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?
YOUR BRAIN IS ACTUALLY BUSY WHEN YOU ARE DOING EXERCISE!
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)
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.
WHAT DO YOU REMEMBER OF PAIN?
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)
STUCTURING THE EXERCISE THERAPY
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.
RIGHT ARM OR LEFT ARM, ARE YOU TREATING THE WRONG ARM?
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.
BRING HOME MESSAGES
- Pain can be modulated through inhibitory pathways and cortical reorganization.
- Cognition-targeted exercise therapy can be used to alter pain memory.
- Thorough pain education should given prior to exercise
- Time-contingency exercise rather than symptom-contingency exercise should be prescribed.
- 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.