If you ask the hypermobility community whether you should stretch, you’ll get roughly as many different answers as there are people in the room. Some will tell you stretching is dangerous because you’re already too flexible. Others insist they couldn’t function without their daily stretching routine. A fair few will have been told by a physiotherapist to stretch their hip flexors, and an equally large number will have been told by a different physiotherapist never to do that. And then there’s the growing crowd who’ve been introduced to “fascial training” or “myofascial release” as the answer to everything, complete with specialised rollers, courses, and a subscription app to go with them.
It’s a mess, this isn’t just about bad advice. And the confusion is completely understandable, because the advice out there is genuinely contradictory, and a large portion of it is built on theoretical frameworks that don’t hold up particularly well when you look at the research. So, that’s exactly what we’re going to do here. We’re going to look at what the evidence actually says about stretching, about what happens to your tissue when you stretch, about why those with hypermobility feel tight when they’re supposedly already flexible, and about why a significant chunk of what’s being marketed to the EDS community under the “fascia” banner deserves some serious scrutiny. We’re going to go deep on that last one, it’s where a lot of money is being spent on premises the evidence doesn’t support.
Fair warning: this is a long one. We’re going to cover a lot of ground, because the topic deserves it and because you deserve good information rather than marketing dressed up as science. So, if you’re ready to dig in, let’s go.
Hypermobility vs Flexibility: They’re Not the Same Thing
Before we get into any of this, we need to clear up a distinction that matters enormously and gets muddled constantly. Hypermobility and flexibility are not the same thing. They’re related, but they’re not interchangeable, and treating them as though they are is where a lot of the bad advice starts.
Flexibility, in the physiological sense, refers to how far a joint can move passively through its range of motion. Hypermobility refers to joints that exceed the normal range of motion, often significantly, due to differences in connective tissue. In hypermobile Ehlers-Danlos syndrome (hEDS) and hypermobility spectrum disorder (HSD), this is driven by a difference in the structural properties of collagen, the protein that gives connective tissue its tensile strength. So, the joints move too far because the ligaments and other soft tissue structures that limit that range are more compliant than typical.
So when someone with hEDS says they feel tight and stiff despite being hypermobile, that’s not a contradiction. It makes complete sense once you understand the mechanisms involved, and we’ll explain exactly why shortly. But the starting point is understanding that having joints which move too far doesn’t mean your muscles are long, mobile, or relaxed. Quite the opposite is often true. If you want the full picture on what hypermobility and EDS actually involve, we’ve covered that in depth elsewhere on the site.
What Stretching Actually Does to Your Body
This is where the popular understanding of stretching falls apart. Most people, including most patients and quite a few practitioners, believe that stretching works by physically lengthening tissue. The story goes: if your hamstring feels tight, it’s because it’s short, so you stretch it out and it gets longer. Sounds logical. But when you look at the research, this just doesn’t hold up.
A 2023 systematic review and meta-analysis by Panidi and colleagues looked specifically at the effect of static stretching on fascicle length at rest. Fascicle length is a direct, ultrasound-measured indicator of actual muscle length. And the pooled effect size was 0.17, which is trivial. Static stretching, even done regularly over weeks, produces essentially no meaningful change in resting muscle fascicle length [1]. And the tissue itself is not changing in any structurally significant way.
So what IS happening when you stretch and your range of motion improves? Well, the answer, supported by a growing body of evidence, is that it’s almost entirely a nervous system effect. A 2017 paper by Bishop and George discussed the role of neural mechanisms in how we experience changes in movement and pain, finding that ROM changes were far better explained by sensory factors than by any soft-tissue changes [2]. In other words, you’re not lengthening anything. You’re training your nervous system to be more tolerant of the sensation of stretch. Your brain decides that this particular position is acceptable, and it stops applying the brakes quite so firmly. That’s stretch tolerance, and it’s neurological, not mechanical.
However, this matters a great deal for those with hypermobility, because if the gains are neural rather than structural, it has significant implications for why you feel stiff, what’s actually going to help, and what you’re wasting your time on. The physical therapist and educator Adam Meakins has made this point clearly and consistently: when someone describes an aggressive six-week stretching programme conducted three times a day, and researchers measure muscle structure before and after with imaging, they find zero physical change to the muscle [3]. The sensation changes. The tissue doesn’t. So, it’s a finding that should reshape how we think about what stretching is actually for.
The “Shortened Muscle” Myth
There’s a story that gets told a lot in clinical and fitness settings: you sit at a desk all day, your hip flexors get “short and tight”, your hamstrings shorten, your thoracic spine stiffens up, and you need to stretch them all out to restore normal length. It’s everywhere. But when it comes to the actual evidence, it’s not particularly well supported.
The mechanism by which muscles genuinely shorten at the level of their sarcomeres (the tiny contractile units that make up muscle fibres) requires sustained immobilisation in a shortened position over a considerable period of time. A 1990 study by Williams looked at exactly this in an animal model, finding that even in fully immobilised muscle, just 30 minutes of daily stretching was enough to prevent sarcomere loss [4]. Thirty minutes. In fully immobilised muscle. If complete immobilisation combined with a minimal daily stretch can preserve normal sarcomere number, the idea that sitting at a desk for eight hours with occasional movement is causing structural muscle shortening looks rather thin.
A 2024 review by Hinks and Power confirmed that sarcomere loss requires at least two weeks of complete immobilisation in a shortened position, and that recovery begins within days of normal movement resuming [5]. We’re talking genuine pathological immobilisation: post-surgical casting, neurological conditions like dystonia or spasticity, or severe contracture. Not sitting at a desk. Not sleeping in a particular position. And not being generally inactive.
Meakins’ argument (and it’s a good one) is that to physically shorten your hip flexors through inactivity, you’d essentially need to be sitting completely still for 23.5 hours a day, every single day, for months at a time, with absolutely no lying flat, no standing, no walking, nothing. Normal daily life, even fairly sedentary daily life, provides more than enough movement to prevent actual muscle shortening. This doesn’t come as a surprise, the body is remarkably efficient at maintaining what it needs. However, the stiffness people feel after sitting or on waking up is real. It’s just not structural. It’s fatigue, deconditioning, nervous system guarding, and those mechanisms matter enormously in hypermobility specifically, and we’ll get to them now.
So you won’t find the usual caveat in this article that “static stretching still has a place for genuinely shortened muscles.” Outside of genuine pathology, shortened muscles simply aren’t the problem for most of the people we work with. That’s not a controversial fringe position. However, it challenges a narrative that is so deeply embedded in fitness and clinical culture that it takes some confronting. That’s what the evidence actually says.
Why Do Hypermobile People Feel Tight?
So if it’s not shortened muscles and it’s not some structural tissue property, why do so many people with hEDS and HSD describe feeling tight, stiff, and restricted? The experience is real and valid. But the explanation is considerably more interesting, and rather more important, than “your muscles are too short”.
There are three main mechanisms at play here, and they often interact with each other in ways that make the overall picture fairly complex. Now, we’ve talked about all three in various contexts across the site, but it’s worth pulling them together here. Understanding them is central to making good decisions about stretching and movement. However, they do get routinely missed in clinical settings, which is part of why so many people with EDS end up with explanations that don’t match their experience.
Protective Muscle Guarding
When your joints move too far and your passive stabilisers (ligaments, joint capsules) aren’t providing the degree of stability they should, your nervous system doesn’t just sit back and let you fall apart. It compensates by increasing muscle tone and activity around the unstable joints. And the muscles essentially work overtime to provide the stabilisation that the ligaments can’t fully deliver. This is protective, it’s adaptive, and it’s exhausting. And it shows up in the body as genuine physical tension.
A 2025 scoping review by Wang, Strutton and Alexander looked at falls and balance in people with hypermobility and found altered muscle activation patterns and increased postural sway, consistent with this kind of compensatory neuromuscular activity [6]. But the muscles aren’t just tight because they’re short. They’re tight because they’re constantly working. We’ve noticed this pattern consistently with our clients: when people with hEDS go through periods of increased stress or fatigue, the “tightness” they feel tends to get significantly worse, even with no change to their physical activity. That’s not a tissue change. That’s a nervous system response. You can read more about the relationship between muscle guarding and core stability in hypermobility on the site.
Central Sensitisation
Central sensitisation is the process by which the central nervous system becomes upregulated, amplifying sensory signals from the body, including pain and the sensation of tightness. It’s not just about pain. And when your nervous system is sensitised, the feeling of restriction or stiffness in a joint or muscle can be amplified well beyond what the tissue state would normally produce.
The prevalence of central sensitisation in EDS is genuinely striking. A 2023 analysis by Willich, Koppe and colleagues found that approximately 90% of affected EDS patients develop central sensitisation [7]. That’s not a small subgroup, almost everyone with the condition. And a study by Schubert-Hjalmarsson and Lundberg in 2023 found signs of central sensitisation in adolescents with HSD and hEDS as well [8]. A paper by Colman and colleagues in the same year showed altered pain modulation and hyperalgesia in classical EDS, consistent with central sensitisation processes [9].
However, when your nervous system is in that state, the sensation of tightness or restriction is genuinely felt. It’s not imagined or exaggerated. But it’s a nervous system phenomenon, not a structural tissue problem, and that has massive implications for what’s going to actually help. We’ve written a full piece on central sensitisation that goes into considerably more depth if this is new territory for you.
Proprioceptive Deficits
Proprioception is your body’s sense of where it is in space, the feedback loop from your muscles, joints and surrounding tissues that tells your nervous system what position you’re in, how fast you’re moving, and how much force is being applied. Those with hypermobility have documented deficits in proprioceptive accuracy across multiple studies, and the implications of this are broader than most people realise.
A 2015 study by Clayton, Jones and Henriques found that people with EDS were significantly less precise at proprioception tasks, and that this correlated with the severity of their hypermobility [10]. A 2025 study by Akaras and colleagues found significantly poorer proprioception at both the elbow and knee in hypermobile individuals [11]. Dupuy and Vlamynck and colleagues in 2017 found greater postural instability in hEDS patients, and Scheper and colleagues in 2017 showed that this proprioceptive inaccuracy actually confounds the relationship between muscle strength and functional limitations in EDS [12, 13].
When you don’t have a clear, reliable map of where your body is in space, your nervous system compensates by increasing tone throughout, essentially creating a kind of background tension that functions as a proxy for the proprioceptive information it isn’t getting clearly. You can think of it as trying to drive in thick fog, the instinct is to slow down and grip the wheel tighter. And that compensation creates genuine tension. We have a dedicated piece on proprioception in hypermobility that goes into the neuroscience in more depth.
And there’s one more piece to add to this picture. A 2022 study by Fernandez and colleagues found that 91% of a sample of 79 people with hEDS or HSD had definite or possible small fibre neuropathy (SFN), meaning damage to the small nerve fibres that transmit pain and sensory signals [14]. That’s a remarkable prevalence, it changes how you should think about the sensory experience of this condition. Small fibre neuropathy produces abnormal sensations: burning, tingling, hypersensitivity, and it can absolutely contribute to sensations of tightness or discomfort that have nothing to do with the mechanical state of the muscles. The pain experience in hypermobility is genuinely complex and multi-layered, and understanding that complexity is half the battle.
So here’s the picture: those with hEDS and HSD often feel tight and stiff not because their muscles are actually short, but because their muscles are working overtime to stabilise hypermobile joints, their nervous system is amplifying sensory input through central sensitisation, their proprioceptive feedback is unreliable and their nervous system is compensating for that, and in many cases there’s underlying small fibre neuropathy contributing to the sensory picture. None of these causes are addressed by static stretching. None of them. And that’s the key point. However, that doesn’t mean the sensations aren’t real. They absolutely are.
The Fascia Industry: What the Evidence Actually Shows
Right. Here we go. This is the section that needs to be said clearly, because a significant amount of money is currently flowing from people with EDS and hypermobility toward products, practitioners, courses and apps built on theoretical foundations that don’t survive contact with the evidence. We’re going to go through it methodically, because the people selling this stuff are often smart, articulate, and genuinely believe what they’re saying. The problem isn’t usually malice. And it’s a theoretical framework that has been adopted prematurely and marketed aggressively before the science has caught up, and it’s being marketed specifically to a community that is vulnerable, in pain, and trying to make sense of a confusing condition.
What Is Fascia, and Why Should You Care?
Fascia is the connective tissue that surrounds and interpenetrates muscles, organs, nerves, and blood vessels throughout the body. It’s a continuous network, which is real and interesting, and it does have mechanical and sensory properties, which is also real and interesting. None of that is in dispute. The dispute is about whether you can specifically target fascia with exercises or manual therapy, whether you can structurally alter it with your hands or with movement, and whether “fascial training” as a concept represents something meaningfully different from regular exercise. Now, when it comes to those questions, the evidence is considerably less flattering to the fascial training narrative than the industry would have you believe.
The short answers are: no, no, and no. Let’s go through why in detail, because each of these points matters and the evidence behind them is solid.
You Cannot Target Fascia Independently
Fascia doesn’t exist in isolation from the rest of your body’s structures. It’s embedded throughout everything. When you move, you load muscles, tendons, ligaments, bones, and fascia simultaneously. And there is no movement that loads fascia while not loading the other structures it wraps around. There is no exercise that “targets fascia” rather than the whole structural matrix. Calling an exercise “fascial training” is, as Meakins has put it, about as meaningful as calling it “bone training” or “nerve training”. You’re loading all of those structures together with every movement you do. And slapping a “fascial” label on it doesn’t make it a different category of thing.
However, the exercises being sold under the “fascial training” brand are frequently perfectly reasonable exercises. Progressive loading, full-range movement, controlled multi-directional patterns: none of that is bad. So if someone is doing those exercises because they genuinely enjoy them and they’re building strength and movement capacity, that’s great, and the exercises are probably working well. But the problem is the theoretical wrapper they’re sold inside. If the fascial framework is why someone avoids proper strength training in favour of gentler “fascial” approaches because they’ve been told the conventional stuff isn’t fascia-friendly, they may be making decisions based on a framework that isn’t well-supported by the evidence.
For those with hypermobility specifically, the implications are potentially significant. When it comes to what actually changes the picture in hEDS and HSD, it’s progressive loading that builds the joint stability and neuromuscular control the body needs. And if the fascial training narrative leads someone away from that, toward gentler approaches that feel safer but don’t provide the mechanical stimulus the body needs, that matters. You can get into the specifics of exercise for hypermobility in our comprehensive guide.
You Cannot Structurally Deform Fascia With Your Hands
This is where the myofascial release, Rolfing, and deep tissue work narrative runs into a problem that’s genuinely hard to argue around. The claim that skilled manual therapy can “release” fascial restrictions, break up adhesions, or realign fascial layers requires that the force applied by a practitioner’s hands be sufficient to produce structural deformation of fascial tissue. And that claim has been directly tested in the mechanics literature.
In 2008, Chaudhry, Schleip, Ji, Bukiet, Maney and Findley published a biomechanical modelling study examining exactly what forces would be required to produce even 1% compression or shear deformation of dense fascial structures like the iliotibial band and the plantar fascia [15]. The results were unambiguous: the forces required were enormous, far beyond anything that human hands can generate. However, this finding somehow hasn’t filtered down into widespread clinical practice, where fascial release is still routinely offered and sold. The iliotibial band, for example, would require forces that are simply not achievable through manual therapy to produce any meaningful structural deformation. Not a small amount. Not something close but not quite achievable. And far beyond what any practitioner’s hands can produce.
Now. Here is the detail that deserves to be noted carefully. So, look at the author list on that paper: Chaudhry, Schleip, Ji, Bukiet, Maney and Findley. Robert Schleip is a co-author on the paper demonstrating that manual therapy cannot structurally deform fascia. Robert Schleip is also one of the most prominent figures in the fascial training and fascial research world. He runs the Fascia Research Congress. He sells courses. And his work has been central to building the commercial fascial training industry. And yet one of his own published papers, a peer-reviewed biomechanical modelling study with his name on it, demonstrates that the structural manipulation premise underlying a significant portion of that industry doesn’t hold up [15].
That’s not a personal attack on Schleip. He’s a prolific researcher and some of what he’s done on fascial anatomy and sensory innervation is genuinely interesting work. But it is important context when you’re evaluating the claims coming out of this space. Likewise, the Stecco family, who developed Fascial Manipulation therapy, have built commercial enterprises on the premise that fascia can be specifically targeted and structurally altered through manual work. These are not disinterested scientists. And they have financial interests built on this framework being true, which doesn’t automatically make them wrong, but it does mean their research should be read with that context in mind.
The Evidence From Imaging and Biopsies
The Chaudhry mathematical modelling paper isn’t the only line of evidence here. Studies that have actually measured tissue properties before and after interventions designed to “release” fascia or alter soft tissue stiffness have consistently come up empty when it comes to structural change, and this consistency across different measurement approaches is quite telling.
A study by Vardiman and colleagues applied vigorous Instrument-Assisted Soft Tissue Mobilisation (IASTM) to calf muscles and measured stiffness, thickness, viscosity, density, and took biological markers from tissue biopsies before and after [3]. They found zero change in any measured parameter, this is not a small or borderline finding. Not a small change. Zero change. The tissue that was being “released” and “mobilised” showed no measurable response to that treatment at any level from gross imaging down to biological markers in biopsies.
A 2015 study by Thomson, Gupta and colleagues applied deep soft-tissue massage to the calf muscle and measured passive mechanical properties before and after. No effect on tissue mechanics [16]. The tissue didn’t change. And the forces applied by the hands are simply not sufficient to remodel the mechanical properties of healthy connective tissue. So, this is consistent across the research that has actually measured rather than assumed.
However, a particularly interesting 2024 study by Hiratsuka, Ikeda and colleagues looked at six weeks of IASTM and found that ROM did improve and stretch tolerance did increase, but there was zero change in muscle or tendon stiffness [17]. This is exactly what you’d expect from the stretch tolerance model: the neural component (ROM and tolerance) changes, the structural component (actual tissue stiffness) does not. The same mechanism as stretching. Neural adaptation, not structural remodelling. And the Konrad data makes the same point from a different direction: an aggressive stretching regime, three times per day for six weeks, produced no physical change to muscle structure whatsoever [3]. People felt more flexible. Their range of motion increased. But the tissue itself was unchanged.
What Does “Myofascial Release” Actually Do?
Given all of the above, what’s actually happening when someone has a myofascial release session and feels better afterwards? The honest answer is that it probably produces real effects, just not the ones claimed. Manual therapy has genuine short-term benefits: reduced nervous system sensitivity, improved perception of movement, reduced guarding, temporary changes in pain threshold. These are real, they’re worth having, and they have a legitimate mechanism. The nervous system responds to touch and pressure by modulating its sensitivity, it’s a nervous system conversation rather than a structural intervention.
But “temporary neural desensitisation through manual contact” doesn’t sell courses or justify premium pricing quite as well as “releasing your fascial restrictions and realigning your connective tissue”. And the neural mechanism, while real and potentially valuable, doesn’t require a specific fascial framework. Any skilled therapist is likely achieving the same thing. Any skilled manual therapist providing therapeutic touch is likely achieving these effects through the same mechanism. The fascial label isn’t doing any additional explanatory or therapeutic work.
For those with hypermobility and EDS, this matters particularly because central sensitisation is so prevalent in this population. Manual therapy can help modulate a sensitised nervous system, and there’s nothing wrong with that at all. However, when patients are being told they have “fascial restrictions” causing their symptoms, that they need specific “fascial release” techniques, or that their fascia is “dysfunctional” in some specific way requiring a certified practitioner using specific protocols, they’re being given an explanation that isn’t well-supported by the evidence. And explanations matter, because they shape what people believe about their bodies, which shapes their behaviour and their recovery. We’ve seen this repeatedly: clients who’ve been told their fascia is the problem spend significant time and money on fascial work and remain afraid of conventional loading, which is the thing most likely to actually help them long term.
The Trigger Point Conversation
Whilst we’re in this territory, it’s worth briefly touching on trigger points, those “knots” that practitioners palpate in muscle tissue and which are central to much of the myofascial release framework. A 2008 systematic review by Myburgh and colleagues examined the structural evidence for myofascial trigger points and found it unconvincing [18]. Interrater reliability for identifying them is poor, the structural correlates are inconsistent, and the mechanism by which they form and persist remains unclear. The sensation of a “knot” being released through pressure is real. The structural explanation for what that means is not.
Again, this doesn’t mean the treatment doesn’t produce genuine benefits, it may. But the theoretical framework it’s sold within has problems, and for those with hypermobility who are trying to make sense of their bodies and their symptoms, being given a clear and accurate explanation really does matter.
The Financial Picture
It’s worth being direct about the economics here, because a lot of the people reading this are making real decisions about where to spend limited money and energy, and the fascia space has significant financial dynamics worth understanding. The fascial training and fascial release industry has grown substantially over the past decade and a half. There are certification courses for practitioners in fascial manipulation, fascial release, and fascial fitness. And there are consumer apps, foam rollers with specific geometries claimed to target fascial tissue, and workshops selling a fascial approach to movement specifically for people with chronic conditions including EDS.
The people behind much of this have built commercial enterprises on the premise that fascia is the key and that they’ve identified the right approach. And the researchers who’ve driven the popularity of fascial frameworks have conferences, courses, and methodologies built around their work. That doesn’t automatically make what they’re saying wrong. But it does mean that when you’re evaluating claims in this space, you’re doing so in a marketplace where there are strong financial incentives to overstate what the evidence shows, and the people most frequently targeted are those who are most vulnerable.
The practical question for someone with hypermobility and EDS is this: if you’re doing exercises sold as “fascial training” and they’re genuinely progressive, they involve loading, they build strength, and they improve your function, then they’re probably working despite the fascial label, not because of it. Good exercise is good exercise. However, if you’re avoiding progressive resistance training and replacing it with gentler fascial approaches because you’ve been told your connective tissue is too fragile for conventional loading, you’re making a decision that the evidence doesn’t support. And the Liaghat series we’ll get to shortly is pretty direct on that point. You can look at the broader picture of exercise rehabilitation for hypermobility in our main guide.
A Word on the Research Landscape
Fascial research is a real field, and we want to be clear about that. There are genuine questions about the sensory and mechanical roles of fascia in health and disease, and some interesting work is being done. We’re not saying fascia isn’t real or that it doesn’t matter as a structure. We’re saying that the jump from “fascia has sensory and mechanical properties” to “you can specifically target, release, and structurally remodel fascia through manual therapy or specific movement patterns” is a very large jump, and the evidence for the second part is not there. The biomechanics says the forces required are too high. The imaging studies say the tissue doesn’t change. And the neural explanation accounts for the effects people experience without requiring any of the structural claims.
For those with hypermobility and EDS who are in pain, who’ve tried a lot of things, and who are being offered an apparently sophisticated explanation for their symptoms, that’s an appealing narrative. We understand entirely why it gets traction. But you deserve to know what the evidence actually says, so you can make good decisions with your time, your money, and your body.
Static Stretching: What the Evidence Shows
Even setting aside the structural lengthening question, there are some specific problems with static stretching as a practice that are worth being aware of, particularly for those with hypermobility. When it comes to static stretching before exercise, the evidence is pretty clear that it creates a force deficit.
A 2024 systematic review and meta-analysis by Warneke and colleagues looked at the acute effects of static stretching on force production and found a clear stretch-induced force deficit [19]. Stretching before activity acutely reduces the amount of force your muscles can produce. If you’re doing a static stretching warm-up before exercise or physical activity, you’re potentially reducing your performance capacity during that session. That’s not ideal for anyone. For those with hypermobility who are already dealing with reduced proprioceptive accuracy and muscle activation challenges around unstable joints, additional acute reductions in force production are not what you want.
A companion paper by Warneke and colleagues, also in 2024, looked at whether stretching and foam rolling are superior to other warm-up activities for acute flexibility gains, and found they are not [20]. You can achieve equivalent or better acute ROM preparation through dynamic movement without the force deficit. So static stretching before exercise isn’t doing anything that couldn’t be done better a different way.
However, for those with hypermobility, there’s a further consideration that goes beyond performance. Static stretching already-hypermobile joints means taking tissue that’s already moving beyond normal range to even greater extremes, and the stabilising muscles that are doing so much work to compensate for the connective tissue laxity are being stretched out and temporarily weakened in the process. So, that’s arguably the opposite of what you need. The research on isometric exercises in hypermobility is instructive here: building stability around joints, not adding range to them, is generally the direction of travel when it comes to what actually helps.
Dynamic Stretching: A Better Option
Dynamic stretching, moving through ranges of motion actively under muscular control rather than holding passive end-range positions, is a more sensible approach and avoids the force production concerns associated with static stretching. Moving joints actively through controlled ranges as part of a warm-up is broadly useful: it warms the tissue, engages the neuromuscular system, and improves movement readiness without the passive end-range loading of static work.
However, even dynamic stretching as a standalone practice misses what’s most important for those with hypermobility. Moving actively through range without the progressive loading stimulus of resistance training doesn’t build the strength and neuromuscular control that stabilise joints. It’s preparation for the main event. And the main event, in terms of what the evidence actually supports for this population, is progressive resistance training. So, let’s get to that.
Strength Training and Flexibility Gains: They’re the Same Thing
Here’s the finding that surprises most people, and it’s one of the more important practical takeaways from the research on this topic. When it comes to flexibility outcomes, strength training and stretching produce equivalent gains in range of motion. Not approximately equivalent. Not roughly similar. And not statistically different.
A 2021 systematic review and meta-analysis by Afonso and colleagues pooled data from 11 randomised controlled trials involving 452 participants and found no statistically significant difference between resistance training and stretching on ROM outcomes [21]. The effect size was -0.22 with a 95% confidence interval of -0.55 to 0.12 and a p-value of 0.206, which means the difference between the two is essentially noise. And this paper is worth sitting with for a moment, because it’s a pretty direct challenge to the idea that you need a separate stretching practice to maintain flexibility. If the strength training you’re doing anyway produces equivalent ROM outcomes, what’s the argument for adding dedicated static stretching on top of it?
A 2023 systematic review and meta-analysis by Alizadeh and colleagues confirmed this finding, showing that resistance training with external loads improves ROM to a moderate magnitude that isn’t significantly different from stretch training [22]. And a 2025 systematic review, meta-analysis and meta-regression by Favro and colleagues pulled together data from 36 studies and 1,469 participants, finding a pooled effect size for resistance training on flexibility of g = 0.6325 (p < 0.0001) [23]. High-intensity protocols showed magnified effects. Heavier loading produces bigger flexibility gains. That’s not what people expect to hear, but that’s what the data says.
But the practical evidence goes further than just meta-analyses. A 2024 randomised controlled trial by Rosenfeldt and colleagues compared resistance training and static stretching directly and found that resistance training improved both flexibility AND strength, while static stretching improved flexibility but didn’t improve strength [24]. So even if both produce equivalent flexibility gains (and they do), strength training does additional work that stretching doesn’t. There is no flexibility argument for stretching that can’t be met by strength training, but there are multiple strength and stability arguments for strength training that stretching simply can’t match.
This is particularly relevant for those with hypermobility, where the entire problem is inadequate dynamic stability, not inadequate range of motion. The exercise and hypermobility guide goes into this in much more depth, but the direction of travel is clear. Progressive resistance training addresses the actual mechanisms behind the problems those with hEDS and HSD experience, and it delivers flexibility benefits as a package deal along the way.
High-Load Exercise in Hypermobility: The Liaghat Series
There’s a persistent belief in the hypermobility community, sometimes reinforced by well-meaning practitioners, that high-load exercise is dangerous for those with EDS and that loads must be kept very low to avoid damage. But the Liaghat research series is fairly direct about challenging this assumption, and it’s a series worth knowing about in some detail.
A 2022 randomised controlled trial by Liaghat and colleagues compared high-load, full range-of-motion exercise against low-load exercise for people with HSD experiencing shoulder problems [25]. The high-load group showed statistically superior outcomes for shoulder function in the short term. And this was an important paper because it provided direct RCT evidence in a hypermobile population that high loading was not only safe but more effective than the cautious, low-load approach that many patients had been advised to follow.
A 2024 follow-up by the same group looking at one-year outcomes found that heavy loading wasn’t statistically superior at twelve months, though it remained better on the emotional wellbeing subdomain [26]. However, neither paper showed that high loading was harmful or caused adverse outcomes in hypermobile joints. Both groups improved. And the key point is that the high-load approach was at least as good as low-load and potentially better, without the harms that many practitioners and patients fear.
The 2025 pain trajectory paper by Liaghat and colleagues is arguably the most reassuring of all. It looked specifically at exercise-induced pain during high-load exercise in people with hypermobility and found minor to no exercise-induced pain in most participants, directly challenging the assumption that loading hypermobile joints will cause symptom flares [27]. For those who’ve been told for years to keep everything gentle and avoid anything heavy, this is significant. We’ve also seen this pattern repeatedly in the people we work with: those who’ve been told to be very careful with loading often discover that carefully progressed, appropriately loaded exercise doesn’t cause the harm they were led to expect. The expectation of harm can sometimes be more limiting than the actual risk.
There’s also a 2021 RCT by Luder and Haupt-Bertschy and colleagues that looked specifically at resistance training in women with generalised joint hypermobility, finding beneficial effects from a structured programme [28]. However, the caveat with all of this is that appropriate progression matters. You don’t start by loading maximally. For those with shoulder pain and hypermobility or knee pain and hypermobility, the Liaghat work is particularly relevant. The evidence for appropriately progressive loading in hypermobility is building. The case for indefinitely avoiding it is not.
Yoga and Hypermobility: A Nuanced Picture
Yoga comes up in virtually every conversation about stretching and hypermobility, and the picture is genuinely mixed. And there are people in the hypermobility community who credit yoga with helping them enormously, and an equally large number who’ve been made significantly worse by it. Both groups are telling the truth, and the difference usually comes down to what type of yoga practice they’re doing and how they’re approaching it.
The issue with standard yoga classes is that they typically encourage moving to the end of range, deepening the stretch, going further. And for those with hypermobility, that’s loading into territory where the passive stabilisers are already insufficient. However, deep passive stretching of hypermobile joints done repeatedly over time may reinforce the very movement patterns that create problems, pushing into end-range positions where the joint is most vulnerable and where the muscles providing dynamic stability are at a mechanical disadvantage. And when it comes to the “flexibility goals” in a standard class context, those goals aren’t really goals for people whose joints already exceed normal range.
A 2024 scoping review by Garreth and colleagues looking at physiotherapy interventions in G-HSD and hEDS found strong evidence for therapeutic exercise and motor function training [29]. However, the context matters enormously. Therapeutic exercise means supervised, progressive, stability-focused work. It doesn’t mean attending a standard vinyasa class and pushing into the deepest expressions of each pose. The distinction between yoga as typically practised in a class setting and modified yoga focused on controlled, stability-building movements within comfortable range is significant for this population.
If yoga is part of your practice and it helps you, that’s worth exploring, there are real benefits in consistent movement and breathwork. However, it’s worth asking which element of the practice is actually providing the benefit. Is it the movement itself? The breathing? The routine? The community? The stress reduction? All of those things have genuine value. But when it comes to the specific question of whether end-range passive stretching in yoga postures is addressing your hypermobility symptoms, the evidence doesn’t particularly support that mechanism.
Kinesiophobia and the Fear Loop
There’s something that happens to a lot of people with hypermobility that doesn’t get talked about enough, and it directly affects how they approach movement and exercise. Now, when you’ve been told your connective tissue is fragile, when movement has caused pain and dislocations or subluxations, when practitioners have repeatedly told you to be careful, it’s completely understandable to develop a fear of movement. This is kinesiophobia, and it’s genuinely common in the hypermobility population.
The 2025 paper by ALMohiza and Reddy found that kinesiophobia mediates the relationship between postural stability and proprioceptive accuracy in hypermobility spectrum disorder [30]. Now, fear of movement isn’t just a psychological side effect of having a connective tissue condition. And it actively worsens both balance and proprioception, which are two of the primary mechanisms driving the problems in the first place. It creates a loop: pain and instability lead to fear of movement, fear of movement reduces activity and load, reduced loading worsens neuromuscular control, worse neuromuscular control makes symptoms worse, which reinforces the fear.
A paper by Dolso, Liaghat and colleagues from 2023 confirmed that higher fear of movement is associated with worse outcomes in people with hypermobility [31]. However, breaking that loop is one of the most important things you can do, and it requires a graduated return to loading rather than an indefinite continuation of avoidance. This connects directly to the fatigue in hypermobility picture as well, because deconditioning from movement avoidance is a major driver of fatigue. The pain and hypermobility guide addresses the kinesiophobia loop in more detail if this is where you find yourself.
I’ve noticed this pattern consistently across the people we work with. Those who’ve been most thoroughly scared off loading, often by well-meaning but overly cautious advice, tend to take the longest to build back to the kind of activity levels that actually improve their function. The fear itself becomes a significant barrier, the “gentler is always safer” message, however kindly intended, can inadvertently reinforce it. That’s nobody’s fault, but it’s worth being aware of.
A Note on Small Fibre Neuropathy
We touched on small fibre neuropathy earlier, but it deserves a dedicated mention here. Because it’s not widely known even within the EDS community. However, it changes how you should think about sensory experiences in your body in ways that are really quite significant. The 2022 Fernandez and colleagues study finding 91% prevalence of SFN in hEDS and HSD patients is striking, particularly given how underdiagnosed it tends to be [14].
If you have abnormal firing in the small nerve fibres throughout your body, you’re going to have abnormal sensory experiences throughout your body: burning, tingling, pins and needles, hypersensitivity, and yes, sensations that might be interpreted as tightness or restriction. Understanding this doesn’t necessarily change what you do on a day-to-day basis, but it does change the explanatory framework. When you feel tight in your thoracic spine or your hip flexors, the cause may not be tissue shortening, fascial restriction, or anything structural. It may be a nervous system firing pattern in the small fibres running through that area. That’s a very different problem with a very different solution, and it underscores why approaches that target tissue mechanically are often missing the point entirely. For more on the neurological complexity of EDS, the main hEDS guide covers a lot of this ground.
Practical Recommendations
So, with all of the above in mind, what should someone with hypermobility and EDS actually do? Here’s our take, based on the evidence we’ve covered.
First, if your current stretching routine is making you feel better and you’re genuinely moving better because of it, that’s not nothing. Stretch tolerance is real. The neurological benefits of regular gentle movement are real. However, it’s worth understanding what’s actually happening: your nervous system is adapting, not your tissue lengthening. And ask yourself whether there’s a more efficient way to get those benefits while also building the strength and stability you need.
Second, progressive resistance training should be your priority. And not because strength training is the answer to everything, but because it addresses the actual underlying mechanisms: it builds the dynamic stability that compensates for ligamentous laxity, it improves neuromuscular control and proprioception, it produces equivalent flexibility gains as a side effect, and the evidence in hypermobile populations is increasingly clear that appropriately progressed loading is safe and effective. The exercise rehabilitation guide can help you understand how to structure that.
Third, if you’ve been doing static stretching before exercise as a warm-up, the evidence doesn’t support that practice. Dynamic movement through comfortable ranges is a better warm-up option. However, if you want to keep some static stretching in your routine, after exercise is a more appropriate time, when the nervous system is already active and the force deficit matters less.
Fourth, be thoughtful about yoga. When it comes to yoga, the type and approach matters enormously. If you’re in a class that repeatedly encourages you to go deeper and further and achieve the full expression of a pose, that’s probably not well-suited to hypermobile joints. If you find a teacher focused on stability, control and breath work rather than range, that’s a different thing. The pelvic floor and hypermobility piece has some relevant discussion of how loading principles apply to areas often thought of as needing stretching rather than strengthening.
Fifth, when evaluating any manual therapy or exercise approach being sold to you with “fascia” as a central concept, apply sensible scepticism. However, scepticism doesn’t mean dismissing everything out of hand. Ask what specific mechanism is being claimed, whether the forces involved could plausibly produce the claimed effect, and whether there’s any imaging or objective measurement evidence that the claimed structural changes actually occur. Based on what we’ve reviewed above, the structural claims for manual fascial work don’t hold up. The neural modulation effects are real but aren’t specific to fascial techniques.
Sixth, if you’ve been avoiding loading because you’re afraid of what it might do to your joints, try to find a practitioner or programme that can help you build back gradually with appropriate support. The evidence from the Liaghat series and others is that appropriately progressed loading in hypermobility is not the catastrophe many people expect. For those with hip pain, CRPS, or POTS symptoms, we have more specific guidance on how exercise fits into those pictures as well.
And finally, if you have POTS or significant dysautonomia alongside your hypermobility, the exercise picture has additional layers. The POTS and dysautonomia guide covers that territory. Similarly, if fatigue is a major factor for you, the fatigue and hypermobility piece is relevant to how you structure and pace activity.
Frequently Asked Questions
Should people with hypermobility stretch?
The evidence suggests that dedicated static stretching provides limited additional benefit for most people with hypermobility, because the flexibility gains from stretching are equivalent to those from strength training, and strength training also builds the joint stability and neuromuscular control that those with hEDS and HSD actually need. Light dynamic movement as warm-up is reasonable. Prolonged static stretching at end range is less well-supported, particularly since it can temporarily reduce muscle force production around already unstable joints.
Why do I feel tight if I have hypermobility?
Feeling tight despite having hypermobile joints is extremely common and has clear mechanistic explanations. The main drivers are protective muscle guarding (muscles working overtime to stabilise joints that lack adequate ligamentous support), central sensitisation (an upregulated nervous system amplifying sensory signals including the sensation of tightness), and proprioceptive deficits (unreliable body position sense causing the nervous system to increase background tension as a compensatory strategy). Small fibre neuropathy, found in around 91% of hEDS patients in one study, can also contribute abnormal sensory experiences.
Is fascial training suitable for people with EDS?
The term “fascial training” is a marketing label applied to exercises, not a distinct category of exercise that specifically targets fascial tissue. You cannot load fascia independently from the other structures it surrounds. The exercises sold as fascial training are often reasonable exercises involving progressive loading and whole-body movement. If those exercises are progressive and build strength and control, they’re likely beneficial. But the theoretical framework around them is not well-supported by evidence, and those who avoid conventional progressive resistance training in favour of “fascial” alternatives may be missing the most evidence-based approach to managing hypermobility.
Can myofascial release help with hypermobility symptoms?
Manual therapy including myofascial release can produce genuine short-term benefits including reduced nervous system sensitivity, improved perception of movement, and decreased pain. However, the effects are neural, not structural. The mathematical modelling evidence (Chaudhry et al. 2008) shows that the forces required to structurally deform fascia are far beyond what human hands can produce. The improvements people experience are real, but they come from temporary neural modulation, not from releasing, breaking up, or realigning fascial tissue.
Is it safe for people with hypermobility to lift heavy weights?
The evidence from the Liaghat research series, which includes randomised controlled trials in hypermobile populations, suggests that appropriately progressed high-load exercise is not only safe but can produce superior short-term outcomes compared to low-load exercise for people with HSD. A 2025 paper from the same group found minor to no exercise-induced pain during high-load exercise in hypermobile participants, challenging the assumption that heavy loading inevitably causes flares. Appropriate progression and good technique matter, but the evidence doesn’t support indefinitely keeping loads very low.
What is stretch tolerance and why does it matter?
Stretch tolerance refers to the nervous system’s adaptation to the sensation of stretch, making a given range of motion feel more comfortable over time. Research including Panidi et al. (2023) and Bishop and George (2017) indicates that most of the ROM gains from stretching are explained by this neural adaptation rather than actual tissue lengthening. This matters because it means the “tight muscle” narrative is often incomplete, and interventions targeting tissue mechanically may be missing the more important neural component.
Wrapping Up
When it comes to stretching and hypermobility, the honest summary is this: stretching doesn’t work the way most people think it does, the “shortened muscle” narrative is largely a myth for most of the people reading this, the reasons those with hypermobility feel tight are neurological and mechanistic rather than structural, and much of what’s being sold under the fascia banner doesn’t hold up to scrutiny when you look at the actual biomechanics and imaging data.
None of which means gentle movement and body awareness work is without value. It isn’t. The nervous system adapts to movement, and any form of consistent, comfortable movement contributes positively to that process. But when it comes to what’s actually going to make the most difference to joint stability, pain levels, fatigue, and functional capacity in hypermobility and EDS, the evidence points clearly toward progressive resistance training done in a way that’s appropriate to where you’re starting from.
The exercises sold as “fascial training” aren’t bad exercises. The outcomes from manual therapy aren’t imagined. But the explanatory frameworks sold alongside them often don’t reflect what the science actually shows, and those frameworks can lead people toward choices that aren’t in their best interest. You deserve accurate information, because you’re making real decisions about real things: your health, your money, and your time.
If you want to explore what a properly structured approach to movement and rehabilitation looks like for hypermobility, the Fibro Guy Academy has programmes built specifically around the evidence base for this population. And if you want to understand more about the broader picture of living with hypermobility and EDS, the hEDS guide is a good starting point.
Take care of yourselves.
The Fibro Guy Team
References
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