Muscles and Connective Tissue
See separate Information page for Muscle Cramps and Night Cramps
Hypermobile Ehlers-Danlos syndrome (hEDS) affects both muscles and connective tissue. Muscles are responsible for movement and stability, while connective tissues such as ligaments, tendons, fascia, and cartilage provide the framework and support that allow muscles to work effectively. These two systems are not separate; they function together as a unit. In hEDS, structural changes in connective tissue alter how muscles work, and muscle weakness and pain in turn place additional stress on connective tissue. This back-and-forth cycle contributes to instability, fatigue, chronic pain, and sometimes abnormal muscle activity such as hypertonicity (tightness) or twitching and spasms. Understanding the interaction between these tissues helps explain many of the challenges experienced by people living with hEDS.
Muscle Involvement in hEDS
Muscle symptoms are common, measurable, and often disabling in hEDS. They appear in childhood, continue into adulthood, and affect daily life at every age.
Why hEDS Affect Muscles
Muscles generate force by contracting, but they depend on surrounding connective tissues (tendons, fascia, extracellular matrix: connective tissues and fibers that are not part of a cell, but provide support) to transmit that force efficiently to bones and joints. In hEDS, the extracellular matrix is altered: collagen fibers are looser, more irregular, and less stiff. This means muscles have to contract more forcefully to achieve the same effect. Over time, this overwork leads to fatigue, pain, and injury. On top of this, nerve regulation of pain and movement is altered, so muscles not only work harder but also become more sensitive to pain signals.
This happens in two ways.
Movement regulation: Normally, nerves send precise signals to muscles, telling them how much to contract and when to relax. In hEDS, because joints are looser and proprioception (the ability to sense joint position and movement) is impaired, the nervous system has to “guess” more. Muscles often tighten too much, stay contracted longer, or fire at the wrong times to try to stabilize unstable joints. This makes them tire and ache quickly.
Pain regulation: Normally, nerves send pain signals only when tissue is stressed or injured. In hEDS, pain pathways become more sensitive — a process called central sensitization. The nervous system amplifies signals, so even mild stress or normal movement can feel painful.
Together, this means muscles in hEDS are both overworked and “louder” in their pain responses. In some cases, especially in children and adolescents with very mobile joints, muscles may tighten excessively in an effort to stabilize. This compensatory tightening tends to lessen with age as laxity decreases, while weakness and fatigue remain more consistent findings.
Weakness and Endurance Loss
Adults with hEDS have 30–49% lower strength in thigh muscles compared to peers, despite normal muscle mass.
Endurance tasks, such as rising from a chair or maintaining a contraction, are reduced by about one-third.
Children and adolescents show early weakness, fatigue, and decreased exercise tolerance, even before chronic pain is established.
Adults with hEDS have 30–49% lower thigh strength compared to peers, despite normal muscle mass, and endurance is reduced by about one-third. These measurable deficits reflect impaired muscle function rather than muscle atrophy.
At a microscopic level, muscle fibers show slower force production, delayed relaxation, and reduced peak torque because their attachment points in the extracellular matrix are overly compliant. This inefficiency has been described as like “pushing off a rubbery surface.”
Why this happens: Weakness is not from muscle shrinkage, but from impaired function. Studies show slower force production, delayed relaxation, and lower peak torque (rotational force) in hEDS. At a microscopic level, muscle fibers struggle to generate effective contraction because their attachment points (via the extracellular matrix) are too compliant (excessively stretchy or flexible). In simple terms, it is like trying to push off from a rubbery surface — energy is lost before it can create useful movement.
Twitching and Spasms
Some people with hEDS experience muscle twitching (fasciculations) or localized spasms, often in the thighs, forearms, or muscles around unstable joints.
These are not considered core diagnostic features of hEDS, but they occur in a subset of patients, particularly when muscles are fatigued or overstressed.
Mechanisms may include
Small fiber neuropathy (SFN): documented in over half of hEDS patients, may alter nerve signaling and contribute to abnormal muscle excitability.
Connective tissue and fascia changes: abnormal extracellular matrix and myofascial tension may predispose muscles to spasm in areas under repetitive strain. In simple terms, the body’s support tissues may be too loose in some places and too tight in others, which puts uneven strain on muscles and can lead to twitching or spasms.
Proprioceptive dysfunction and overuse: muscles that are working harder to stabilize joints may fire irregularly, leading to twitching or spasms.
These symptoms differ from hypertonicity (persistent tightness). Twitching/spasms are usually brief and localized, while hypertonicity reflects sustained contraction.
Although bothersome, twitching and spasms are typically benign (harmless) once other causes (such as electrolyte imbalance, medication effects, or neurological disease) are excluded.
Management: Physical therapy, pacing of activities, hydration, magnesium supplementation, and gentle manual therapies may help reduce frequency and discomfort. For most people, knowing that these symptoms are not dangerous and having ways to reduce discomfort is enough to manage them.
Pain
Muscle pain usually starts in childhood (around age 10) and becomes persistent by early adulthood.
By age 20, nearly all individuals with hEDS experience pain, often described as severe and disabling.
Pain is most often felt in muscles around joints in the lower body but can become widespread, including the spine, arms, and face.
Central sensitization — when the nervous system becomes overly sensitive to pain — contributes to the intensity and persistence of symptoms.
Why pain is so common: Continuous muscle overuse around unstable joints leads to micro-injury, spasm, and ischemia (reduced blood flow). This peripheral pain is amplified by central sensitization, where the spinal cord and brain become hyper-reactive to normal input. This explains why many patients describe pain that spreads beyond the injured area and lingers longer than expected. The analogy is a “volume knob” turned up too high — the nervous system broadcasts pain signals more loudly than the tissue damage alone would justify.
Injury and Healing
Lax ligaments and tendons make muscles more prone to strain. Subluxations and full dislocations add extra stress.
Injuries may occur from minimal trauma or even everyday activity.
Recovery is often delayed because of differences in the extracellular matrix, the structural scaffolding that supports cells and transmits force. In hEDS, the extracellular matrix is looser and less effective, slowing healing.
Recovery is often incomplete, with scar tissue that is weaker and less durable.
Recurrent sprains, prolonged soreness, and incomplete recovery are frequent in hEDS due to these extracellular matrix differences.
See the Recovery and Healing page for more detail.
Why healing is harder: Normal tissue repair depends on fibroblasts (cells that produce collagen) laying down strong, organized fibers. In hEDS, fibroblasts produce collagen that is thinner, more disorganized, and breaks down faster due to upregulated enzymes like matrix metalloproteinases. The result is weaker scar tissue and slower healing. Clinically, this shows up as recurrent sprains, prolonged soreness, and injuries that never fully heal.
Muscle Group–specific Issues
Face and jaw: temporomandibular joint (TMJ) dysfunction, headaches, chewing and speech difficulties
Respiratory muscles: breathlessness and reduced exercise tolerance due to altered lung mechanics, including dynamic hyperinflation and reduced chest wall recoil during exercise
Pelvic floor: urinary or fecal incontinence, pelvic organ prolapse, and pelvic pain, particularly common in women due to overstretched ligamentous supports
Why this happens: These areas are vulnerable because they combine constant use with fragile connective support. For example, TMJ dysfunction is linked to abnormal loading of jaw cartilage plus spasm in surrounding muscles. Respiratory changes arise from dynamic hyperinflation and limited chest wall recoil during exercise. Pelvic floor problems reflect overstretched ligaments and connective tissue support, making the muscles less effective as a “hammock” for pelvic organs.
Prevention in Muscle Health
Since hEDS cannot be cured, prevention focuses on reducing injuries, slowing symptom progression, and supporting independence.
Why prevention matters: In hEDS, muscles are always compensating for unstable joints. Without support, they become overworked and vulnerable to chronic injury. Preventive therapy gives muscles better efficiency and protection, reducing the cycle of pain and weakness.
Issues in Prevention
Regular monitoring: Annual assessments for strength, endurance, pain, and comorbidities help identify problems early.
Therapy: Physical and occupational therapy are the foundation of prevention. Tailored exercise improves strength, muscle tone, and proprioception (the body’s sense of joint position and movement). Braces and splints can support joints during activities, while adaptive equipment (wide-grip pens, supportive mattresses, ergonomic tools) helps reduce strain.
Patient education: Learning safe movement patterns, pacing activities, and making small environmental changes empowers patients to avoid flare-ups.
Sport and exercise choices: Avoiding high-impact sports and repetitive joint loading in favor of low-impact sports and controlled strengthening lowers injury risk.
Unsafe exercises and movements for hEDS
High-impact sports: running, basketball, gymnastics, or martial arts with repetitive jumping/landing.
Repetitive joint loading: heavy weightlifting, push-ups, or planks that repeatedly strain the same joint under load.
End-range stretching: yoga poses or splits that push joints to their maximum flexibility.
Contact sports: football, rugby, or wrestling with high risk of joint trauma.
Safer exercises and movements for hEDS
Controlled strengthening: resistance training with light to moderate weights, elastic bands, or bodyweight — done slowly, with attention to joint alignment and avoiding overextension.
Low-impact cardio: swimming, water aerobics, cycling, or elliptical training.
Closed-chain exercises: movements where hands or feet remain in contact with the ground or equipment (e.g., mini-squats, step-ups) that reduce shear on joints.
Balance and proprioception training: using wobble boards, stability balls, or guided exercises to improve joint awareness in safe ranges.
Pilates or gentle core work: focused on stability and posture, not extreme flexibility.
Body treatment choices: Avoiding deep, forceful or sudden movements when receiving chiropractic, massage or other body treatments lowers injury risk.
For detailed information on safe and unsafe exercise practices, see the Exercise page.
Unsafe manual therapies for hEDS
High-velocity chiropractic manipulations (“joint cracking” or thrust techniques).
Aggressive joint mobilizations that push joints past their natural range.
Deep or forceful massage that causes bruising or lingering pain.
Stretching therapies that encourage extreme flexibility.
Safer manual therapies for hEDS
Gentle massage aimed at relaxation and reducing spasm.
Myofascial release applied carefully without forcing joints.
Supportive joint taping or bracing combined with gentle handling.
Guided soft tissue work that relieves tension but avoids overstretching.
For detailed information on manual and body treatments, see the Alternative and Non-Western Treatments page.
Managing comorbidities: Fatigue, pain, anxiety, and depression add to muscle strain.
Multidisciplinary care, including psychological support and cognitive behavioral therapy, improves coping and reduces the risk of disability.
Connective Tissue Involvement in hEDS
Connective tissues — ligaments, tendons, cartilage, skin, fascia, bone, and blood vessels — are at the heart of hEDS. Their fragility explains many of the core features of the condition.
Why hEDS Affects Connective Tissue
Collagen, the main protein in connective tissue, normally acts like strong ropes that provide both stiffness and elasticity. In hEDS, collagen fibers are less uniform and more fragile. This makes tissues stretchier but less able to withstand load. The result is joints that slip, skin that bruises, and fascia that does not glide normally. At the microscopic level, electron microscopy shows collagen fibrils that are irregular in size and arrangement, leading to weaker tissue mechanics.
Joints, Tendons, and Ligaments
Over 95% of people with hEDS show generalized hypermobility.
Looser tendons and ligaments make joints unstable.
Subluxations and dislocations may happen from minor movements, causing acute pain and repeated injury.
Why this happens: Ligaments and tendons contain type I collagen bundles that normally resist stretch. In hEDS, these bundles are thinner and more disorganized, so they fail to stabilize joints. This explains why someone with hEDS might dislocate a shoulder while reaching overhead or sprain an ankle while walking on flat ground.
Cartilage and Bone
Cartilage wears down over time from unstable joints, leading to early-onset osteoarthritis.
Bone density is often reduced, raising the risk of osteoporosis with age, although fractures are not a defining feature.
Why this happens: Unstable joints increase shear stress on cartilage, which accelerates wear. Bone density changes may be linked to altered signaling between connective tissue and bone-forming cells (osteoblasts), as well as reduced weight-bearing activity due to pain and fatigue.
Skin and Fascia
Skin may be soft, mildly stretchy, and prone to bruising. Scars may become wide or thin.
Fascia, the sheet-like tissue surrounding muscles and organs, shows abnormal stiffness and reduced gliding in hEDS, contributing to pain and mobility difficulties.
Why this happens: In hEDS, dermal collagen is less dense and more fragile, explaining easy bruising and atrophic scarring. Fascia, which normally acts as a smooth sliding surface for muscles, thickens and remodels abnormally. This interferes with movement and contributes to chronic pain.
Vascular and Other Tissues
While major blood vessel fragility is not typical of hEDS, mild features such as easy bruising, mitral valve prolapse, or mild aortic enlargement are more common than in the general population.
Other connective tissues may also be affected, leading to crowded teeth, dry eyes, pelvic floor dysfunction, or hernias.
Why this happens: Connective tissue defects in valves and vessel walls reduce their stiffness, which may allow valve floppiness (prolapse) or mild dilation of the aortic root. Dental crowding is linked to altered craniofacial connective tissue growth, while pelvic floor dysfunction reflects overstretched ligamentous supports.
Prevention in Connective Tissue Health
Because connective tissue is more fragile in hEDS, prevention focuses on protecting joints, skin, bone, and vascular tissue from cumulative stress and long-term damage.
Why Prevention Matters: Connective tissue in hEDS is weaker and more elastic than normal, which makes joints unstable, skin prone to injury, and supporting structures more vulnerable to wear. Since these tissues cannot be fully repaired once damaged, careful protection helps preserve stability and reduce complications across the lifespan.
Issues in Connective Tissue Health
Regular monitoring: Routine checkups may include joint stability assessments, skin and wound checks, bone density scans, and cardiac evaluations (for mitral valve prolapse or aortic dilation). Detecting problems early allows timely interventions.
Therapy and supports: Physical and occupational therapy focus on stabilization rather than flexibility. Braces, orthotics, and compression garments can support fragile connective tissues and reduce strain on joints. Ergonomic aids — such as supportive seating, customized orthotics, and abdominal binders — help prevent injury during daily activities.
Patient education: Learning about joint protection, safe skin care, and activity modification empowers patients to avoid unnecessary tissue stress. Education also helps families, schools, and workplaces provide safer environments for children and adults with hEDS.
Lifestyle choices: Avoiding activities that overstretch joints or strain tissues reduces long-term damage. Gentle, supportive movements and careful handling of skin and joints are emphasized instead of forceful or extreme practices.
Unsafe practices for connective tissue in hEDS
Extreme flexibility activities: gymnastics, cheerleading, or advanced yoga that push joints to their maximum range.
Heavy lifting without support: carrying weights that strain ligaments, fascia, or abdominal walls, raising the risk of hernias.
High-contact or collision sports: football, rugby, or martial arts that increase trauma risk to joints and soft tissues.
Prolonged pressure on skin: tight bandages, strong adhesives, or equipment straps that bruise or tear fragile skin.
Repeated straining: chronic coughing, heavy lifting, or constipation-related straining that worsens hernia or prolapse risk.
Safer practices for connective tissue in hEDS
Stabilizing activities: Pilates, gentle core strengthening, and low-resistance exercise that improve control without overstretching.
Low-impact movement: swimming, cycling, or water aerobics that support joints while promoting strength and cardiovascular fitness.
Protective skin care: using gentle adhesives, cushioned padding, and attentive wound care to prevent bruising and scarring.
Joint and posture supports: braces, orthotics, compression garments, and ergonomic seating to reduce stress on fragile tissues.
Pelvic floor therapy: guided exercises that strengthen supportive structures and reduce the risk of prolapse or incontinence.
Unsafe manual therapies for connective tissue in hEDS
Forceful spinal or joint manipulations (high-velocity chiropractic thrusts).
Aggressive fascial scraping or cupping that damages fragile skin and fascia.
Deep-tissue massage that bruises or overstretches soft tissue.
Joint stretching techniques that push beyond safe ranges.
Safer manual therapies for connective tissue in hEDS
Gentle massage to reduce tension without bruising.
Careful myofascial release applied in a controlled, pain-free manner.
Supportive taping and bracing to stabilize joints and reduce stress on tissues.
Gentle mobilization that respects safe ranges of motion and avoids overstretching.
Managing comorbidities: Conditions such as osteoporosis, hernias, pelvic organ prolapse, and vascular changes can worsen connective tissue fragility. Regular bone scans, pelvic floor therapy, cardiovascular surveillance, and coordinated multidisciplinary care help prevent complications.
Shared Mechanisms
The changes in muscle and connective tissue are closely related. The extracellular matrix in hEDS is more compliant, meaning it stretches more easily. While this flexibility may seem like an advantage, it weakens the transmission of force between muscle and bone. Muscles then must contract harder to stabilize joints, causing fatigue and pain. Weakness in hEDS reflects impaired function rather than loss of muscle mass, highlighting that deficits arise from inefficiency in force transmission rather than atrophy. Muscle fibers adapt by stiffening proteins like titin, which partly compensates but increases discomfort and risk of injury. Fascia may also thicken and glide less effectively, altering proprioception and encouraging protective co-contraction. Central sensitization can lower the threshold for muscle guarding, adding to the sense of tightness even when true hypertonicity is not present. Chronic inflammation, nerve changes, and central sensitization magnify both muscle and connective tissue symptoms.
Why this happens: This cycle reflects altered mechanotransduction, the process by which cells sense and respond to mechanical forces. In hEDS, abnormal extracellular matrix proteins disrupt these signals, leading to maladaptive remodeling in both muscle and connective tissue. This disruption of mechanotransduction helps explain why deficits in strength and endurance occur in hEDS even without muscle atrophy, underscoring that weakness is primarily functional and connective-tissue–driven.
Comorbidities That Worsen Symptoms
Comorbid conditions increase the burden on muscle and connective tissue.
Chronic fatigue and sleep disorders
Fibromyalgia and central sensitization
Postural orthostatic tachycardia syndrome (POTS)
Gastrointestinal issues and malabsorption
Anxiety and depression
Neuropathy, including small fiber neuropathy
Why this matters: Comorbidities amplify the effects of hEDS through overlapping biological mechanisms. For example, dysautonomia reduces blood flow to muscles, worsening fatigue. Fibromyalgia intensifies central sensitization. Nutrient malabsorption limits tissue repair. These overlapping processes explain why many patients experience multisystem symptoms beyond joints alone.
Management Approaches
There is no cure for hEDS, but supportive management reduces symptoms and complications.
Physical and occupational therapy are first-line treatments.
Braces, splints, and ergonomic aids help reduce joint strain.
Medications may relieve pain or neuropathic symptoms but are usually adjunctive (supplementary to other treatments such as physical and occupational therapy, braces and splints).
Complementary approaches such as TENS, dry needling, or cognitive behavioral therapy can provide additional benefit.
Surgery is a last resort due to higher complication rates in hEDS.
Strategies shift by age: children need motor skill support, adults focus on preventing disability, and older adults prioritize fall prevention and bone health.
In patients who show excessive muscle tightening, strategies such as safe stretching, aquatic therapy, magnesium supplementation, or gentle manual therapy may help reduce discomfort. Muscle relaxant medications are rarely used, as they may worsen instability or cause sedation. Management also involves evaluating comorbidities such as dystonia, neuropathy, or tethered cord if abnormal tone is suspected.
Why management works: Although abnormal collagen cannot be corrected, muscles and connective tissues are adaptable. With the right combination of strengthening, support, and protection, patients can offset much of the instability and reduce pain.
Summary
Muscles and connective tissue in hEDS are inseparable parts of one system. Fragile connective tissue makes joints unstable, while muscles must work harder to compensate, leading to fatigue, pain, and weakness. This weakness reflects impaired muscle function rather than atrophy. In some individuals, muscles may also show abnormal activity such as compensatory tightening (hypertonicity) or twitching and spasms, particularly in the context of fatigue, neurological comorbidities, or joint instability. However, weakness and instability remain the dominant features across the lifespan.
Prevention and treatment work best together. Preventive measures such as protecting joints, strengthening muscles, pacing activities, managing comorbidities, and educating patients reduce the risk of long-term disability. Treatments such as individualized physical and occupational therapy, supportive devices (braces, splints, ergonomic aids), pain management strategies, and complementary approaches (like TENS or cognitive behavioral therapy) help patients manage symptoms and improve daily function.
With early recognition, proactive prevention, and supportive treatment, many complications of hEDS can be minimized. This integrated approach allows people with hEDS to preserve independence and maintain a better quality of life.
