Exercises are usually prescribed as part of treatments for tendinopathy. Resistance exercise can regain the strength after prolonged unused of the muscles due to pain. Stretching exercise can restore the flexibility of the muscle and enhance the movement. Whereas eccentric exercise is the most common modality used to treat tendinopathy clinically. Besides the strengthening effect, eccentric exercise was proposed that can enhance collagen fibre cross-linkage formation of the tendon and the realignment of collagen fibre is improved. (Woodley et al., 2007)

Regarding to the speed of movment, the eccentric exercise is proposed to perform in a slow speed in order to allow tissue healing and avoid any re-injury to the tendon tissue, and the speed can be increased according to patient’s response. Clinically, 15 repetitions for 3 sets and twice per day is suggested. (Dimitrios, 2015) For the optimal speed and dosage of eccentric exercise, they are proposed according to the clinical experience and patients’ response rather than the pathophysiological response of the tendon tissue, hence more well constructed studies in confirming the dosage maybe needed.


In a more recent systematic review, 13 articles were reviewed for the effectiveness of eccentric exercise to tendinopathy. Tendinopathy types including achilles tendinopathy, patella tendinopathy and lateral epicondyle tendinopathy. It suggested that there is no strong conclusion can be made that eccentric exercise is more effective than other interventions. (Woodley et al., 2007) The possible reason of the conclusion may due to low sample size and large confidence intervals. The long term effect of the exercise is also debatable as only 3 of the studies investigate the treatment effect after 1 year of time.

Most of the studies are emphasized on the effect on the tendon itself, the pain response and functional improvement of the patient. When we are doing exercise, is it only our muscles and skeletal structures are moving? Are there something far beyond the tendon happening in our body?


People often said that they can be relaxed during exercise because they can concentrate their mind and thinking nothing else. But is it true that our brain is doing nothing when we are exercising? No! Your brain is actually very busy!

In the cortical level, performing exercise with pain will cause cortical reorganization and intra-cortical inhibition. The pain reduction by exercise may due to cortical changes and supraspinal activation strategies. (Rio et al., 2015) Rostral ventromedial medulla (RVM) is an important site in the central nervous system mediating opioid receptors. Also, when we are doing exercise, central inhibitory pathways are triggered on and hence analgesia effect produced. (Vera-Portocarrero et al., 2006)

An interesting rat model study investigated exercise effect on pain. Acute pain was generated by injection of sulphated polysaccharide; Chronic pain of muscle was induced by injection of low pH saline; Whereas exercise-enhanced pain was induced by fatiguing exercise task. It showed that regular physical activity can significantly reduce the opportunity of hyperalgesia for the central mediated chronic pain. (Sluka et al., 2012)

RVM is labelled as structure No.5

It is proposed that there is phosphorylation of receptor at the protein kinase in the RVM which would further facilitate the pain sensation of muscle. (Tillu, Gebhart and Sluka, 2008) Yet opioid receptors would be activated under regular exercise and hence the inhibitory pathway for pain is also initiated. In addition, exercise can also affect the interaction of joint afferents and cutaneous nociceptive afferents. At the interneuron level often summarizing the afferent signals from different part of body, hyperalgesia is modulated under altered interaction of afferent signals. (Hosseinzadeh et al., 2013)

An important implication for this study is that, the change for pain modulation by exercise is tremendously plastic and reversible. Which means the pain can be modulated within a short period of time after exercise, yet the effect can also be diminished after withdrawal of exercise. (Nijs et al., 2015) Patients often work very hard after having the physiotherapy session, while after experience some of improvement in symptoms, they may gradually retrieve from regular exercise and hence the risk of recurrence of chronic pain may increase. Hence it is crucial to advice and explain to the patient with chronic pain that maintenance of active exercise can reduce the risk of develop recurrence of symptoms.



Prefontal cortex and anterior cingulate cortex are recorded to be overactive for the patients with chronic pain. Amygdala is often blamed as the centre of fear memory for pain movement. (Nijs et al., 2015) Besides the role of memorizing fear memory, negative emotions are also processed in the amygdala. Negative emotions such as anxiety may contribute to the process of central sensitization of chronic pain. It is confirmed by the study showing that the lesion in the amygdaloid complex can relieve the development of chronicity of pain in rat. (Li et al., 2013)


As we aimed to change the pain memory of the patient, several stage of exercise should be implemented. Precisely, cognition-targeted exercise therapy should be termed for this kind of exercise therapy.

Firstly, in the preparation stage of the exercise therapy, pain education is of the utmost important. The therapist should have profound knowledge in the pain neuroscience. And therapists should explain thoroughly to the patient about the pain. The education should be based on the patients’ perspective, rather than just stuffing knowledge into patients’ head. It is important to know about what patient is really afraid of and avoiding to do so. (Adams and Turk, 2015)


Secondly, exercise is important to be structured in time-contingent rather than symptom-contingent. (Nijs et al., 2015) In the classical method of prescribing exercise, dosage is usually based on the symptoms, which means we often advice patients do the exercise and may stop when experience of pain.

For cognition-targeted exercise, we aim at changing the perception of pain, which means targeting the time of exercise rather than the symptoms only. As mentioned, we should set goals with the patient in order to change the perception of what they are really afraid of. As the exercise goes on, therapists can further reveal some of the worry of the patient towards painful movement may be unreal and overly exaggerated. (Moseley, 2003) The movement should not be overprotected since the protective mechanism adopted by the patient may turn out to make them emphasize on the painful structure.


In the clinical situation, giving treatment such as electro-modalities and exercise to the symptomatic side of the patient sounds perfectly reasonable. But is it always true to all of musculoskeletal pain? Is it possible to giving exercise to the side that with no pain?


Cross-transfer effects are proposed that exercising the contralateral side of limb would alleviate hyperalgesia effect to the symptomatic limb. The possible mechanism behind is that, firstly, it may facilitate the spinal and cortical motor pathways of the opposite limb (Lee and Carroll, 2007); secondly, it enhances accessibility of the opposite limb to motor control area of the cortical structure; thirdly, the sensory afferents is altered when the axons of the muscle are activated. (Zhou, 2000) But the actual mechanism is still debatable and need for further investigation.

Study investigated the cross-transfer effect on pain sensitivity showing that the pain pressure threshold and withdrawal reflex were decreased after the repeated bout of eccentric exercise of either ipsilateral or contralateral side of symptomatic limb. It suggested that it is effective to reduce pain sensitivity by exercising even the opposite side of symptomatic limb. (Hosseinzadeh et al., 2015) One drawback of this experiment is that the patients were normal patient without chronic pain, hence it is difficult to generalize the result to the patients which chronicity of pain is already developed.


Patient maybe puzzled when you ask them to exercise their limb that without symptoms and response of treatments should be closely monitored. (Adams and Turk, 2015) Clear explanation of neural adaptation should be given to the patient in order to enhance the efficacy of the patient on the exercise task; otherwise anxiety may build up.

Besides considering exercise for bilateral limbs, different joints of the symptomatic limb should also be taken into consideration. Fernández-Carnero et al. (2009) investigated the pain sensitivity of different non-symptomatic area of the painful limb of patients with unilateral epicondylagia. It is found that there is a decrease of pain threshold for peripheral nerve trunks in the upper limb, and C5-C6 zygapophyseal joint. It suggested that the peripheral sensitization might contribute to the central sensitization problem of lateral epicondylgia. Possible mechanism may due to enhanced spatial summation and increased recruitment of central neurons.

When therapists are prescribing exercise to the patient, we should not just focus on the symptomatic joint or area only. Multiple joint condition and sensitization condition should be checked. Exercise to the cervical and the different joints of symptomatic side for the lateral epicondylgia case should be taken into account as a whole picture. It may be a potential study direction in the future.



  1. Pain can be modulated through inhibitory pathways and cortical reorganization.
  2. Cognition-targeted exercise therapy can be used to alter pain memory.
  3. Thorough pain education should given prior to exercise
  4. Time-contingency exercise rather than symptom-contingency exercise should be prescribed.
  5. Exercise bilateral limbs rather than symptomatic side only can be considered.



Adams, L. and Turk, D. (2015). Psychosocial Factors and Central Sensitivity Syndromes. CRR, 11(2), pp.96-108.

Dimitrios, S. (2015). Exercise for tendinopathy. World J Methodol, 5(2), pp.51-54.

Fernández-Carnero, J., Fernández-de-las-Peñas, C., de la Llave-Rincón, A., Ge, H. and Arendt-Nielsen, L. (2009). Widespread Mechanical Pain Hypersensitivity as Sign of Central Sensitization in Unilateral Epicondylalgia. The Clinical Journal of Pain, 25(7), pp.555-561.

Hosseinzadeh, M., Andersen, O., Arendt-Nielsen, L. and Madeleine, P. (2013). Pain sensitivity is normalized after a repeated bout of eccentric exercise. European Journal of Applied Physiology, 113(10), pp.2595-2602.

Hosseinzadeh, M., Samani, A., Andersen, O., Nosaka, K., Arendt-Nielsen, L. and Madeleine, P. (2015). Ipsilateral resistance exercise prevents exercise-induced central sensitization in the contralateral limb: a randomized controlled trial. European Journal of Applied Physiology, 115(11), pp.2253-2262.

Lee, M. and Carroll, T. (2007). Cross Education. Sports Medicine, 37(1), pp.1-14.

Li, Z., Wang, J., Chen, L., Zhang, M. and Wan, Y. (2013). Basolateral Amygdala Lesion Inhibits the Development of Pain Chronicity in Neuropathic Pain Rats. PLoS ONE, 8(8), p.e70921.

Moseley, G. (2003). Joining Forces – Combining Cognition-Targeted Motor Control Training with Group or Individual Pain Physiology Education: A Successful Treatment For Chronic Low Back Pain. Journal of Manual & Manipulative Therapy, 11(2), pp.88-94.

Nijs, J., Lluch Girbés, E., Lundberg, M., Malfliet, A. and Sterling, M. (2015). Exercise therapy for chronic musculoskeletal pain: Innovation by altering pain memories. Manual Therapy, 20(1), pp.216-220.

Sluka, K., O’Donnell, J., Danielson, J. and Rasmussen, L. (2012). Regular physical activity prevents development of chronic pain and activation of central neurons. Journal of Applied Physiology, 114(6), pp.725-733.

Tillu, D., Gebhart, G. and Sluka, K. (2008). Descending facilitatory pathways from the RVM initiate and maintain bilateral hyperalgesia after muscle insult. Pain, 136(3), pp.331-339.

Vera-Portocarrero, L., Zhang, E., Ossipov, M., Xie, J., King, T., Lai, J. and Porreca, F. (2006). Descending facilitation from the rostral ventromedial medulla maintains nerve injury-induced central sensitization. Neuroscience, 140(4), pp.1311-1320.

Woodley, B., Newsham-West, R., Baxter, G., Kjaer, M. and Koehle, M. (2007). Chronic tendinopathy: effectiveness of eccentric exercise * COMMENTARY 1 * COMMENTARY 2. British Journal of Sports Medicine, 41(4), pp.188-198.

Zhou, S. (2000). Chronic neural adaptations to unilateral exercise: mechanisms of cross education. Exerc Sport Sci Rev, 28(4), pp.177-84.




“Next patient please!” “Oh! Therapist! My elbow pain is still there and as intense as before! I really worry about whether I can back to cook and how to make ends meet..” Similar scenario I think every therapists would have encounter throughout his or her work; with patient telling you that the pain is still there or even worse after you already had given all of the applicable modalities and exercises. I still remember this patient very much, he is a middle-aged cook suffered from tennis elbow who is the sole breadwinner of his family. During the treatment session, more than three-quarter of time he was telling me that his financial worries rather than the pathology itself. By the time, I knew that something must be happening far beyond the inflamed or injured “tendon” and it is time to look beyond the biomedical model in management of pain in tendinopathy.


Tendinopathy is one of the common and challenging conditions, which the management approaches and timeframe are still debatable. (McCreesh and Lewis, 2013) In the classic biomedical model, tendinopathy involved three phases. Firstly non-inflammatory tissue reaction stage that the tissue exhibits tensile property with proliferation of tissues under strain. Secondly tendon disrepair stage, tendon exhibits tissue matrix disruption due to more intense strain. At last the irreversible stage of degenerative tendinopathy shows extensive damage of collagen that lead to pathology condition. Pain can be experienced throughout the stages because of the inflammation response of the tissue. Bio-chemical substance released, peritendinous structure inflammation and neural and vessels ingrowth are also be blamed for the irritable condition. (McCreesh and Lewis, 2013)

Besides anti-inflammatory physical agents such as ultrasound and electrophoresis, exercises are prescribed to different conditions of tendinopathy. Extensive research was conducted throughout the decades. Study showed improvement of patellar tendon stiffness and microcirculation with eccentric extension knee exercise. (Yin et al., 2014) Editor also agreed that eccentric exercise is effective for patient with Achilles tendinopathy, while the heavy loading protocol may not be applicable for the frail and non-athlete patients. (Silbernagel, 2014) Yet a more recent clinical review stated that there is not enough evidence to show isolated eccentric exercise is more beneficial than concentric exercise with the same load. (Couppé et al., 2015)

Most of the studies carried out are emphasizing on the strain, loading and duration of the exercise that are extensively based on the tendon physiological property. The reasoning behind is all about how well the neurovascular structure will be regrowth and how well the collagen fibre will be realigned.



For a usual clinical practice pathway for tendinopathy usually start with the diagnosis with ultrasound imaging. Followed by referral and medication, then possibly to the physiotherapy department for exercises and rehabilitation. (Morrissey, 2015) Surgical intervention maybe needed if conservative treatments are not applicable for the problem. Diagnosis sounds very important for the rehabilitation pathway since it comes at the beginning and also drives the patient to different kind of medical services. The question comes to me is that, is it always good to emphasize on the diagnosis to the patient?

Back to the case of my tennis elbow patient, he was worried for the tennis elbow symptoms and had been surfing around the internet about the information of tendinopathy, which turned out worrying a lot more because he can see the information about “tissue inflammation”, “disruption of tissue structure” etc.. Those wordings maybe scary to an originally healthy person, which drives him emphasize to the local tendinopathy problem and the pain symptom even more.

Ultrasound has been used for assessment of tendinopathy as a common practice and to exclude any tear. However it is not always true that the symptomatic patient would have altered morphology detected in the ultrasound imaging. Neovascularity has been suggested as a predictive factor for the pain level of tendinopathy. But in the later research suggested stated that insignificant correlation was found with symptoms, thickness of tendon or extent of neovascularity. (Clarke et al., 2010) Which means not all of the patients with symptomatic ultrasound imaging would experience pain. On the other hand, Ryan, Bisset and Newsham-West (2015) also stated that almost half of asymptomatic individuals (without pain) still can be detected with altered presentation of tendon structure.

During our classical training as a therapist, we had always been taught to explain the detailed condition to the patient. The word of “inflammation”, “damage” and “pain” maybe often used for the explanation. Some clinicians always proposed that self-fulfilling prophecy when giving the patient a label. (Broom and Woodward, 1996) Which means that a healthy patient may become symptomatic after they are given a label of certain diagnosis or condition. It may eventually become a stressor of psychosocial aspect for the patient and worsening the central sensitization problem.


Sometimes in the clinical practice situation, patient would get certain extent of improvement after having the exercise, but some of them may not exhibit same response or even not response at all. Are we missing something? Are something invisible happening inside the patient? Should we directly label the patient as a “difficult patient” if they keep saying that the pain is always there?



Central sensitization may be one of the explanations for the chronic pain in tendinopathy. For a normal person, pain sensation would be interpreted in brain when a nociception signal was fired from the tissue to central nervous system. Yet with central sensitization, patient would have a lower pain threshold, and even a very light touch would generate a nociception stimulus and hence a pain feeling. (Rio et al., 2013) With increased in pain sensitivity is called “hyperalgesia” and feeling pain with a non-nociception stimulus is named “allodynia”. Cause of the hypersensitivity of pain may due to the reorganization pathway within the central nervous system. Further studies are required to confirm the actual mechanism in the nervous system. Usually central sensitization is tested by quantitative sensory testing, such as measuring different mechanical and thermal tactile stimulation. Psychosocial factors such as fear and avoidance, beliefs of pain, social support, stigma etc. are often blamed as causes leading to central sensitization.

Plinsinga et al. (2015) conducted a systematic review of 16 articles with different tendinopathy conditions. With mechanical and pain threshold as the main outcome measurement, hypersensitivity and lowered pain threshold was reported across the different studies of tendinopathy including lateral epicondylitis. At the same time, central sensitization confirmed by mechanical and thermal measurement can be a prognostic factor of tendinopathy. While one restriction of this systematic review is that Achilles tendinopathy study is not included. Psychosocial factors such as stress and fear of symptoms are well addressed to be contributing factors to central sensitization and eventually chronic pain.

It further confirms that my patient with persisted lateral epicondyle pain may have some central components contributing to this chronic problem. Such inappropriate symptom appraisals, thinking that he will not be getting better again. Socio-economical context such as worrying of losing his job because of unsatisfactory job performance; as well as the subsequent financial worry since he is a breadwinner for his family. Furthermore, fear-avoidance of painful movement because of worrying that he will further deteriorate the pain problem. (Adams and Turk, 2015).question-mark-1020165_1280.jpg


Although central sensitization is getting more and more recognized by massive research regarding chronic pain problem, we still not yet have make a clear diagnosis method in the clinical settings. In the researches, quantitative sensory testing such as thermal and mechanical stimuli would be tested as a comparison of chronic pain and healthy subjects in order to find out whether they have hypersensitivity to nociception stimulus and lowered pain threshold. (Plinsinga et al., 2015) While absolute score for thermal and mechanical sensitivity different or standardized survey for diagnosis is not yet available. This would bring difficulties for diagnosis in the practical situation. Another problem is, if we notice some psychosocial stressors of the patient, to what extent should we as physiotherapist to be a mediator of the stressors and; to what extent should we refer the patient to the respective specialties such as clinical psychology or social workers? Obviously future researches are needed to investigate the multidisciplinary interaction towards the central components problem.


In the clinical situation in Hong Kong, we as physiotherapist cannot directly refer the patient to the clinical psychology and social workers. If we once identify the psychosocial stressors that are beyond our scope of practice, then we may refer back the patient to the doctor in-charge and that may probably lengthen the treatment course of the patient. Secondly, patients may expect to have physical modalities such as manual therapy, electro-modalities and acupuncture etc. when having a physiotherapy treatment session. Explanation on the central components to the patient should be taken carefully otherwise may make patient have deviation in what they are expecting to have in a physiotherapy treatment session. How we address the psychosocial factor to the patient and how we incorporate these factors into our conventional therapy would be of the utmost important in the treatment session. (Barron, Klaber Moffett and Potter, 2007)


Next blog will be about how we incorporate exercise therapy to our treatment dealing with chronic tendinopathy problem and the clinical implication of that. Please feel free to comment!



Adams, L. and Turk, D. (2015). Psychosocial Factors and Central Sensitivity Syndromes. CRR, 11(2), pp.96-108.

Barron, C., Klaber Moffett, J. and Potter, M. (2007). Patient expectations of physiotherapy: Definitions, concepts, and theories. Physiotherapy Theory and Practice, 23(1), pp.37-46.

Broom, D. and Woodward, R. (1996). Medicalisation reconsidered: toward a collaborative approach to care. Sociol Health & Illness, 18(3), pp.357-378.

Clarke, A., Ahmad, M., Curtis, M. and Connell, D. (2010). Lateral Elbow Tendinopathy: Correlation of Ultrasound Findings With Pain and Functional Disability. The American Journal of Sports Medicine, 38(6), pp.1209-1214.

Couppé, C., Svensson, R., Silbernagel, K., Langberg, H. and Magnusson, S. (2015). Eccentric or Concentric Exercises for the Treatment of Tendinopathies?. J Orthop Sports Phys Ther, 45(11), pp.853-863.

McCreesh, K. and Lewis, J. (2013). Continuum model of tendon pathology – where are we now?. International Journal of Experimental Pathology, 94(4), pp.242-247.

Morrissey, D. (2015). Guidelines and Pathways for Clinical Practice in Tendinopathy: Their Role and Development. J Orthop Sports Phys Ther, 45(11), pp.819-822.

Plinsinga, M., Brink, M., Vicenzino, B. and van Wilgen, C. (2015). Evidence of Nervous System Sensitization in Commonly Presenting and Persistent Painful Tendinopathies: A Systematic Review. J Orthop Sports Phys Ther, 45(11), pp.864-875.

Rio, E., Moseley, L., Purdam, C., Samiric, T., Kidgell, D., Pearce, A., Jaberzadeh, S. and Cook, J. (2013). The Pain of Tendinopathy: Physiological or Pathophysiological?. Sports Med, 44(1), pp.9-23.

Ryan, M., Bisset, L. and Newsham-West, R. (2015). Should We Care About Tendon Structure? The Disconnect Between Structure and Symptoms in Tendinopathy. J Orthop Sports Phys Ther, 45(11), pp.823-825.

Silbernagel, K. (2014). Does One Size Fit All When It Comes to Exercise Treatment for Achilles Tendinopathy?. J Orthop Sports Phys Ther, 44(2), pp.42-44.

Yin, N., Chen, W., Wu, Y., Shih, T., Rolf, C. and Wang, H. (2014). Increased Patellar Tendon Microcirculation and Reduction of Tendon Stiffness Following Knee Extension Eccentric Exercises. J Orthop Sports Phys Ther, 44(4), pp.304-312.

Hello there!



I am a physiotherapist from Hong Kong and currently studying MSc in University of Nottingham in The United Kingdom. My area of interest are musculoskeletal and sport rehabilitation. This is the very first web blog of me and I would like to share some of my thoughts towards the profession and at the same time, learn from others and to improve.

Please feel free to make any comment and this is valuable for me to improve! Hope this marks a good start of my blogging journey!

Raymond Wong