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Hormones & Tendinopathy

  • Writer: Luke Nelson
    Luke Nelson
  • 3 days ago
  • 4 min read

Why tendon pain isn’t just about load


When we talk about tendinopathy, the conversation almost always revolves around:

  • Training load

  • Biomechanics

  • Programming errors

And rightly so, these are critical.


But there’s a piece of the puzzle that often gets overlooked: The endocrine system.


Because tendons don’t just respond to load.

They respond to the environment in which they exist.



Tendons are NOT just passive structures


It’s easy to think of tendons as ropes connecting muscle to bone.

They’re not.


Tendons are living, metabolically active tissue, made up of cells (tenocytes) that are constantly:

  • Building collagen

  • Breaking down collagen

  • Adapting to mechanical stress


And importantly, these cells contain receptors for multiple hormones, including:

  • Estrogen

  • Thyroid hormones

  • Cortisol

  • Growth hormone

  • Testosterone


So when the hormonal environment changes, tendon behaviour changes too.


Estrogen and tendon adaptation


Estrogen is one of the most studied hormones in tendon physiology.


Research suggests that estrogen can:

  • Reduce collagen synthesis following exercise

  • Influence tendon stiffness

  • Alter mechanical properties of the tendon


What does this mean clinically?


It may help explain:

  • Differences in tendon injury patterns between males and females

  • Why some female athletes respond differently to load

  • Why certain life stages matter more than we realise


Menopause: a key transition point

One of the most clinically relevant hormonal shifts is menopause.


With declining estrogen levels, we see:

  • Reduced tendon collagen synthesis

  • Changes in tendon mechanical properties


In practice, this may present as:

  • Increased tendon stiffness or irritability

  • Slower adaptation to load

  • More persistent symptoms


For masters runners, this is a critical but often under-recognised factor.



Hormonal contraceptives

Hormonal contraceptives also influence the endocrine environment.


Some studies suggest they may:

  • Suppress tendon collagen synthesis

  • Alter connective tissue turnover


This doesn’t mean they’re harmful, but it does mean: They may influence how tendons respond to load and training.



Thyroid hormones and tendon health

Thyroid hormones play a key role in cell metabolism and tissue repair.


Tenocytes have thyroid hormone receptors, and these hormones can:

  • Stimulate cell growth

  • Reduce cell death

  • Influence tendon matrix turnover


Clinically, thyroid dysfunction has been linked to tendon disorders.


So if you’re seeing:

  • Persistent tendinopathy

  • Atypical presentation

  • Poor response to rehab


…it may be worth considering thyroid screening as part of a broader work-up.


Cortisol and corticosteroids

Glucocorticoids (like cortisol and corticosteroid medications) have well-documented effects on tendon.


They can:

  • Reduce collagen synthesis

  • Alter tendon structure

  • Reduce mechanical strength


This helps explain why:

  • Repeated corticosteroid injections increase rupture risk

  • Tendons can feel “better” short-term but worse long-term


There’s a place for these interventions, but timing and context matter.



Growth hormone and tendon adaptation

Tendon adaptation isn’t just mechanical, it’s biological.


The growth hormone axis plays a role in:

  • Collagen synthesis

  • Tissue turnover

  • Adaptation to load


If this signalling is impaired, tendon adaptation may be limited, regardless of how well you program load.



Testosterone and tendon risk

Testosterone is often associated with strength and performance.


But some studies have shown that testosterone therapy is associated with:

  • Increased tendon injury risk

  • Higher rates of rupture


One likely explanation: Muscle adapts faster than tendon.


So if strength increases rapidly, the tendon may not yet have the capacity to tolerate the load being placed on it.



So what does this mean clinically?

It doesn’t mean we abandon load management.

It means we broaden our lens.


When tendinopathy is:

  • Persistent

  • Recurrent

  • Disproportionate to load

  • Not responding as expected


…it may be worth considering systemic contributors, including:

  • Menopause

  • Thyroid dysfunction

  • Hormonal therapy

  • Corticosteroid exposure

  • General metabolic health


Because tendons sit at the intersection of: Load + Capacity + Biology


The take-home message

Tendinopathy is not purely mechanical.


It’s a condition influenced by:

  • Mechanical load

  • Tissue capacity

  • Systemic health

  • Hormonal regulation


If we only focus on load, we risk missing part of the picture.


And in some cases, that’s the part that explains why the tendon isn’t improving.



References

  • Abate, M., Salini, V. and Andia, I. (2017) ‘Therapeutic use of hormones in tendinopathies: a narrative review’, Muscles, Ligaments and Tendons Journal, 6(3), pp. 445–452.

  • Albright, J.A., Nwachukwu, B.U., Kunze, K.N. and colleagues (2023) ‘Testosterone replacement therapy is associated with increased odds of Achilles tendon injury and surgery: a matched retrospective analysis’, Journal of Foot and Ankle Research, 16, p. 30.

  • Dean, B.J.F., Gettings, P., Dakin, S.G. and Carr, A.J. (2014) ‘The risks and benefits of glucocorticoid treatment for tendinopathy: a systematic review of the effects of local glucocorticoid on tendon’, Seminars in Arthritis and Rheumatism, 43(4), pp. 570–576.

  • Doessing, S., Heinemeier, K.M., Holm, L., Mackey, A.L., Schjerling, P., Rennie, M. and Kjaer, M. (2010) ‘Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myofibrillar protein synthesis’, The Journal of Physiology, 588(2), pp. 341–351.

  • Hansen, M., Kjaer, M., Magnusson, S.P. and colleagues (2008) ‘Ethinyl oestradiol administration suppresses collagen synthesis in tendon in response to exercise’, The Journal of Physiology, 586(12), pp. 3005–3016.

  • Hansen, M., Kongsgaard, M., Holm, L., Skovgaard, D., Magnusson, S.P. and Kjaer, M. (2009) ‘Effect of estrogen on tendon collagen synthesis, tendon structural characteristics, and biomechanical properties in postmenopausal women’, Journal of Applied Physiology, 106(4), pp. 1385–1393.

  • Hansen, M., Couppe, C., Hansen, C.S., Skovgaard, D., Kovanen, V., Larsen, J.O., Aagaard, P., Magnusson, S.P. and Kjaer, M. (2013) ‘Impact of oral contraceptive use and menstrual cycle phase on patellar tendon morphology, biochemical composition, and biomechanical properties in female athletes’, Journal of Applied Physiology, 114(8), pp. 998–1008.

  • Oliva, F., Berardi, A.C., Misiti, S., Verga Falzacappa, C., Iacone, A. and Maffulli, N. (2013) ‘Thyroid hormones enhance growth and counteract apoptosis in human tenocytes isolated from rotator cuff tendons’, Cell Death & Disease, 4(8), e705.

  • Oliva, F., Giai Via, A., Maffulli, N. (2016) ‘Hormones and tendinopathies: the current evidence’, British Medical Bulletin, 117(1), pp. 39–58.

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