Why Am I Stiff If I'm Hypermobile? What's Actually Happening in Your Tissue
An exploration of what’s happening when we are both bendy and stuck.
Steven Murdoch
Hypermobility with stiffness — being both bendy and stuck
Not everyone who is hypermobile knows that they are hypermobile. But most know they are double jointed, flexible, bendy or a bit more stretchy than the average person. That basically sums up hypermobility — that one or more joints in the body has more range of motion than average.
Hypermobility without pain, tension or other symptoms (asymptomatic hypermobility) isn’t usually a problem — it may even be handy for dance, gymnastics, party tricks, or yoga.
But sometimes it does become problematic — joints can feel unstable, whilst other places can feel stuck and painful (symptomatic hypermobility). This combination of being both bendy and stuck is one of the most common and confusing things about living with symptomatic hypermobility.
It is rare for people to get a diagnosis such as Hypermobile Spectrum Disorder (HSD), or hypermobile Ehlers-Danlos Syndrome (hEDS). Both are difficult to diagnose and people often fall through the cracks — not being believed, being misdiagnosed and usually having to discover for themselves what may be going on.
This article is to help make sense of what is going on — both in the tissue, and in the brain when we are both bendy and stuck. We’ll look at what creates this combination of hypermobility with stiffness.
Research into hypermobility and the tissue is still in its early stages — but it’s moving quickly, and what’s emerging is genuinely fascinating. I’m going to reference the studies as we go, so you can see that there’s a logic to what we’re exploring. Many are small studies, but they throw up some remarkable findings.
Understanding the tissue — fascia
To understand that sensation of being both stretchy and stuck, it helps to first understand the tissue involved — fascia.
Fascia is connective tissue. It exists throughout your entire body — wrapping muscles, surrounding joints, connecting structures to each other. Fascia is a continuous web holding everything in place. It allows everything to move in relation to everything else.
Fascia is made up of layers. Each layer contains collagen fibres (which provide strength and structure), elastin fibres (which allow stretch and recoil), and a water-rich ground substance that sits between and around the fibres (Wiktor Świątek et al., 2023).
For the body to move freely and comfortably, these layers need to slide over each other. What enables that sliding is a substance called hyaluronic acid — a slippery lubricant that sits between the fascial layers.
When hyaluronic acid is healthy and evenly distributed, the layers glide smoothly. That glide is what gives you the sensation of easy, unrestricted movement.
Fascia is constantly being maintained by cells called fibroblasts. These cells produce the collagen, maintain the ground substance, and respond to what’s happening mechanically in the tissue.
When fascia is loaded or under tension, fibroblasts adjust their activity — more tension tends to lead to more collagen production (Wiktor Świątek et al., 2023). Less movement can also lead to changes in the tissue composition.
Importantly — fascia is directly connected to the nervous system. It contains a huge number of sensory nerve endings — far more than muscle tissue.
This is how the brain knows where the body is in space (proprioception) — and how it detects potential threats.
Fascia researcher Robert Schleip has described fascia as the body’s richest sensory organ for proprioception, containing six to ten times more receptors than muscle (Schleip et al., 2021, pp.156–159). These include receptors that detect pressure, stretch, tension, and position (Stecco et al., 2010).
What's different about fascia in hypermobility?
This is where the research gets really interesting.
In 2016, researcher Nicola Chiarelli and his team in Italy made a significant discovery. They found that in people with hEDS, the fibroblasts — the cells that maintain the connective tissue — were behaving differently. They were shifting into a more active state, becoming what are called myofibroblasts (Chiarelli et al., 2016).
Myofibroblasts are normally involved in wound healing — they lay down new tissue to repair damage, and then they switch off. But in hEDS, they appear to stay switched on. They continue to produce excess collagen and extracellular material — essentially building too much tissue, and tissue that is disorganised.
What’s really interesting here is that in hEDS (unlike some other forms of EDS) the changes do not appear to be down to a genetic mutation (Malfait et al., 2017). There is something else creating the change. This has led researchers to look towards the broader connective tissue environment — and that’s where fascia research is starting to provide answers.
It’s also worth noting that much of the research I am referencing in this article generally includes people with both hEDS and HSD — and the fascial changes appear in both. The current clinical distinction between the two is based on a diagnostic checklist, not on any known biological difference. A major update to the diagnostic criteria is due to be published in December 2026, which may well change how these conditions are classified (The Ehlers-Danlos Society, 2026).
In 2021, Dr Tina Wang used diagnostic ultrasound to show what Chiarelli’s cellular findings actually look like in living tissue. She found that the deep fascia in people with hEDS and HSD was measurably thicker than in people without these conditions — the first time these structural changes had been documented in living patients (Wang & Stecco, 2021).
But it wasn’t just thicker. It was also stickier.
Why the fascia stops gliding
The hyaluronic acid between the fascial layers — the lubricant that allows the layers to slide — appears to become clumped and more viscous (less fluid) in people with hEDS and HSD. Wang’s 2021 paper noted that this increased viscosity leads to reduced lubrication and reduced sliding movement of the fascia.
Earlier research by Antonio Stecco had shown that when hyaluronic acid behaves normally, the fascial layers glide smoothly. But when it clumps — becoming thick and sticky — the layers start to stick together instead of sliding, and restrictions follow (Stecco et al., 2011).
In 2023, Wang then tested this in people with hEDS and HSD. Using advanced ultrasound, she was able to show that the fascial layers weren’t sliding properly over each other (Wang et al., 2023).
In 2025, Tina Wang joined forces with Antonio Stecco, Alan Hakim and Robert Schleip to make sense of it all. They published a comprehensive review bringing all the threads together: the thickening of the fascia; the reduced gliding; and the presence and activity of the myofibroblasts (Wang et al., 2025). The authors described it as a self-reinforcing cycle — the overactive cells laying down excess tissue — thus disrupting the lubrication — which then impairs the gliding — which creates restrictions and pain.
It’s worth noting — as Wang herself emphasises — that whilst these findings show what is happening, we don’t yet know why. The changes are present in people with hEDS and HSD — but what sets the whole process in motion? The research is moving quickly, but we’re still in the early stages of understanding the full picture. Wang’s 2026 book Fascia and Hypermobility Disorders brings together much of what is currently known.
In summary - why you are both bendy and stuck
I know we have gone into a bit of detail, but I do think getting up to date with the science helps with making sense with what to do in terms of treatment and self-care. Before I share some thoughts on that — here’s what we’ve said in a nutshell:
Your connective tissue is more stretchy than average. But the cells that maintain your fascia appear to be overactive, laying down excess collagen, disrupting the lubrication between the fascial layers, and reducing the glide. That’s why you experience being both stretchy and stuck.
What this also means is that the joints have too much movement, whilst the fascia between and around them doesn’t move enough. And your nervous system — which relies on fascia for much of its sensory feedback — is responding to all of this by tightening muscles up to try and create the stability it can’t find elsewhere.
What does this mean for treatment and self-care?
So what can you do to interrupt the cycle? How do you restore the glide without triggering the nervous system to tighten everything back up again?
I’m going to sow a few seeds here. I cover these topics in more detail in other articles and on my site dedicated to jaw pain, tmjpaincare.com.
Is massage helpful?
It can be — but the approach matters. The brain needs to sense that the massage is not a threat. If it’s too painful, you are likely to experience more tension soon after. If it feels safe, the body is more likely to let go. Myofascial release incorporates this way of thinking. It forms the core of my in-person treatments for hypermobility and it’s something you can explore yourself at home.
Is stretching a good idea?
Stretching may be easy for you, and it may give some immediate relief — but it may also be sending the wrong signals to the brain. If the nervous system is already sensing instability, stretching can amplify that. The likely response? More tension elsewhere.
Instead of stretching the tissue, think about how you could bring the tissue in on itself — a bit like taking a stretched elastic band and letting it come back together. This reassures the brain, and the tissue is more likely to let go. I explore that concept and demonstrate it in a video in this article on releasing neck tension.
Should I be doing strength training?
People with HSD, hEDS and symptomatic hypermobility are often told to strengthen. And if done appropriately, it can significantly improve symptoms. But the wrong kind of strengthening has a real risk of overloading the joints — resulting in flare-ups, dislocation and injury.
Think about what’s happening close to the joint (laxity) and away from the joint (tension). The type of strengthening matters enormously. I’d recommend working with an hEDS-informed trainer — you may find one through the EDS Society directory. An hEDS-informed trainer is likely to incorporate isometric exercises — where the muscle works hard without the joint moving through its range. For a nervous system that’s seeking stability, this can make a real difference. They will help ensure your body feels safe throughout — sending signals of stability rather than instability.
Frequently asked questions
These are questions I’m often asked about hypermobility and tension. If something isn’t covered here, please feel free to get in touch.
In hypermobility, the fascia — the connective tissue that wraps and connects everything in the body — can become thickened and lose its ability to glide. The joints themselves remain mobile, but the tissue between and around them gets stuck. Your nervous system responds by tightening muscles to create the stability it can’t find elsewhere. That’s the stiffness you feel.
Yes. This is one of the most common experiences in symptomatic hypermobility. The joints move too much because the connective tissue is stretchier than average. But the fascia between and around them can become stuck and restricted. The result is a body that feels both bendy and braced at the same time.
Not everyone with hypermobility experiences pain — many people are hypermobile without any issues at all. But when pain does occur, it often relates to the fascia becoming thickened and restricted, changing the quality of information reaching the brain. The nervous system struggles to sense where the joints are, so the body compensates by tightening muscles to create stability. Those muscles work overtime, causing fatigue and pain.
Fascia is connective tissue that exists throughout your entire body — wrapping muscles, surrounding joints, connecting structures to each other. In people with hypermobility, hEDS, and HSD, research has shown that the fascia can become thickened and lose its ability to glide smoothly, contributing to pain, stiffness, and restricted movement. information reaching the brain. The brain can’t properly sense where the joints are, so it increases muscle tension to protect them. Those muscles work overtime, fatigue, and ache.
Massage can be helpful — but the approach matters. If the massage feels safe to the nervous system, the body is more likely to let go of tension. If it’s too forceful, the brain may interpret it as a threat and tighten things up further. Gentle approaches like myofascial release tend to work better for hypermobile bodies.
Stretching may give immediate relief, but it can also send signals of instability to an already protective nervous system. Instead of stretching tissue that’s already lax around the joints, it may be more helpful to bring the tissue in on itself — reassuring the brain rather than challenging it.
Strength training can significantly improve symptoms — but the type and how it is done matters enormously. The wrong kind of strengthening can overload joints and lead to flare-ups, dislocation, or injury. Working with an hEDS-informed trainer who incorporates isometric exercises — where the muscle works without the joint moving through its range — is a good place to start.
References
Chiarelli, N., Carini, G., Zoppi, N., Dordoni, C., Ritelli, M., Venturini, M., Castori, M. and Colombi, M. (2016). Transcriptome-Wide Expression Profiling in Skin Fibroblasts of Patients with Joint Hypermobility Syndrome/Ehlers-Danlos Syndrome Hypermobility Type. PLOS ONE, [online] 11(8), p.e0161347. doi:https://doi.org/10.1371/journal.pone.0161347.
Malfait, F., Francomano, C., Byers, P., Belmont, J., Berglund, B., Black, J., Bloom, L., Bowen, J.M., Brady, A.F., Burrows, N.P., Castori, M., Cohen, H., Colombi, M., Demirdas, S., De Backer, J., De Paepe, A., Fournel-Gigleux, S., Frank, M., Ghali, N. and Giunta, C. (2017). The 2017 International Classification of the Ehlers-Danlos Syndromes. American Journal of Medical Genetics Part C: Seminars in Medical Genetics, [online] 175(1), pp.8–26. doi:https://doi.org/10.1002/ajmg.c.31552.
Schleip, R., Stecco, C., Driscoll, M. and Huijing, P.A. (2021). Fascia : the tensional network of the human body : the science and clinical applications in manual and movement therapy. Amsterdam: Elsevier, pp.156–159.https://www.amazon.co.uk/Fascia-Tensional-Clinical-Applications-Movement/dp/0702071838
Stecco, C., Macchi, V., Porzionato, A., Morra, A., Parenti, A., Stecco, A., Delmas, V. and De Caro, R. (2010). The Ankle Retinacula: Morphological Evidence of the Proprioceptive Role of the Fascial System. Cells Tissues Organs, 192(3), pp.200–210. doi:https://doi.org/10.1159/000290225.
Stecco, C., Stern, R., Porzionato, A., Macchi, V., Masiero, S., Stecco, A. and De Caro, R. (2011). Hyaluronan within fascia in the etiology of myofascial pain. Surgical and Radiologic Anatomy, 33(10), pp.891–896. doi:https://doi.org/10.1007/s00276-011-0876-9.
The Ehlers-Danlos Society (2026). A Major Update Is Coming to EDS and HSD Diagnosis – The Ehlers Danlos Society. [online] The Ehlers Danlos Society. Available at: https://www.ehlers-danlos.com/new-global-diagnostic-criteria-2026/.
Wang, T. (2026). Fascia and Hypermobility Disorders. [online] Singing Dragon – US. Available at: https://us.singingdragon.com/products/fascia-and-hypermobility-disorders [Accessed 3 Apr. 2026].
Wang, T.J. and Stecco, A. (2021). Fascial thickness and stiffness in hypermobile Ehlers‐Danlos syndrome. American Journal of Medical Genetics Part C: Seminars in Medical Genetics, 187(4), pp.446–452. doi:https://doi.org/10.1002/ajmg.c.31948.
Wang, T.J., Stecco, A., Hakim, A.J. and Schleip, R. (2025). Fascial Pathophysiology in Hypermobility Spectrum Disorders and Hypermobile Ehlers–Danlos Syndrome: A Review of Emerging Evidence. International Journal of Molecular Sciences, [online] 26(12), pp.5587–5587. doi:https://doi.org/10.3390/ijms26125587.
Wang, T.J., Stecco, A., Schleip, R., Stecco, C. and Pirri, C. (2023). Change in gliding properties of the iliotibial tract in hypermobile Ehlers–Danlos Syndrome. Journal of Ultrasound, 26, pp.809–813. doi:https://doi.org/10.1007/s40477-023-00775-7.
Wiktor Świątek, Olgierd Kłodziński, Brzęczek, J., Ignacy Kosiorowski, Grzybowska, N., Paul Edward Mozdziak and Wiesława Kranc (2023). Components of the fascia – cells and extracellular matrix. Medical Journal of Cell Biology, 11(1), pp.13–19. doi:https://doi.org/10.2478/acb-2023-0002.