by Martin Krause
The Achilles tendon is a thick strong mass of avascular collagen fibres who attains it's nutrition through the process of diffusion of nutrients down a pressure gradient. Achilles injuries are usually classified into acute tears and paratendonosis. The latter occurs frequently in males over the age of 40, whose high testosterone and reduced chondroitin-6-sulphur levels mean that their collagen matrix has become drier and more brittle. Ironically, these people can present with swelling in the mid substance of the tendon due to neovascularization of the tendon. In contrast, acute ruptures of the tendon can occur at any age, and hence these people may present clinically with complete rupture of the Achilles substance from the bone, mid tendon or musculotendonous junction ruptures. It commonly occurs in sprinting and jumping sports where fast changes in muscular lengthening and shortening occur. People with large tight calves and those with a pes cavus (high arched) foot are at greater risk of getting such a tear. On the other side of the coin, are the people with long flattened arches which make them slow and/or weak in their supination component of push-off. These people frequently develop a mid medial calf tear. Over-active lateral gastrocnemius and underactive soleus have also been implicated as has excessive eversion of the ankle during the stance phase of gait. Finally, some people have a very low insertion of their deep calf muscle (the soleus) on the Achilles making the tendon inherently shorter. Complete and partial tears are treated with camwalker boots, complete immobilsation or surgery with or without autologous grafts such as using the plantaris tendon.
Chronic swelling inside the tendon sheath can lead to severe pain. Depending upon pathology a necrotic area of degeneration within the tendon may occur with concommittant blood vessel infiltration leading to further pain and swelling. Other factors leading to a potential Achilles problem also include myofascial-immune pathology, metabolic-immune-bursa pathology, and low back pathology (L5/S1 intervertebral disc), the latter resulting in neurologically generated tightness and weakness in the muscles of the calf and ankle. Additionally, people with chronic lateral ankle instability also seem to be at risk of Achilles tendonopathy. In fact, the inverse dynamics of energy transfer, where muscles crossing 2 joints are seen as energy straps, implicate the entire lower limb in Achilles pathology.
Creaby et al (Medicine & Science in Sports & Exercise . 49(3):549-554, March 2017.) found the impulse of the hip adduction and external rotation moments as well as the peak hip external rotation moment to be significantly increased in runners with AT compared with their healthy counterparts. However, the two groups displayed similar hip and ankle joint angles as well as ankle joint moments during running. The identified differences in hip joint biomechanics found in the present study compliments previous research that provided evidence of altered hip neuromuscular control in runners with AT (Azevedo et al, Br J Sports Med. 2009;43(4):288–92; Franettovich Smith et al, Med Sci Sports Exerc. 2014;46(3):594–9 ). Taken together, these findings reinforce the need to consider proximal lower-limb function in the assessment and rehabilitation of runners with AT.
- Ultrasound images
- The Kinetic Chain
- Clinical implications of inverse dynamics (mind map of cause and effect)
- Cognitive filtering for decision making
Refinement of the working hypothesis
- Multimodal approach to treatment
- Predictive reasoning
- Treatment options
- Lateral ankle instability
- Countermovement jumps
- Plyometric exercises and eccentric muscle contractions (biomechanics)
- Conclusion : Swedish method of eccentric calf training for collagen alignment and intra-tendon swelling
- Videos of exercises
The Achilles tendon forms part of a kinetic chain of accelerating levers (bones) around which energy is transfered and dissipated through lengthening (eccentric) and shortening (concentric) contractions between the foot and thorax.
Inverse dynamics in an accelerating lower limb include the capture and release of kinetic energy through the conservation of angular momentum.
Tendons act as buffers, delay energy absorption by muscles and therefore act as attenuators and shock absorbers and hence have implications for neural control (Roberts & Konow 2013, Ex Sp Sc Rev, 41, 4, 186-193). If tendons are injured, or if a pain state exists the ability to engage the elastic components of movement is diminished. In fact, people with chronic ankle instability (CAI) have been shown to have decreased energy dissipation at the knee during jumping (Terada et al 2013, Med Sc Ex Sc, 44, 11, 2120-2128). CAI makes those people more likely to have injuries to the knee, hip and spine. Mind maps can be generated which illustrate the multifactorial nature of calf tightness and achilles pathology. It should be noted that this 'mind map' was generated 7 years before researchers vindicated the use of such an approach. This is a 'classic' example whereby clinical reasoning can define the treatment rationale even in the abscence of evidence based physiotherapy (EBP). In this case, the amelioration of clinical signs and symptoms provides the face and construct validity to drive the EBP, where the 'mind map' is a construct from a combination of energy transfer biomechanics and clinical reasoning.
The mind map highlights the need to develop a structured approach to treating an Achilles tendon problem. Multiple hypotheses testing requires a mechanism of filtering multiple information so that the clinical signs and symptoms can be integrated with knowledge from pathophysiology, which subsequently generates decision making and treatment strategies based on testable clinical pattern generation.
All clinical findings (impairments measures) need to be assessed in relationship to the subjective examination (disability measures, past and current history w.r.t mechanism of injury/onset and/or aggravating/easing factors) in order to determine a diagnosis and prognosis based on the stage, stability, irritability and severity of the disorder. This process should also identify whether we are dealing with misuse, overuse, abuse or disuse as a precipitating factor in it's onset and/or chronicity. By defining the disorder into these categories the clinician is consciuosly 'filtering' the multitude of information to form a 'clinical picture'.
The clinical reasoning process is used to confirm and negate correlations between the multiple variables. These findings must then be integrated into the neuro-matrix to determine a management plan which encompasses the goals and asperations of the client.
The ultimate goal for the musculoskeletal physiotherapist is to integrate the neuro-matrix into a clinically useful management strategy where predictive reasoning enhances the clients confidence in their therapist and in their own decision making processes
Treatment could consist of
- Camm walker boot
Dry needling, myofascial release & soft tissue massage
- Kinetic or dynamic taping
Foot - ankle taping, orthotics/heel raise
Muscle energy techniques for lumbar spine - SIJ dysfunction
Metabolic consideration - Mg-Ca, Na-K balance
Nutritional Considerations - protein-carbohydrate, creatine supplementation
Joint mobilisation to the foot, inferior and superior fibula, hip, sacrum & lumbar spine
Functional closed chain oscillatory eccentric - concentric exercises for lumbar spine, hip, knee and ankle
Countermovement jumps have been demonstrated to improve with eccentric Achilles tendon loading. Neural modulation of the muscle -tendon control strategy was shown to change after 1 bout of practice. These changes included a decrease in the magnitude of fascicle lengthening and shortening, which was accompanied by an increase in tendon shortening without a change in ankle ROM (Hirayama et al 2012, Med Sc Sp Ex, 44, 8, 1512-1518). Motor control suggests that the 'degrees of freedom' are controlled using a mass spring analogy of oscillations around a point of CNS stability. This stability is based on the balance of muscle tone as well as predicted feedforward movement oscillations.
The eccentric component to this exercise cause more profound changes to the connective tissue of the muscle (broadening and streaming of Z bands). Investigations into eccentric exercise revealed pain 8 hours after initial exercise which was maximal 48 hours later (Newham, Mills, Quigley, Edwards 1983). These investigators found low frequency fatigue 10 minutes after a 20 minute period of stepping (Newham et al 1983). Additionally, they demonstrated progressive increases in IEMG during the exercise in the rectus femoris (160% increase) and vastus medialis (140% increase) in the eccentric contracting leg (Newham et al 1983). Mechanical damage to the sarcoplasmic reticulum resulting in less calcium release for each excitatory action potential was suggested as the cause of the low frequency fatigue (Newham et al 1983).
Muscles undergo fatigue and weakening after several bouts of concentric and eccentric exercise. Moreover, this fatigue and weakness is usually more extreme after eccentric exercise in the untrained individual. A number of sites in the myo-fibrillar complex such as reduce binding sensitivity and capacity of Troponin C for calcium, altered troponin-tropomysosin interaction to impaired binding and force generation by actin and myosin have been implicated in impaired force generation (Green 1990). Indeed, in the absence of any association between relaxation rates and Calcium kinetics raises support for the notion of a rate-limiting process controlling the relaxation of fatigued muscles being located in the contractile proteins (Hill et al 2001). During fatigue the relaxation times can be prolonged as much as 50% (Bigland-Ritchie et al 1986) thus resulting in increased force generation during sub-maximal stimulation due to tetanic fusion despite a substantial fall in the maximum tetanic force (Bigland-Ritchie et al 1986).
The initial overall loss of force production seen may be due to Desmin and Titan damage (Lieber & Friden 2002). Desmin acts as an extra-sarcomeric mechanical stabilizer between adjacent Z discs and the attachment to the costomere at the sarcolemma (Lieber, Shah & Fridén 2002). The costomere complex contains Talin, Vinculin & Dystrophin which attach to the trans-sarcolemmal proteins Integrin and Dystrophin associated proteins. These proteins allow the lateral transmission of force from actin to the basal lamina containing type IV collagen which is contiguous with the endomysium (Kovanen 2002). Desmin loss after eccentric exercise can occur within 5 minutes, possible as a result of increased intracellular Calcium leading to Calpain activation and selective hydrolysis of intermediate filament network (Lieber & Fridén 2002). This may result in the ‘popping of sarcomeres’ of different length may loose their myofilament overlap of actin and myosin (Lieber & Fridén 2002). Hence, reduced force production would be expected. Additionally, the release of matrix metalloproteinase (MMP) which may degrade the extramyocellular type IV collagen (Korskinen, Kovanen, Komulainen et al 1996). However, this effect occurs many days after exercise (Korskinen et al 1996) and could even effect torque production 28 days after exercise (Lieber & Fridén 2002). This has significant implications in exercise training prescription.
Tendon properties under loading
A meta-analysis of increased loading on in-vivo tendon propeerties (Wiesinger et al 2016, Med Sc Sp Ex,47, 9, 1885-1895) confirmed a nearly systematic change in tendon properties with training. The patella tendon appears more amenable to change than the achilles tendon in terms of tendon stiffness. A rapid increase in Young's modulus is often paired with tendon stiffening and remains elevated within the first months of trainng in a rather monotonic fashion, whereas long term, years of training was associated with a larger tendon cross sectional area, without any evidence of differences in material properties. Mechanisms of change include extracellular matrix (ECM) enzymes involved in collagen turn-over, such a matrix metalloproteinases. Furthermore, an up-regulation of the stress response cytokines and growth factors (insulin like growth factor or transforming factor-beta-one) have been observed in Acchiles tendons in vivo and patella tendons in vitro.
Is muscle injury the result of an imbalance between intra-muscular transverse and longitudinal forces?
Is muscle tightness due to an imbalance between force and velocity and hence the development of power? This highlights the need for specificity with training and rehabilitation.
Force damping and recoil leads to efficient transfer energy which in the case of walking has been related to sinusoidal movement. Longer lower limb tendons, especially the Achilles Tendon, and stiffer lower limb joints have been shown to lead to improved running efficiency (Hunter et al 2011, Med Sc Ex Sp, 43, 8, 1492-1499). Clinically, however, we need to differentiate between the 'floppies' and the 'stiffies' as tendon-muscle complexes can be long and stiff as well as short and stiff in individuals with strong collagen complexes versus those with weaker more pliable ones. Other investigators also found that six weeks of plyometrics training improved running performance and the ECR (energy cost of running) despite no measurable changes in MHC (myosin heavy chains) and titin isoforms. This plyometric intervention improved 3000m time trial performance and oxygen consumption. Plyometric training consisted of 15 sessions. The sessions included total contact time of between 60 to 228, and the intensity of vertical jumps increased progressively using a slightly modified Spurrs protocol to avoid injury. Vastus lateralis was used as a biopsy site. (Pellegrino et al 2015, Med Sc Sp Ex, 48, 1, 49-56). In my clinical experience, regardless of the site of lower limb tendonopathy, similar to principals of myofacial trains (eg deep myofascial train of the calf is continuous with underside of the patella), the entire kinetic chain needs to be treated and the plyometric exercise protocol should resemble sporting specificity. For example, soccer players should be able to do at least 3 sets of 30 heal drop/raises, 3 sets of 90 one leg bridging, 3 sets of 90 hip drop/hitches and 6 sets of 60 quads 'hover' eccentric/concentric activity.
The concepts of Young's modulus of elesticity and the Hills Model of viscoelasticity should not be confused with the Mass-Spring Concept of motor control and Inverse Dynamics.
Conclusion : the Swedish method of treatment using eccentric calf loading for optimal collagen alignment
The Swedish method of rehabilitation for Achilles Tendinosis has used the concepts of eccentric loading to propogate nutrition to the muscles, encourage lengthening of the actin-myosin resting position as well as improve viscoelasticity through enhanced collagen turnover. Thereby, a mechanical input is transduced to a cellular response. However, Achilles tendinopathy has an aberrant strain response to eccentric exercise. Researchers concluded that Achilles Tendinosis is a bilateral systemic process where they found that both the symptomatic and asymptomatic tendons were thicker and hypoechoic when compared with control tendons. Furthermore, they showed altered fluid movement within the tendon matrix which was characterized by lower acute anteroposterior response to eccentric exercise (Grigg et al 2012, Med Sc Sp Ex, 44, 1, 12-17). Moreover, human muscle proteome modification after acute or repeated eccentric exercises is towards a switch to an oxidative metabolism Hody et al 2011, Med Sc Sp Ex, 43, 12, 2281-2296), which suggestive of protection against DOMS as well as a progenetor for recovery and repair.
The science behind a 12 week eccentric training for Achilles Tendonosis are an increase in collagen synthesis (Langberg et al 207) and reduced neovascularization (Ohberg et al 2004) leading to reduced capillary engorgement and improved venous return (Knobloch et al 2007). These latter authors demonstrated a 45% improvement in capillary blood flow and reduced pain on a VAS after a 12 week eccentric training progam. Furthermore, Webborn (2008) suggested that clinical improvements were also related to nerve blood flow issues coined "neoneurovascularization". Achilles tendon stiffness has been shown to increase with plantar flexion training by between 16% and 29% (Kubo & Ikebukuro 2012 Med Sc Sp Ex, 44, 11, 2111-2117). However, these values are lower than increases of between 58% and 83% in patella tendon stiffness after knee extensor training. These results suggest a difference in the plasticity of the two tendon types. Furthermore, sprinters appear to have a more elastic patella tendons, whereas endurance runners had stiffer patella tendons when compared to lesser trained individuals. These differences appear to be the result of higher blood flow in the patella tendon when compared with the achilles tendon (Kubo & Ikebukuro 2012). Improvements in blood flow to the Achilles tendon was only shown after repeated contractions of 70% MVC whereas 50% MVC showed no change in perfusion. Furthermore, these investigators demonstrated improvements (7.7%) in achilles tendon perfusion (total haemoglobin and oxygen saturation) from 20 minutes of heating using a hot pack. The generalised reduction in Achilles perfusion when compared to the patella tendon may partially explain the greater propensity to rupture achilles tendons.
Achilles tendon stiffness has been shown to increase with plantar flexion training by between 16% and 29% (Kubo & Ikebukuro 2012 Med Sc Sp Ex, 44, 11, 2111-2117). However, these values are lower than increases of between 58% and 83% in patella tendon stiffness after knee extensor training. These results, in line with previous comments, suggest a difference in the plasticity of the two tendon types. Furthermore, sprinters appear to have a more elastic patella tendons, whereas endurance runners had stiffer patella tendons when compared to lesser trained individuals. These differences appear to be the result of higher blood flow in the patella tendon when compared with the achilles tendon (Kubo & Ikebukuro 2012). Improvements in blood flow to the Achilles tendon was only shown after repeated contractions of 70% MVC whereas 50% MVC showed no change in perfusion. Furthermore, these investigators demonstrated improvements (7.7%) in achilles tendon perfusion (total haemoglobin and oxygen saturation) from 20 minutes of heating using a hot pack. The generalised reduction in Achilles perfusion when compared to the patella tendon may partially explain the greater propensity to rupture achilles tendons.
Knobloch K et al (2007) Eccentric training decreases paratendon capillary blood flow and preserves paratendon oxygen saturation in chronic Achilles tendinopathy. Journal Orthopeadic Sports Physical Therapy, 37, 5, 269-276
Kubo K, Ikebukuro T (2012) Blood circulation of Patella and Achilles tendons during contractions and heating. Med Sc Sp Ex, 44, 11, 2111-2117
Langberg H et al (2007) Eccentric rehabilitation exercises increases peritendinous type I collagen synthesis in humans with Achilles tendinosis. Scandinavian Journal Medicine Science Sports, 17, 3, 298-299.
Webborn ADJ (2008) Novel approaches to tendonopathy. Disability Rehabilitation, 1-6.
See links to
Achilles Tendonosis (Pdf)
Last update : 20 February 2017