Can You Be Hypermobile but Not Flexible? 

• About
• Latest Posts

Adam Foster

Director at The Fibro Guy

Adam Foster is the founder of The Fibro Guy and one of the leading voices in hypermobility, EDS, and chronic pain rehabilitation. A former Reconnaissance Soldier, he developed chronic pain after an IED blast in Afghanistan and built his approach from the ground up when the medical system had no answers. Since 2009 he has worked with thousands of people across eight countries, drawing on pain neuroscience, motor learning, and sensorimotor rehabilitation. He co-authored "No Pain, No Pain" with trauma psychologist Dr Mairi Harper, directed the documentary "Invisible Monster," and has been featured in Forbes, BBC Radio 4, ITV News, LiveScience, and The Telegraph.

Latest posts by Adam Foster (see all)

• Why ADHD and Hypermobility Keep Turning Up Together - 16 September 2026
• Hypermobility and Early Development: Milestones, Motor Delay, and Predictions - 12 September 2026
• Fibromyalgia and Itching: Why It Happens, What the Science Actually Says, and What You Can Do About It - 9 September 2026

Yes, really easily, and it’s one of the most common things our hypermobile clients turn up confused about, as the thumb folds back towards the forearm, the elbows go past straight, somebody at school once called you double jointed, and yet you still can’t get your palms anywhere near the floor and your hamstrings and neck feel permanently short. That combination is completely ordinary and it does have a decent explanation behind it, as hypermobility and flexibility are two different measurements of two different things, and they come apart all of the time ^[1][2].

Hypermobility describes how far a joint is capable of travelling, mostly because of what the passive structures around it will allow, whereas flexibility describes how far the soft tissue will let you go, and it’s only one of several things deciding what you can actually do on the day ^[2][3]. Bone shape, tissue extensibility and the nervous system’s willingness to let the movement happen all feed into your usable range, so “not flexible” was never the clean opposite of “hypermobile” ^[2].

The confusion does cause real harm though, as people get told they can’t be hypermobile because they failed the toe touch, and other people get handed a stretching programme that makes them feel worse. A fair bit of what you’ll read online about why hypermobile muscles feel tight is also stated far more confidently than the evidence actually allows (which honestly happens a lot in this space).

Hypermobility and Flexibility Are Measuring Different Things

Joint hypermobility means a joint moves beyond what’s considered a usual range, either actively or passively ^[1]. The terminology around joint movement is genuinely messy in the literature though, as different words get used for overlapping ideas, which is a decent chunk of why the internet is so confused about it ^[3].

Flexibility is the narrower of the two, as it’s about how far the muscles, tendons and the other soft tissue around a joint will lengthen and permit motion ^[1][2]. Range of motion is the thing you can actually measure on a person, and it’s the output of several inputs at once, some of which you can train and some of which you really can’t ^[2].

So, a hip can be hypermobile at the joint and still refuse to go anywhere in a forward fold, as the hamstrings, the current pain level, and how safe the movement feels are all sitting in the way ^[1][4]. That presentation is completely ordinary.

It cuts the other way too, as plenty of people are extremely flexible from years of training without being hypermobile in any constitutional sense, given that measured range can be pushed around by training, stretching, sport and previous injury ^[4][5]. Being bendy in a yoga class and being hypermobile are two different claims about your body.

What the Beighton Score Actually Looks At

The Beighton score is the screen nearly everybody meets first. Nine points, most of them at the fingers, thumbs, elbows and knees, plus the one forward bend where you keep your legs straight and put your palms flat on the floor ^[6].

That forward bend is the item that causes all of the trouble, as it’s heavily influenced by hamstring length, it’s trainable, and it can come back negative in someone who is genuinely hypermobile simply because the muscles won’t allow the manoeuvre ^[6][7][8]. So, failing the toe touch tells you something about your hamstrings on the day and very little about your ligaments.

The rest of the score has its own problem though, as it’s weighted towards the upper limb and skips several of the joints that actually hurt people ^[1][6]: hips, shoulders, ribs, jaw, ankles, the spine. You can be scoring badly on a test that never went anywhere near the joint that keeps subluxating.

None of that makes the score useless, as it’s quick, it’s consistent enough between clinicians, and it’s the common language, which does matter ^[6][9]. It’s a screening tool though, and it was never designed to be the whole assessment ^[1][6].

The Cutoff Moved, and Most of the Internet Hasn’t Caught Up

A flat “four or more means generalised joint hypermobility” is out of date as a general statement, as the threshold depends on age, and the current data driven cutoffs are higher than that for most people ^[10][11][9]. In children, six or more ^[11]. In adults, six or more between the ages of 18 and 25, five or more between 26 and 65, and four or more above that ^[10].

Which does explain something that otherwise looks a lot like your body betraying you, as scores drift down with age as tissue changes, so the same person can clear the bar at twenty and sit under it at fifty without a single thing having improved ^[10][11]. And no single threshold works cleanly across every population anyway, which is why the number is a starting point rather than a verdict ^[9].

Now, there’s a framing problem sitting underneath all of it. Hypermobility is a graded trait that sits on a spectrum, running from perfectly asymptomatic bendiness through to hypermobility spectrum disorder and hypermobile Ehlers-Danlos syndrome, and where a given person sits depends on symptoms, which joints are involved, age and context rather than on the score alone ^[12][13][14]. So it isn’t really a thing you either have or you haven’t, like a spare rib.

That distinction gets fumbled in both directions, all of the time. A high score on its own doesn’t establish HSD or hEDS, and plenty of people with a high score are fine and should be left alone ^[1][15][14]. A low score doesn’t rule out symptomatic hypermobility either, particularly if the symptomatic joints aren’t ones the test bothers to look at ^[1][6].

Asymptomatic hypermobility is common, and medicalising it does nobody any favours. What warrants a fuller look is the symptomatic version, which needs a joint by joint and functional assessment rather than another go on the nine point screen ^[1]. So, the useful question isn’t really whether you clear a threshold, it’s which joints give you trouble, what they do under load, and what’s happening around them.

Loose Doesn’t Mean Usable

A joint with generous passive capacity still has to be controlled by something. The passive structures, so the ligaments and the capsule, give you static restraint, while the muscles, tendons and the sensorimotor system give you dynamic restraint, and when the passive side is contributing less, the active side has to do a great deal more work ^[1][16]. Symptoms tend to show up at the point where mobility outstrips the capacity to control it, rather than at any particular number on a goniometer ^[1][7].

There’s a tissue level part to this as well, which gets left out of the usual explanation. In hEDS and HSD, reduced tendon stiffness and altered muscle and tendon mechanics have been documented, and those changes can interfere with force transmission, coordination and functional stability even when the passive range is enormous ^[17][18]. Measured stiffness of the tissue itself comes out lower in HSD at the patellar and Achilles tendons, and lower at the ankle ligaments in young women, so what you feel as tightness is not simply the opposite of what a clinician measures as looseness ^[19][20].

The clearest illustration of that gap comes from outside hypermobility entirely. In knees with a deficient anterior cruciate ligament, so plenty of passive laxity on examination, the amount of forward and backward motion the knee actually used during active movement was decreased rather than increased ^[21]. Loose on the examination table and guarded in use, in other words. It hasn’t been shown that the same mechanism explains hypermobile tightness, but it does demonstrate that passive laxity and active excursion can point in opposite directions in the same joint.

It isn’t a uniform impairment across everybody either, which is worth saying before anyone reads themselves into a worse position than they’re actually in. In hypermobile children, some measures come out lower, such as isometric lower limb strength and dynamic balance, while proprioception is preserved and functional lower limb strength on certain tasks is actually better ^[22]. One model does not fit every hypermobile body.

Which is also why two people with more or less identical Beighton scores can live completely different lives. One has proprioception, strength and motor control that are up to the job and stays entirely asymptomatic, while the other becomes unstable, sore and exhausted at the point where the active system either fails or deconditions ^[1][8][23]. The score didn’t decide any of that, what was governing the range did.

Mobility and stability get used interchangeably a lot of the time, and they’re asking genuinely different questions, so it’s worth separating the two words properly. Mobility is about how much range the passive structures and the shape of the joint will allow, whereas stability is about control of that range under load, and its restraints are the muscles, the tendons and the sensorimotor system ^[1][16]. The failure mode differs as well, as a mobility problem looks like excess excursion, while a stability problem looks like giving way, mistrust of the joint and poor control, which is something you experience rather than something a clinician measures on a table ^[1]. Functional instability and measured laxity are related, and they’re still not the same finding.

What the Muscles Are Actually Doing

The popular explanation is that the brain locks the muscles down to protect an unstable joint, and that story is partly supported. It’s also stated with far more certainty online than anybody has earned.

What has actually been measured is altered muscle activation, more bracing, and compensatory recruitment patterns ^[17][24]. Hypermobile girls produced torque faster in the early phase of a contraction and ran higher ratios of muscles working against each other around the joint, which reads as motor adaptation to laxity ^[24]. During ordinary walking, hypermobile women used more activation in the knee and calf muscles than you’d expect, consistent with the system working harder to hold the knee together ^[25]. Knee control during landing from a jump comes out altered in hypermobile children ^[26], and knee function and activation differ in both children and adults ^[27]. At the wrist, recruitment strategies differ as well, and the pattern is compensation rather than straightforward weakness ^[28].

So, the guarding idea is reasonable, and a protective neuromuscular response is one plausible explanation for the tightness, sitting alongside altered tissue mechanics and symptom limited range. Direct proof that a single neurological lockout is the cause of it just isn’t there though ^[17][29].

What’s worth taking from all of that is that the tight feeling is usually a muscle doing a job rather than a muscle that’s too short. A hamstring bracing to keep a knee honest will feel exactly like a short hamstring, and it’ll respond to being stretched by tightening up again about twenty minutes later, as nothing has changed about the reason it was working in the first place.

The Signal Coming Back Is Less Precise, in Some Joints

Proprioception is the other half of it, as your brain is making movement decisions on the information it gets back from the joint, and in hypermobility that information is often less reliable.

Poorer joint position sense turns up at the elbow and knee ^[30], in the neck ^[31], and in the lumbar spine, where worse proprioception tracks with poorer limits of stability ^[32]. Balance has been looked at across a range of measures in hypermobile adults, and impairments do show up there too ^[33]. Adults with symptomatic hypermobility were less able to normalise their joint motion after being pushed off balance, which reads as a control problem rather than a range problem ^[34], and trunk stability during walking comes out lower in both hypermobile children and adults ^[35].

It’s genuinely mixed though. Shoulder joint position sense came out normal in one group with EDS while vibratory sense was affected ^[36], shoulder proprioception did differ in women with generalised laxity ^[37], and adolescent competitive swimmers with hypermobility showed no clear shoulder sensorimotor deficit at all ^[38]. Poorer proprioception also doesn’t automatically mean poorer function, as the elbow and knee deficits sat alongside perfectly normal performance on closed chain functional tasks, which suggests the system compensates ^[30].

So, the honest version is that the signal is less precise in some joints, in some people, and the adaptations built on top of it are joint specific and population specific rather than universal ^[8][34].

And nobody has sorted out the direction of causation, as it’s still unclear whether the proprioceptive and strength differences cause the symptoms, follow from them, or feed each other in both directions ^[8].

Not Everything That Feels Tight Is Mechanical

Pain in hEDS and HSD doesn’t behave like a purely mechanical problem, and that’s part of why the tightness doesn’t respond to mechanical answers.

Lowered pain thresholds and increased wind up have been found in joint hypermobility syndrome and hypermobility type EDS, without the standard signs of damage to the large sensory fibres, which points towards central sensitisation as a contributor ^[39]. At the same time, small fibre neuropathy turns up in hEDS and HSD ^[40], and the sensory and autonomic involvement in hEDS looks distinguishable from idiopathic small fibre neuropathy rather than identical to it ^[41]. Both things can be true in the same population, and possibly in the same person.

The autonomic side shows up in the pattern as well. In hypermobile and neurodivergent adults, the number of hypermobile joints mediated the link to dysautonomia and pain ^[42], and there’s a proposed model connecting hypermobility to altered interoception and anxiety related circuitry ^[43]. Interoception, by the way, being how your brain reads what’s going on inside you, which is a different channel from proprioception and can be off independently of it.

All of which means the system generating that tight sensation has several inputs feeding it, and a hamstring stretch only ever addresses the one.

Fear, Fatigue and the Loop That Keeps It Running

The last piece is behavioural, and it’s the one people get defensive about, usually because it’s been used against them by somebody who wasn’t listening.

The evidence is fairly consistent here though. In lumbar hypermobility syndrome, fear of movement and fatigue both mediated the relationship between poorer stability and worse proprioception, so they aren’t a side issue sitting outside the mechanics ^[32]. In hypermobile adolescents with chronic musculoskeletal pain, heightened pain related fear is proposed as a route from hypermobility to disability, alongside physical deconditioning ^[44]. And in the broader chronic pain evidence, greater fear of movement goes with greater pain intensity and greater disability, and predicts disability later on ^[45].

Symptomatic hypermobile people are specifically described as avoiding sport and recreation because of a fear of subluxation, dislocation, pain or injury, and that avoidance narrows what they can do day to day ^[46]. Which is a completely rational response to a joint that has let you down before, and it still costs you.

The cycle is straightforward enough. The joint feels unreliable, so movement gets smaller and more guarded, and less movement means less conditioning and less exposure, so the joint gets less reliable still. Higher walking cost and exercise intolerance in hEDS and HSD make the whole thing more expensive to push against ^[17].

Naming that cycle isn’t the same as blaming you for it, and it’s a reason for the movement to be graded properly rather than a reason to be told to move more and try harder.

Injury Risk Is Joint Specific

This is where a lot of hypermobility advice goes wrong, as “hypermobility causes injuries” gets repeated as though it applies evenly across every joint and every person, and it really doesn’t.

The knee is the clearest signal, as hypermobility goes with higher odds of knee injury in contact sport ^[47]. Shoulder injury risk is also higher in athletes with hypermobility, though the underlying evidence there is weak ^[48]. Generalised joint laxity is much more common in people who dislocate a patella, and it looks like a genuine risk factor for patellar instability, again on low quality evidence ^[49]. Higher anterior cruciate ligament injury risk shows up in some groups, along with worse laxity and outcomes after reconstruction ^[50].

Second injuries after returning to sport are the strongest part of the picture. The odds of a second ACL injury within a year of returning to sport after reconstruction are substantially higher in generalised hypermobility ^[51], and in female footballers followed over five years, generalised hypermobility and excess knee hyperextension were associated with second ACL injury but not with the first one ^[52].

Now, the other half, which gets quoted a great deal less often! Ankle injury risk wasn’t elevated ^[47]. In university aged people ^[53] and in pre professional contemporary dancers ^[54], overall injury rates weren’t higher in generalised hypermobility. In one small multisport group, hypermobile athletes actually had fewer sprains, though that does sit on very shaky ground, and continued dislocations happened only in the hypermobile group ^[55].

What ties it together is symptoms rather than score. In a college population, injury rates weren’t different for generalised joint laxity on its own, but they were higher for joint hypermobility syndrome, which also went with sprains, back pain, stress fractures, clumsiness and balance problems ^[23]. Asymptomatic bendiness and symptomatic hypermobility are not the same risk profile, and treating them as one is how bendy teenagers end up frightened of sport for no reason.

Mechanically that pattern makes sense, as the knee leans heavily on its passive restraints at end range and under rotation, so laxity there is harder to compensate for than at joints where a different movement strategy can cover the gap ^[7][47].

What Actually Helps

The direction the evidence points is consistent, and it’s more or less the opposite of what most people with hypermobility get told first. Graded strengthening, proprioceptive work, posture and motor control, rather than more passive stretching of joints that are already lax ^[7][56][57].

– Stability before range: Active control strategies are consistently favoured over adding passive range, because the problem is rarely that the joint can’t get there, it’s that nothing is governing it once it does ^[1][7][56].

– Active over passive: In proprioceptive rehab more broadly, active movement approaches can outperform passive ones, so an actively held end range is worth more to you than somebody pushing you into one ^[58].

– Stretch what’s genuinely tight, leave the lax joint alone: Aggressive passive stretching of a lax joint adds very little and can aggravate the instability, but targeted stretching of a muscle that’s actually short is still perfectly appropriate. The blanket “never stretch if you’re hypermobile” line overshoots what the evidence says ^[7].

– Graded and symptom guided: Movement looks most useful when it’s built up gradually and guided by symptoms, and when the psychological barriers get addressed alongside the physical ones rather than instead of them ^[7][32][57].

– Expect it to be joint by joint: Given how joint specific the proprioceptive and activation findings are, a programme that treats every joint as equally affected is going to waste a lot of your time ^[30][38].

Graded is doing a lot of work in that list, and it’s worth being specific about what it means, as it isn’t a synonym for gentle. It means the load goes up in steps small enough that the system doesn’t have to brace its way through them, and it means the size of the step gets decided by what the symptoms do afterwards rather than by what the plan said on Monday. Movement in hypermobility is also genuinely more expensive than it looks from the outside, as walking costs more and exercise tolerance is lower in hEDS and HSD, so a programme built for somebody with ordinary tissue mechanics will overshoot ^[17].

On the calming side, breathing work and mindful movement are widely used to reduce the sense of tension and improve how much movement feels tolerable, and graded exercise does tend to reduce fear of movement in chronic pain, though the quality of that evidence varies ^[59]. There’s no direct hypermobility specific evidence for the breathing piece though, and it’s reasonable, a lot of our clients do find it useful, and it still hasn’t been tested properly in this population.

One thing to keep in mind though. If stretching has never touched the tightness, that’s information rather than a personal failing, as you’ve most likely been treating a muscle that’s working when the actual problem is what it’s working to compensate for.

What Nobody Knows Yet

The mechanism isn’t settled. Exactly how altered tissue properties, proprioception, pain processing, fatigue and fear interact to produce tightness and instability in different hypermobile subgroups is still unresolved ^[17][18][8].

The causal order is the biggest open question, as nobody has established when the proprioceptive deficits, altered recruitment, fear and deconditioning are causing the symptoms and when they’re the consequence of them, and it’s likely to be both depending on the person and the stage they’re at ^[8][4].

What has genuinely shifted is the framing. Hypermobility used to be treated as extra range and an injury risk, and it’s now treated as a system where passive laxity, active stabilisation, sensory reliability, pain processing and behaviour all interact ^[8][18]. The biomechanics didn’t get abandoned, they just stopped being the whole story.

The practical consequence of all that uncertainty is smaller than it sounds though. You don’t need the mechanism settled to know that the joint needs governing, that the signal coming back from it can be improved, and that the load has to go up in steps you can absorb ^[1][7][56]. Anyone selling you the complete explanation of why hypermobile muscles feel tight is comfortably ahead of what’s actually been shown.

The Fibro Guy

References

[1] Nicholson, L.L., Simmonds, J., Pacey, V., De Wandele, I., Rombaut, L., Williams, C.M. et al. (2022) ‘International Perspectives on Joint Hypermobility’, JCR: Journal of Clinical Rheumatology. https://doi.org/10.1097/rhu.0000000000001864

[2] Afonso, J., Blazevich, A.J., Behm, D.G., Tilp, M. and Warneke, K. (2026) ‘One of These Things Is Not Like the Others: Disentangling the Concepts of Range of Motion Versus Flexibility, and Flexibility Training Versus Stretching’, Sports Medicine. https://doi.org/10.1007/s40279-026-02425-4

[3] Jagar Omar Doski (2024) ‘Terms Used to Describe Abnormalities of Joint Kinematics: An Overview’, Kufa Medical Journal. https://doi.org/10.36330/kmj.v20i1.14725