Tendons attach muscles to bone. Tendinopathy is a painful condition of the tendon due to a mismatch in the rate of healing and the frequency of loading. It was previously known as tendonitis or tendinosis. But research has shown that the inflammatory response is lacking in most cases of tendon injury and may only be present in the early stages (itis means inflammation). Hence, the term tendinopathy is more scientific as it encompasses the structural changes associated with tendon changes observed in this condition.
Tendons attach muscles to bone. Though the muscles and tendon are both made up of structural proteins, there is a basic difference in their architecture. The muscles have more contractile proteins allowing them to generate speed and power on contraction. On the other hand, the tendons are made up of densely packed collagen protein, making it a more tensile structure designed to bear a lot of weight.
Repeated stresses to the tendon cause micro-injury. Overtraining and lack of rest, does not allow the normal healing process to occur. Thus, at some point, the rate of healing is slower than the rate of injury. This puts the tendon in a degenerative phase leading to tendinopathy. A degenerated tendon becomes weak and liable to rupture at the smallest load.
Achilles tendon and patellar tendon in the legs are more prone to overuse injury. Sports like rugby and athletics put a lot of explosive forces on these tendons.
Tendinopathy initially presents with pain before and after the activity. As the condition progresses, the pain comes on during the activity as well. In later stages, early morning and night time pain and stiffness is a common complaint. There is swelling, redness and tenderness around the affected tendon.
Tendinopathy initially presents with pain before and after the activity. At this stage, there is no pain during the activity. As the condition progresses, the pain comes on during the activity as well. In later stages, early morning and night time pain and stiffness is a common complaint. There is swelling, redness and tenderness around the affected tendon.
Repeated stresses to the tendon cause micro-injury. Overtraining and lack of rest, does not allow the normal healing process to occur. Thus, there comes a point when the rate of healing is slower than the rate of breakdown. This puts the tendon in a degenerative phase leading to tendinopathy. Consequently, a structurally compromised tendon is prone to produce pain with sudden or inappropriate loading and this is why athletes often find the pain returns quickly as soon as they go back running. In other words, despite a period of rest, the structure of the tendon has not changed and therefore the pain returns when they go back running.
Excessive training, change in training equipment (heavier), altered biomechanics in the adjacent joints, incorrect training surfaces, shorter rest periods and back to back tournaments are a few identifiable risk factors that put excessive stress on the tendon.
Usually the weight bearing tendons of the legs like the achilles tendon and patellar tendon are more prone to overuse injury. Sports like rugby and athletics put a lot of explosive forces on these tendons. Similarly, in the arms, the supraspinatus tendon and the biceps tendon are the more commonly affected. Games like gaelic and basketball have repeated jumping action which causes injury to these tendons. Biceps tendinopathy is also commonly seen in swimmers proficient in backstroke and breaststroke.
A simple injury to the tendon turns into a chronic tendinopathy, when the micro-ruptures in the tendon do not get sufficient time to heal. Altered biomechanics in the adjacent joints, undulating training surfaces, excessive training, shorter rest periods and back to back tournaments are a few identifiable risk factors that put excessive stress on the tendon.
In elderly individuals, a lack of structural integrity due to ageing of the collagen fibres (the fibres that make up tendons), just like other tissues can increase the risk of tendon injury. When these individuals take up running or increase their training intensity suddenly, the already compromised tendon is subjected to greater relative loads and can give rise to tendinopathy in elderly athletes.
Obesity also increases the total load on the tendons. In patients with diabetes mellitus, the problem lies with the neurological and vascular supply of the tendon. The tendons inherently are less vascular than the muscles. Diabetes further disrupts the microvasculature of the tendons. In addition, diabetes also reduces the neuronal proliferation in the tendons. This means reduced neuronal feedback of pain and stress. Simply put, the tendons are unable to convey to the brain that they are being overloaded. The resulting lack of pain perception and the inability to convey distress to the brain, leads to further overuse damage.
With the changes occurring in the biological and mechanical properties of the tendon, they respond differently to injury and healing is impaired when compared to tendons of a healthy person. The metabolic disorders affect the structural integrity of the tendons making them prone to injury or rupture.
The key to successful rehabilitation is the early recognition of the injury. Training through the injury in the initial phases slows down the recovery (J. Swimming research, Vol 18, 2011). Once a tendon injury is suspected, the person must alter their loading schedule and a strengthening program is commenced which is aimed at improving the capacity to perform the daily activities of the individual.
A study (Rheumatology, 2013) found an interesting link between individuals with metabolic disorders and tendon injuries. According to this study, tendon degeneration was found more often in individuals suffering from metabolic disorders like diabetes mellitus, gout, hypercholesterolemia and obesity.
The study argues that changes in the metabolism of carbohydrates, proteins and fats, results in accumulation of toxic byproducts in the tendons which can then alter the properties of the collagen proteins which form the tendon. Infiltration of low density lipoproteins (LDL) or bad cholesterol and monosodium urate crystals in the tendons cause a persistent low level inflammatory response in the tendons.
As tendinopathy is not an inflammatory condition, the usual anti-inflammatory interventions such as NSAIDS or corticosteroid injections are not effective in the long term (Clinical Orthopedic Related Research, 2008). The same research also reports inconsistent results with therapy modalities like ultrasound and laser therapy when used for pain relief.
Application of ice has been found to be effective in controlling the swelling and redness in the early and late stages. Cessation of all pain inducing movements is advised to allow healing to occur.
Eccentric strengthening exercises (muscle contracting and lengthening simultaneously) have shown to be effective in increasing cross linkages between the collagen fibers in the tendon that helps in tendon remodeling and neovascularization (Rheumatology, 2008). The benefits of loading include improved alignment of regenerating tissue and minimisation of atrophy. (Jarvinen et al. 2007). In fact, a combination of eccentric training and static stretching has shown to be more effective in reducing pain and improving function (Clinical Rehabilitation, 2012). A small study indicates that manual therapy (mobilisation of the underlying joints) improves joint mobility, which indirectly improves muscle-tendon efficacy (J Manipulative therapy, 2017).
Every muscle-tendon unit has a representation in the brain. After an injury, there is a change in the input messages from this unit to the brain. Consequently, there is an alteration in the area of the brain that controls this muscle-tendon unit. This in turn leads to an altered nerve message relay from the brain to the muscle-tendon unit, causing a change in its excitability (British Journal of Sports medicine, 2017). This change can result in the tendon being more sensitive to pain and this may impact on how the patient responds to early rehab.
According to this latest study, the present exercise protocol involving eccentric training and heavy slow resistance training (involving both eccentric and concentric components) improves the muscle tendon structure and mitigates against pain production. But this does not address the altered neural component. Since this change is not factored into the rehabilitation, there are more chances of recurrence.
Thus, these authors (Rio et al.) have proposed a new neuroplasticity training technique that focusses on the excitability of the muscle tendon unit. An externally paced training program that makes the athlete contract and relax a muscle to random visual or auditory cues uses excitability properties of the muscle-tendon unit to retrain brain control. The right neural input to the brain will get the right output to the contractile unit.
The authors believe this Tendon Neuroplasticity Training program bridges the gap between the muscle and the brain. It combines the strength based loading program with external strategies that optimise the message pathway from the muscle –tendon unit to the brain and back.
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