance programme in women with generalised hypermobility didn’t produce measurable gains in strength or function at all [22]. So it isn’t strength against sensory work. It’s supervised, individualised and sequenced, against a sheet of exercises and good luck.

What Does Seem To Help

The evidence in this population is small, mixed, and mostly not built to compare one approach against another, so anybody handing you a definitive protocol is handing you their preference. The direction of it is fairly consistent though.

Physiotherapy of various kinds improves pain, joint sense, function and quality of life in hEDS and HSD, across studies that are few, small, and quite different from one another [21]. Pull the physical therapy work together and the approaches with the most behind them are exercise, and training aimed at how movement gets organised. The passive treatments, the ones where something is done to you while you lie there, come out weakest [20].

Training the sense of position directly has the broadest evidence base of anything here, although most of it comes from outside hypermobility. Across a large review spanning a lot of conditions, programmes that trained joint sense improved both how well people could feel position and how well they moved, and the versions that worked best involved active movement with something to work out, rather than being put passively through a range [23]. That isn’t hypermobility specific and we’re not going to pretend it is. The principle travels though.

There’s a neat demonstration of the same logic from somewhere else entirely. After a knee replacement, home based training that worked on sensation and movement together beat the usual functional exercise on quadriceps force, on how well the muscle switched on, and on the size of the muscle itself, with the same amount of exercise time going into both groups, which is what makes it a fair fight [24]. The sensory work built more muscle than the muscle work did! Different population, and the mechanistic point stands.

Closer to home, a rehab programme built around retraining how the brain organises movement improved pain, fatigue, fear of moving and disability in people with hEDS and long standing back pain [25]. Multidisciplinary programmes combining physical training with work on the fear side have improved disability, strength and motor performance in hypermobile adolescents [26], and a controlled programme in hEDS held onto its gains at short and medium term follow up [27]. Most of those are small, several have no control group at all, and the authors say so themselves. So they point one way, and they settle nothing, which is more or less the state of everything in this field. If the fear half of that is the bit that rings true for you, our piece on fear of movement in hypermobility and EDS is the one to read next.

How We’d Train Tone

What follows is how we sequence it, and it’s our read rather than a settled finding. Nobody has run the study that compares doing it in this order against doing it the other way round. Part 1 says the same thing and it’s still true.

– Sort the information out before you add load. Adding weight to a joint that nobody can locate accurately mostly adds consequences. Get the signal and the movement strategy sorted, then load it. Skin contact, textures, different floors and tape all help here, and our piece on KT tape for hypermobility and Ehlers Danlos syndrome walks through what tactile cueing actually looks like.

– Train the letting go, not only the switching on. Readiness runs in two directions and nearly every programme only ever trains one of them. Going from effort down to nothing, deliberately, is a skill, and for most of those with hypermobility it’s the missing one. The breath and the abdominal wall are where this shows up first, which is covered in our piece on hypermobility core exercises.

– Give the system something to decide. Part 2 went into this properly. The touch training that changed anything was the version where people had to work something out, rather than the version where they simply received sensation. Which surface is this, which foot is further forward, which way did that just move.

– Work near the end of the range, gradually. That’s where the tissue has least to say and the signal gets thinnest, and it’s also where your joints genuinely spend their time, whatever your programme is pretending.

– Vary it rather than repeat it. Same action, different speed, surface, direction, load and head position. You’re after a rule your nervous system can use in a situation it has never met, and you can’t build one of those out of three identical sets.

– Judge the session by tomorrow. Not by how it felt and not by what you lifted. Whether the thing is still there the next morning is the honest measure, and it’s the first thing we change with a new client.

– Keep strength in and put it in the right place. Load isn’t the enemy here. Loading a joint that nobody can accurately locate, is.

– Expect the first few weeks to look like nothing. The early stretch of a well built programme is deeply unimpressive from the outside, as what’s changing is the quality of the information rather than the size of anything. That’s the stage where most people quit, and it’s the stage that decides everything after it.

How all of that lands depends on the joint, as the principles are the same everywhere and the practicalities really aren’t. There are worked versions on the blog for knee instability, for hypermobile flat feet, for the ribs, and for the hypermobile jaw, if you want to see it applied rather than described.

What Nobody Knows Yet

The list is a fair bit longer than the marketing in this space would suggest, and it’s worth having anyway.

Nobody has directly measured resting muscle tone in symptomatic hEDS or HSD, which is quite the hole given how often the phrase gets said to people. There’s decent evidence for lower resistance when a limb gets stretched, and for altered activity during tasks, and almost nothing on what the muscle is doing when you’re genuinely at rest [7][11].

Readiness tone is a teaching idea rather than a validated category, and we’d rather keep saying that than let it harden into something it isn’t. If anybody offers to measure yours, they’ve made the measurement up.

Which mechanism is running your particular week is a judgement call. Tissue, the way pain gets processed, the automatic side of the nervous system that runs your heart rate and your blood pressure, doing less over a lot of years, and what you expect a movement to cost you, all load the same system, and the mix differs enormously between people [28]. There’s no test that tells you which one is yours.

And the order of operations is unproven. Information before load is our read, built on the mechanism and on watching a great many people go through it in the studios. The head to head study doesn’t exist. If it comes out and says we had it the wrong way round, we’ll say so and teach the other thing.

The Fibro Guy


References

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[2] Masi, A.T. and Hannon, J.C. (2008) ‘Human resting muscle tone (HRMT): narrative introduction and modern concepts’, Journal of Bodywork and Movement Therapies. https://doi.org/10.1016/j.jbmt.2008.05.007

[3] Cacciatore, T.W., Anderson, D.I. and Cohen, R.G. (2024) ‘Central mechanisms of muscle tone regulation: implications for pain and performance’, Frontiers in Neuroscience. https://doi.org/10.3389/fnins.2024.1511783

Read More

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[6] Doolan, B., Lavallee, M., Hausser, I., Schubart, J., Pope, F., Seneviratne, S. et al. (2023) ‘Extracutaneous features and complications of the Ehlers-Danlos syndromes: A systematic review’, Frontiers in Medicine. https://doi.org/10.3389/fmed.2023.1053466

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[22] Luder, G., Aeberli, D., Mebes, C., Haupt-Bertschy, B., Baeyens, J. and Verra, M. (2021) ‘Effect of resistance training on muscle properties and function in women with generalized joint hypermobility: a single-blind pragmatic randomized controlled trial’, BMC Sports Science, Medicine and Rehabilitation. https://doi.org/10.1186/s13102-021-00238-8

[23] Winter, L., Huang, Q., Sertic, J.V.L. and Konczak, J. (2022) ‘The Effectiveness of Proprioceptive Training for Improving Motor Performance and Motor Dysfunction: A Systematic Review’, Frontiers in Rehabilitation Sciences. https://doi.org/10.3389/fresc.2022.830166

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[28] Syx, D., De Wandele, I., Rombaut, L. and Malfait, F. (2017) ‘Hypermobility, the Ehlers-Danlos syndromes and chronic pain’, Clinical and Experimental Rheumatology.