Conservative Treatments for Tendinopathy

, S. Della Villa1 and A. Giannini 

Isokinetic Medical Group, Bologna, Italy



A. Giannini

15.1 Exercises Therapy

15.1.1 Introduction: The Importance of Loading Program in Tendinopathy

In 1998 Alfredson et al. published a key paper that changed the way we look at tendons (1998). The authors prospectively studied the effect of heavy-load eccentric calf muscle training in 15 recreational athletes who had the diagnosis of chronic Achilles tendinosis with a long duration of symptoms despite conventional nonsurgical treatment. At week 0, all patients had Achilles tendon pain not allowing running activity, and there was significantly lower eccentric and concentric calf muscle strength on the injured compared with the non-injured side. After the 12-week training period, all 15 patients were back at their preinjury levels with full running activity. There was a significant decrease in pain during activity. A comparison group of 15 recreational athletes with the same diagnosis and a long duration of symptoms had been treated conventionally. No one of the control group improved, and all patients were ultimately treated surgically.

However, despite the first encouraging results, subsequent studies have failed to reproduce the same outcome. In fact, most authors reported successfully returning 60% (Silbernagel et al. 2001; Roos et al. 2004) of participants back to sport, which contrasts with the 100% reported to have returned to sport in Alfredson’s original paper. It was proposed that the lower success rates observed can be due to a poorer response to isolated eccentric exercises in nonathletic and female individuals when compared with athletic subjects (Maffulli and Longo 2008). A recent systematic review confirmed the success of eccentric exercises (Sussmilch-Leitch et al. 2012) even if the mechanism by which the effect is achieved remains unclear. However there is no evidence that eccentric regime is more effective than other loading programs (Malliaras et al. 2013).

Biologic tissues have the unique capacity to adapt over time increasing load tolerance and energy absorption. In tendons, changes in stiffness seem to be attributed more to adaptations of the material rather than to morphological properties. We don’t know for sure if a program regime is better than other in optimizing this response. Type I collagen response to high load in normal tendon peaks at around 3 days after intense exercise (Langberg et al. 2000). Interestingly this response appears to be greater in pathological tendons than normal tendons (Kjaer et al. 2005). However, the majority of the tendon is composed not of cells but of extracellular matrix (ECM), which is a passive structure. The tendon ECM is a viscoelastic material, which means that slower loading regimes can yield greater strains than faster loading regimes, as the tendon has more time to creep (Pearson et al. 2007). This viscoelastic behavior depends on the amount of time the tendon is under load and is therefore unaffected by the mode of muscle contraction (eccentric or concentric). Slow loading may therefore produce particularly strong cell stimuli that can be beneficial to the tendon if the strain is sufficient. Taken together, all these data from in vitro and normal or pathological tendon studies suggest that loading magnitude plays the key role in contrast to muscle contraction type (Couppé et al. 2015) since contraction is slow enough.

Most of the tendinopathic area is located on the deep surface of tendons at, or close to, the bone–tendon junction. It’s not possible that this is due to tensile overload because there is less elongation in this region than in the superficial portion of the tendon. The joint side of the tendon is exposed, in fact, to less tensile load (stress shielded) but may be subjected to high compressive loads against the bone (Cook and Purdam 2012). For example, with proximal hamstring tendinopathy, the tendon is thought to be compressed against the ischial tuberosity when the hip is flexed, such as during sitting. The tendon insertion and the “enthesis organ” are well engineered to absorb most functional loads and will adapt over time to higher levels of load. However, these tissues are slow to adapt to high loads and slow to resolve after insult. Reducing compressive loads in insertional tendinopathies therefore can provide an important unloading strategy for the “sensitized” tendon and must be tailored based on site of compression (Goom et al. 2016).

15.1.2 Not All Tendons Are Created Equal

Basically tendons serve to transfer tension from their respective muscle to their bony attachment. Tendons that are common sites of tendinopathy have large different morphology, so that no single characteristic emerges as key factors common to the development of tendon pain. From a clinical point of view, the differences between different sites of tendinopathy are huge. Patients with supraspinatus tendinopathy frequently report pain during night (Terabayashi et al. 2014), while Achilles tendinopathy is generally more severe at the first step in the morning. Achilles and patellar tendinopathies occur most commonly in people participating in sporting and physical activity (Järvinen 1992). Rotator cuff tear is, instead, extremely common even in normal population (Minagawa et al. 2013), and asymptomatic tear is twice as common as symptomatic tear.

Lower limb tendons have a precise biomechanical role: energy storage and release. In fact, they behave similar to a spring reducing the energy cost of human movements and to a source of power amplification for many high-powered movements (Roberts 2002). There is some evidence that this may be true even for upper limb tendons; however the muscle tendons more involved seem to be pectoral major or subscapularis, while most of rotator cuff tears are located in the supraspinatus (Roach et al. 2013). Energy storage seems not to be a key factor for upper limb tendons. Conversely upper limbs are mainly involved in reaching and pointing, movements that require a precise adjustment of muscle activity to achieve the necessary precision.

Unlike the single-joint movement, the dynamics of multi-joint movement is complex. Take the case of flexing your elbow with your arm in the horizontal plane. If your central nervous system (CNS) simply activates the biceps muscle, the elbow will flex, but its motion will impose a torque, called an interaction torque, on your shoulder. If you do not want that torque to move your upper limb while you move your lower arm around the elbow, you need to activate shoulder muscles in advance to negate interaction force. The same is true for elbow muscle. The more you need to be precise, the more muscle activation control needs to be fine adjusted. This behaviour can be different for lower limb activity, such as walking and running, that appears to be more “automatic” (Narita et al. 2002).

A recent systematic review shows that in people with tendinopathy sensory and motor system are altered bilaterally even in unilateral tendinopathy (Heales et al. 2014). This implies a potential central nervous system involvement. Interestingly among 20 studies included, there are only two studies on lower limb tendinopathy. Greater error in detection of movement was found in affected elbows of participants with lateral epicondylalgia (LE) (Juul-Kristensen et al. 2008). Consistently patients with LE have impairments in reaction time and speed of movement with reaching task (Pienimäki et al. 1997). Motor deficit may also be present in sites distant to the original site of pathology (Alizadehkhaiyat et al. 2007). All these motor control alterations may have a deepest impact where more precise muscle activation is needed, such as in reaching.

Exercises aimed to improve proprioception showed to be no more effective to improve pain compared to traditional treatments in shoulder tendinopathy (Dilek et al. 2016). Exercises to improve “stability,” advocated for low back pain in the recent past, are currently reviewed for lack of any positive evidence to support their use (Wang et al. 2012). Data from low back pain studies also report hypo-activity or hyperactivity depending on the muscle and tasks investigated (Hungerford et al. 2003). Based on what we have already shown, all these data are not surprising. Proprioception is only a part of motor control and probably not the more involved in tendon pathology. Generalized muscle contraction for stability is not a good solution in movement.

To achieve correct stabilization, you have to predict the force your arm is going to experience and produce muscle contraction of the right intensity at the right time: no more, no less. In practice, this means that your CNS is “implicitly” adapted to the physical world (or, from a computational neuroscience prospective, that CNS has acquired an internal model of dynamics). This type of knowledge is, fortunately, implicit and has to remain so. Rather than focus on how to change motor control, it seems logic to reduce, in the short term, the need for stability, reducing the load in the tendon. There is moderate evidence for the immediate effect of several manual therapy techniques on pain and strength (Vicenzino et al. 2001). For example, in “lateral elbow mobilization with movement,” a lateral humeroulnar accessory glide is applied while the patients, suffering from tennis elbow, perform their painful action (Coombes et al. 2015). For rotator cuff related shoulder pain, Lewis has proposed a method of assessment called Shoulder Symptom Modification Procedure (SSMP) (2009). The SSMP systematically investigates the effect of modifying thoracic posture, three planes of scapular posture, and humeral head position in terms of shoulder symptoms. In this process, external forces are applied to joint and painful movement tested. If this reduces or alleviates symptoms, the technique(s) founds to be beneficial during the assessment process forms part of the treatment (Lewis 2016). The common features for these proposed treatments for shoulder and elbow are that external force is applied to joint and so it may increase the articular stability changing motor command.

Predicting force is not a unique feature of the upper limb, and energy storage is not only an exclusive feature of lower limb. Rather, the relative importance of the two functions may vary between anatomical sites and be based on the prevalent activity. That has to be taken in account when we think at the rehabilitation program. We can’t approach, for example, in the same way a rotator cuff tendinopathy of a professional swimmer and of a housewife.

15.1.3 Pain and Psychological Variables

Like other chronic pain conditions, in tendinopathy, there is discrepancy between tissue damage seen on clinical imaging and clinical presentation, which creates confusion for both patients and clinicians. Contradictory evidence exists on the substances responsible for pain generation, the source of these substances, and the pathways of transmission to the central nervous system.

The relationship between tendon pain and mechanical load, together with the mechano-responsiveness of tenocytes and lack of sensory innervation of the deep tendon tissue, may implicate paracrine signaling by the tendon cells. Researchers suggest that abnormal tendon cells produce signaling proteins and receptors for epinephrine, acetylcholine, glutamate, substance P, tumor necrosis factor α (TNFα), and other neuropeptides. Upregulation of these substances can produce a local response driving vascular and tenocyte responses and may also cause a neural response and provoke pain. Increases in receptors for nociceptive substances have been reported such as N-methyl-D-aspartate (NMDA) (Alfredson et al. 2001) and neurokinin-1 (NK-1) receptors (substance P) (Ljung et al. 1999).

These nociceptive signals are assessed by the CNS, but pain will not emerge until the input to the brain has been evaluated, albeit at an unconscious level. Allodynia and primary hyperalgesia are attributed to sensitization of the primary nociceptor and relate to the area of usual pain. Secondary hyperalgesia is attributed to sensitization of nociceptive neurons within the central nervous system (CNS). Tenderness and evoked pain that spread, in a non-dermatomal, non-peripheral nerve distribution, is best explained by central sensitization (Woolf and Salter 2000). The rule of central sensitization in tendinopathy is debated in literature. Plinsinga et al. (unpublished data) found no evidence of central sensitization but a reduction in lower limb loading pain threshold and an increase in pain on pain onset. This data suggest predominantly peripheral mechanisms. Conversely, there are evidences of central sensitization in tennis elbow and in rotator cuff related shoulder pain (Lim et al. 2012; Coombes et al. 2008, 2012; Gwilym et al. 2011). Again it seems that there is important difference in proportion of central involvement between the upper and lower limb.

Nociceptor signals are not the only input evaluated by the brain. Previous experiences, cultural factor, expectation of consequence, and beliefs all together contribute the implicit perception of threat to body tissues. This means that pain can be conceptualized as the conscious correlate of the implicit perception of threat to body tissues. Fear of pain develops as a result of a cognitive interpretation of pain as threatening (pain catastrophizing), and this fear affects attention processes (hypervigilance) and leads to avoidance behaviors, followed by disability, disuse, and depression. In the absence of fear-avoidance beliefs about pain, individuals are more likely to confront pain problems head-on and become more engaged in active coping to improve daily function (see Linton and Shaw (2011) for a review). In their multicenter longitudinal cohort study, Chester et al. (2016) found that in shoulder pain, psychological factors were consistently associated with patient-rated outcome, whereas clinical examination findings associated with a specific structural diagnosis were not. Mallows et al. (2016) conducted a systematic review of psychological variables in tendinopathy. While they found that there is moderate evidence that links catastrophizing and distress with LE, and moderate evidence that kinesiophobia and catastrophizing are associated with rotator cuff tendinopathy, limited evidence suggests that patellar tendinopathy is not associated with anxiety or depression and kinesiophobia may be linked with suboptimal outcomes in Achilles tendinopathy. Again literature seems to suggest that psychological factors may have different impact between the upper and lower limb.

15.1.4 To a Comprehensive Model of Tendinopathy

Recently, Coombes et al. (2008) proposed an integrative model for treating LE: they propose that LE can be conceptualized as comprising three interrelated components: (a) local tendon pathology, (b) changes in the pain system, and (c) impairment in the motor system. In their model, the authors recognized that not all LE patients have the same clinical presentation, then through comprehensive evaluation, different proportions of tendon pathology, pain system dysfunction, and motor system impairments can be used to define subgroups of LE. The healthcare practitioners should identify the relative expression of local pathology, pain, and motor system dysfunction in individual patients, so that treatment strategies may be better matched to the clinical presentation. However, this model can’t be apparently generalized to other tendinopathy sites. There are different ways through which tendinopathy may produce nociception. Based on Cook et al. (n.d.), “continuum” model pain in tendon can fall into two categories: (1) reactive tendon with a first presentation of tendon pain following acute overload and (2) reactive-on-late disrepair/degenerative tendon pathology. A painful reactive or reactive-on-degenerative tendon may increase expression of nociceptive substances and their receptors, stimulating the peripheral nerve, and be interpreted as pain (Fig. 15.1). Since the degenerative portions of the tendon appear mechanically silent and structurally unable to transmit tensile load, the pain-free tendon may contain substantial matrix and cell abnormalities, but limited nociceptive substance production, signaling ability, or receptor activation, which is in summary an insufficient nociceptive stimulus. This may explain, in parts, the low correlation between symptoms and alteration in traditional imaging exams.


Fig. 15.1
Different burden (width of dark blue arrows) of various components on pain, based on upper or lower location of tendinopathy

Morphological alteration seems to produce different centralization of pain between tendinopathy sites, despite always being a chronic disease. This can be due to different impact on motor control between different sites. The presence of pain leads to inhibition or delayed activation of specific muscles or muscle groups that perform key synergistic functions. This produces alterations in the patterns of motor activity and recruitment during functional movement (Hungerford et al. 2003; Hodges and Moseley 2003). Interesting alteration in motor pattern activity is present even in expectation of pain (Tucker et al. 2012). This type of alteration exists also in lower limb tendinopathy (Chang and Kulig 2015) although may have a deepest impact where more precise control is needed. Proprioceptive representation of the painful body part in primary sensory cortex changes when pain persists (Flor et al. 1997). This may have implications for motor control because these representations are the maps that the brain uses to plan and execute movement. It is known that experimental disruption of cortical proprioceptive maps disrupts motor planning (McCormick et al. 2007). Several minor motor planning alterations may be less relevant where tendon have mostly an energy storage function.

There are different theoretical ways through which motor activity alteration may produce pain. The need to modify feed-forward control may permanently increase contribution from synergistic muscles and reduce the variability in movement. Movement variability is thought to minimize load accumulation in a specific region and to be protective for tendon morphology alteration (Stergiou and Decker 2011). Another possible mechanism is that exaggerated muscle contraction, beyond the needed for movement stability, due, for example, to error in the internal calculation of tendon load (Rio et al. 2014), significantly increases load on tendon (Maganaris and Paul 2002).

Exaggerated muscle contraction, limiting the movement of the involved area (Lund et al. 1991), can be helpful but can become detrimental if the other factors (psychological variable and morphological alteration) are relevant. Fear of pain develops as a result of a cognitive interpretation of pain as threatening (pain catastrophizing), and this fear affects attention processes (hypervigilance) and leads to altered motor behaviors, followed by tissue sensitization and then pain. Both negative affectivity (a tendency to see the cup as “half empty” rather than “half full”) and threatening types of illness information can help to fuel catastrophic thoughts about pain. In absence of fear-avoidance beliefs about pain, individuals are more likely to confront pain problems head-on and become more engaged in active coping to improve daily function. If pain is framed as solely a biomedical problem, problem-solving efforts inevitably will be based on strategies to remove or reduce pain. When multiple attempts to get rid of pain fail, worries are further reinforced, and patients are stuck in an endless loop of increasing worries and failed problem-solving attempts to alleviate pain (Linton and Shaw 2011). From these descriptions, it will be clear how motor control may have an enhancement effect on relationship between pain and psychological variables. It will then not be surprising that tendinopathy in anatomical sites involved in more precise tasks is more likely to have a psychological components when compared to tendons involved more in energy storage. We are not auguring that there are some tendons that have a purely energy storage function and are not involved in joint stability, rather same tendons are more related to one aspect than the other and a different clinical presentation. In the model, we are proposing the three different components which are separated for the sake of explanation. They are, in fact, in closed correlation between them. The relative contribution from these different factors and their interactions with each other are variable, fluctuating, and unique to each individual. It is not impossible to have a patient with Achilles tendinopathy and depression and kinesiophobia; it is only less probable. Therefore also in tendinopathy, there is a need of a multidimensional clinical-reasoning approach to patient examination. This enables the clinician to recognize the relative burden and dominance of the various factors that are unique to each patient’s presentation.

15.1.5 Rehabilitation Program Phase 1: Reduce Pain (The Load Management)

Although loads appear to be the key factor, different tendons may respond differently based on their pathological state. Cook et al. (Forsdyke et al. 2016) have proposed a model of tendon pathology that can be useful to guide clinical approach. Based on this model, tendon pain presentations fall into two categories: reactive tendon with a first presentation of tendon pain following acute overload or reactive-on-late disrepair/degenerative tendon pathology. Since reactivity to load seems to be the key factor, the most important intervention in this stage is load management. This means reducing both tensile and compressive load on the tendon. Complete rest from tensile loads for a tendinopathy is contraindicated as it can decrease mechanical strength of the tendon (Reeves 2006). It’s reasonable than to modify load with the goal of reducing pain. This means, in particular, reducing high-load energy storage activities that may be aggravating the pain. Volume and frequency of the highest-intensity activities, such as maximal jumping or throwing, may need to be reduced eventually in consultation with both the athlete and coach. For example, a reduction in an athlete’s training load may diminish symptoms to a level that allows an athlete to continue competing. Simple training changes can reduce compressive load while maintaining tensile loads. One effective way to do this is to reduce loads in the outer muscle range, as compression of the tendon against the bone proximal to the enthesis is increased with longer muscle lengths. For upper limbs, an effective way is applying external force to joint. It is important to consider the 24-h pain behavior when implementing and progressing rehabilitation programs for tendinopathy.

Pain monitoring is a good way to control training load. A slight increase in tendon discomfort or pain is acceptable as a result of the rehabilitation program, but only for a limited period of time. Normally an increase in pain by 2–3 points on the visual analogue scale the day after taking part in rehabilitation exercises is normal, as long as it subsides within 24 h (Kountouris and Cook 2007). Any pain increase that lasts longer than 24 h should be viewed as a contraindication to progress the rehabilitation program, and appropriate adjustments should be made. The Victorian Institute of Sport Assessment (VISA) (Robinson et al. 2001) questionnaires are a series of specific validated pain and function outcome measures that can also be used to assess severity of symptoms as well as to monitor outcomes in different tendons (such as hamstring, Achilles, and patellar tendon). VISA is a 100-point scale, with higher scores representing better function and less pain. However, because of the large domain of sporting function in the VISA scores, they are not sensitive to change over a short period, and at last, 4 weeks are required between each submission. In patellar tendinopathy, Malliaras et al. (2015) suggest to measure pain response using a “pain-provocation test,” such as single-leg decline squat. If the pain score on the load test (e.g., one repetition of the single-leg decline squat test at the same depth) has returned to baseline within 24 h of the activity or rehabilitation session, the load has been tolerated. If the pain is worse, load tolerance has been exceeded. The test is to be administered daily, at the same time of day, throughout the entire rehabilitation process. This approach can be extended to other tendinopathies such as LE using, for example, pain-free grip test, which is a reliable, valid, and sensitive measure (Stratford and Levy 1994). Littlewood et al. (2014) used a someway similar approach for rotator cuff related shoulder pain. However caution has to be taken in reactive shoulder and especially when psychological factors are associated (Lewis et al. 2015). Pain education may be crucial in this phase. Patient has to understand that pain is not equal to damage (Moseley 2007). Finally clinicians have to be aware of appearance of new symptoms during the course of treatment or of symptoms that expand to sites outside and remote from the first site of presentation. This, in fact, may represent a possible sign of central sensitization (Nijs et al. 2010).

Subjecting tendons to tensile, moderate isometric loads while protecting against compression may improve recovery. Isometric also seems to be able to reduce pain through central modulation. Rio et al. (2015) show that a single resistance training bout of isometric contractions, in patients with patellar tendinopathy, reduced tendon pain immediately for at least 45 min post-intervention. The reduction in pain seems paralleled by a reduction in cortical inhibition. However, another study conducted by O’Neil et al. (unpublished data) shows that the above mentioned pain reduction does not seem to appear in patients with Achilles tendinopathy. Even if other researches are needed, isometric contractions with high load (up to 80% of maximum voluntary contraction) can be used as initial strategy if a reduction of pain is obtained. The isometric work must be composed of 5 repetitions lasting 45–60 seconds each, with a 2 minutes rest interval between the series to allow recovery. These loads can be repeated several times a day. A good prognostic sign after isometric work is an immediate reduction of pain in pain-provocation test after exercise. Even isometric must be designed in a way that compression at enthesis, in insertional tendinopathy, is not increased.

There is not a clear boundary between Phase 1 and Phase 2. Exercises that involve distant site from the original site of pathology should be introduced as soon as tolerated while maintaining Phase 1 exercises. Phase 2: Recover Flexibility (Look at Distant Sites)

Little is known about range of motion (ROM) among patients with tendinopathy. Chimenti et al. (2016) found that during stair ascent patients with insertional Achilles tendinopathy used greater end-range dorsiflexion, less plantar flexion and lower peak ankle plantar flexor power than the control group 2016. These data seem to show that there is not restriction in ROM or isometric plantar flexor strength; altered ankle biomechanics during stair ascent were linked with greater symptom severity and likely contribute to decreased function. Conversely other authors found that patients with patellar tendinopathy showed decreased ankle dorsiflexion range of motion (Malliaras et al. 2006). Witvrouw et al. (2001) looked for risk factors for development of patellar tendinosis. They found that the only determining factor was hamstring and quadriceps reduced flexibility. From all this, albeit not conclusive data, we can hypothesis that reduced range of motion and flexibility in site of tendinopathy is not the crucial part. However altered flexibility in distal sites from the actually painful may be partial relevant because it can create biomechanical alteration.

Different tendinopathies may have different biomechanical alterations in different sports activities. People suffering ultrasuond abnormalities at their patellar tendons showed different landing patterns compared to controls (Edwards et al. 2010). Paradoxically better jumping ability has been shown to be a risk factor for developing patellar tendinopathy (Visnes et al. 2013). This may be due to a better ability to use elastic energy of tendon for force production. An altered “energy flow” from the trunk to the hand has been shown to be correlated with injury risk (Martin et al. 2014). It’s difficult to find general principles that can guide functional assessment for all the tendons; however “minimum jerk” is a common feature especially of upper arms movement (Flash and Hogan 1985). Physically “jerk” is defined as the time derivative of acceleration or as the third time derivative of location. In practice, it means that if your CNS has to move your hand or some other end effector smoothly from one point to another, it should minimize the rate of changes of acceleration. If during functional assessment rapid change of acceleration is observed, this may be signs of alteration. If other flexibility, coordination, or strength deficit elsewhere in the limb are found, specific exercises can also be initiated during this initial phase. Sports with markedly different use profiles (such as baseball pitchers) may surprisingly demonstrate bilateral pathology implicating systemic or nervous system involvement in tendinopathy (Rio et al. 2016). For these reasons it is important to do a bilateral assessment and start rehabilitation as needed.

If an alteration in “kinetic chain” range of motion is found, it should be corrected with exercises that do not load the original site of pathology. Meanwhile, it is important to continue Phase 1 exercises. Finally general exercises aimed to maintain general fitness, without load altered tendon, have to be included. Phase 3: Recover Strength (The Muscle–Tendon Specific Function)

Isotonic loads can be introduced when they can be performed with pain less than 3/10 on a numeric pain rating scale. If range of motion is restricted, for example, in the shoulder, it has to be progressed as resistance training. It is useful in the first steps of this phase to avoid compression on tendon and to maintain, if required, an external force to joint. As the symptoms improve, progression may be made by performing movement using a less stable base such as physioball and reducing external load. Then patients can switch to short lever (i.e., elbow bent for shoulder) initially without, then with, increasing weights and resistances (Lewis 2016).

In a randomized control trial, Beyer et al. found that both traditional eccentric and heavy slow resistance training (HSR) achieved equally good results in patients with Achilles tendinopathy, but that the latter tends to be associated with greater patient satisfaction after 12 weeks (2015). Kongsgaard et al. found similar results in patellar tendinopathy (2009). In HSR training three to four sets were performed progressing from an initial load based on 15 repetition maximum (15RM) to 6RM performed every second day. Different methods have been proposed to estimate RM (Niewiadomski et al. 2008). A simple way is to consider that 80% of 1RM is more or less equal to 8RM: the maximal weight that can be lifted eight times. Initially for the aim of be specific and to reduce motor control task, it’s better to use single-joint specific exercises, avoiding multi-joint exercises and, for the lower limb, using only one leg. It’s important, especially for energy storage tendons, to achieve heavy load (6RM) because they are associated with tendon adaptation. The clinicians have to consider both short-term and long-term reaction to load. In the short term, there will be a net loss of collagen production for 24–36 h post-exercise; for these reasons is mandatory to adequate rest days between strength sessions (Magnusson et al. 2010). In the day off isometric exercises for pain can be continued.

When heavy loads are reached (6RM), eccentric training can be introduced. Achilles tendon load and stretch are identical during the concentric and eccentric components of the traditional heel rise/drop exercise (Chaudhry et al. 2015). Muscles can produce greater maximal force eccentrically than concentrically (Enoka 1996). This can produce higher strain on tendon; however this potential is rarely utilized in practice because rehabilitation exercises seldom approach to concentric 1 RM (Malliaras et al. 2015). It’s important that eccentric trainings have to be performed using significant progressive overload. Formally, the patients have to use an overload that, to be raised, need contralateral help in concentric phase. Eccentric phase has to be well performed with “minimum jerk.” There are other theoretical techniques showing eccentric training useful in tendinopathy (see O’Neil et al. for a review (2015)). There is also some evidence that eccentric training may be helpful also in the upper limb (Camargo et al. n.d., 2014). We suggest to perform eccentric training only in the final steps of this phase to prepare patient to more demanding activity. Phase 3 exercises should be continued throughout rehabilitation and to return to sport. Phase 4: Recover Coordination (The Kinetic Chain Function)

The purpose of Phase 4 is to introduce more functional tasks: during this rehabilitation period the differences between tendons increase. According to the hypothesis already presented the functional task of lower limbs is to store and release energy, whereas upper limbs have to predict forces. As already described this distinction depends also from the patient activities. Upper limbs multi-joint coordination exercises have to be firstly introduced as closed chain exercises, such as push-up or modified push-up. Progression is performed using less stable base and/or open chain. For example, to treat a shoulder tendinopathy we can introduce external rotation exercises with unsupported abduction/flexion, with progressive increase of elastic resistance or free weight loads as tolerated. (Lewis et al. 2015).

Treat movement dysfunction may be extremely tricky. It is difficult to find an optimal coordination for most of the human movement, if not impossible nowadays. Imposing a “correct” way to move is complicated and may be even detrimental especially when variability is needed (Stergiou and Decker 2011). Giving learners instructions that refer to the coordination of their body movements—as is typically done in teaching motor skills—has not been shown to be optimal for learning (Wulf et al. 1998) and may reduce variability. Most of the motor learning happens without any formal instructions. A 1-year-old child normally walks easily even if he’s not able to understand a single word. His brain has an “internal model of dynamics” that is well adapted to physical forces such as interactional torque and is able to predict it. This is called unsupervised motor learning. Reinforcement learning (RL) is learning by interacting with an environment. It means learning from the consequences of one’s actions, rather than from being explicitly taught and selecting actions on the basis of past experiences (exploitation) and also by new choices (exploration), which is essentially trial-and-error learning. There are good evidences that the CNS uses some forms of RL (Graybiel 2005; Tanaka et al. 2004). According to the constrained action hypothesis (CAH), an internal focus is associated with “conscious” control processes interfering with automatic control processes (Wulf et al. 2001). Learning from error implies that we need to reduce error in the long run. In movements such as hitting a nail with a hammer, minimalizing errors means that the center of the hammer must get as close as possible to the center of the nail. This achieves reducing variability at the end effector. Then it is generally mandatory to increase “good variability” (Wu and Latash 2014) elsewhere (Todorov and Jordan 2002). For this reason, conscious control, for example, of shoulder may reduce variability in shoulder movement that may be detrimental for tendon and function. So during this phase of rehabilitation, exercises have to be focused to end effector (external focusing) trying to forget as much as possible the painful tendon.

During the landing phase of a vertical jump, peak patellar tendon forces have been estimated to be 5.17 ± 0.86 body weight, with a loading rate of 38.06 ± 11.55 body weight per second (Janssen et al. 2013). In contrast, bilateral leg press (which is not an energy storage loading exercise) performed with a resistance equal to three times the body weight exerts a patellar tendon force equivalent to 5.2 body weight and a loading rate estimated at around 2 body weight per second (Reeves et al. 2003). The major change through these activities is rate of loading of the tendon, which should be progressed gradually through relevant energy storage activities for patients. Initially, simple weight-bearing exercises, such as single-leg squats, step downs, or lunges, can be performed at a speed appropriate for the patient’s functional level. The speed of the exercise is progressively increased until the patient becomes proficient to perform the exercise as fast as athletic or functional activities.

After satisfactory completion of simple faster movements, more demanding exercises, such as hopping, skipping, or jumping squats, can be added to improve the kinetic chain function. Progression is guided by pain experienced in provocation test 24 h after exercise. A helpful habit is to use a training diary on which the athlete keeps the level of pain during activity and during the next day (especially morning stiffness). Exercises that implement energy storage can be very demanding for tendons; for this reason, it is better to perform this type of exercise every third day, in consideration of collagen turnover (Cook and Purdam 2012). It’s important to continue Phase 1, Phase 2, and Phase 3 exercises in the days off, with a progressive and careful load increase. Malliaras et al. (2015) suggest that the volume is progressed before the intensity. Especially in athletes, the purpose of Phase 4 is to build power. Power is a function of strength (force) and speed (velocity) of movement and is important in most sporting activities. Power has to be at least as in the contralateral limb. We advise to use a functional test that mimics sport-specific demands of the subject such as maximal vertical hop height. If pain rises during Phase 4, it is important to return to Phase 1 exercises and progress as soon as the pain has returned to normal.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Sep 6, 2017 | Posted by in ORTHOPEDIC | Comments Off on Conservative Treatments for Tendinopathy

Full access? Get Clinical Tree

Get Clinical Tree app for offline access