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Achillies tendinopathy treatment revolution of sorts

Discussion in 'Biomechanics, Sports and Foot orthoses' started by mike weber, Jan 30, 2010.

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    The below was written by Simon Spooner and has got me thinking...

    Now Simon was discussing a study protocol (http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=39056 ) In this thread.

    Now as we know the Gastroc and soleus main job is as a plantarflexors thru pull on the achillies tendon on the posterior calc. There will depending on the position of the subtalar joint axis be a pronatory, supinatory or no movement when considering STJ motion.

    Now the thread was discussing medial skive orthtoics so that indicates to me that the patients have a medial deviated axis. If we work with this idea in mind whether its often seen in the real world or not.

    So the STJ axis is medially deviated,

    Here are two quote to consider about an axis from Simon Spooner
    and Eric Fuller
    Note when using achillies tendon I also include the muscles gastroc and soleus and their action of contraction and excentic contraction

    Now as stated the pull of the achillies tendon can cause 3 different motions at the STJ, if the STJ is medially deviated the motion around the STJ axis will most likely be an external pronation moment. Now the the insertion point is lateral to the STJ axis the load on the achillies tendon will be less, it has a mechanical advantage. ie the natural motion of the foot is pronation the achillies is at a mechanical advantage.

    So if we use a medial skive device as part of our treatment plan we maybe adding to the load of the achillies tendon.

    As the medial skive will cause an external STJ supination moment the axis will also deviate laterally, which may mean either a shorter level arm or the insertion point of the achillies will be medial to the STJ axis which would then mean the muscle must help "control" the natural motion of pronation of this patient and the type of work will change and if the load placed on it by the body is too much an increase in symptoms.

    Now this may be obvious to most and if so sorry for being a bit dense but I could not find this discussed anywhere and if I´m wrong in my revolution of sorts let me know.

    The opposite would work for a lateral deviated axis as well.

    I also though that this might be a good discussion to get the orthotics consensis project going again ?

    What do others think?
  2. musmed

    musmed Active Member

    Dear Michael

    May I suggest that you anatomy is not quite correct and thus your assumptions follow that line.
    The soleus is inserted into the medial posterior aspect of the calcaneum and is thus a supinator of the foot and not a plantar flexor as its primary role.
    The reason why I say the soleus is a supinator of the foot is because almost nobody has a mobile subtalar joint.
    As I have posted many times, why is OA to the subtalar joint a very rare event if there is no history of a fracture to the joint line?
    Regards from bleak Stratford UK
    Paul conneely
  3. musmed

    musmed Active Member

    \Dear MichaelNo2.May I be so bold as to suggest that the gastroc is a knee extender as its primary role.The next few patients with OA of the knee check the strength of the gastroc.It will be weaker on the OA side.This is to compensate for the joint changes.Oh I can see some sunPaul Conneely
  4. Paul you keep saying these thing and most people ignore your comments. I will put these in with the below comments which you have made which make no sense and kind of make me laugh and cry at the same time.
    But please don´t comment here make a new thread the stj dosen´t move or something like that or the Gastroc is not a plantarflexer.
  5. I been thinking again.....

    If we could by some sort of technology identify when the STJ axis is in such a position as to not cause pronation and supination of the STJ and have the orthotic working in such a way that the STJ is in that position when the Gastroc, soleus are contracting to cause a plantarflexion moment at the talocural joint, our heel lift would have a greater effect as well in our treatment plan, but I guess this would not be possible due to the fact that our biomechancis will be slightly different every step.
  6. It appears I´m having a bit of a conversation with myself, but I try one more time by asking a question.

    If you prescribe an orthotic in Achillies related issues and you shorten the level arm of this muscle in relation to pronation/supination of the STJ, could you be adding load to the achillies tendon ? Is it signifiacant?

    I would of course be using a heel lift, massage, exentric training, stretching, ice, rest, FMT etc etc in my 1st line of treatment, but as an educational exercise could an orthotic increase the loads?
  7. Craig Payne

    Craig Payne Moderator

    attached is some slides i use on the boot camps on this

    Attached Files:

  8. Thanks Craig.

    Here is the full text of the Dixon article

    This was very intersting..


    Attached Files:

  9. I wouldn't be so sure these researchers were accurately measuring Achilles tendon tension. It appears as if they were measuring total ankle joint plantarflexion moment and assuming all of this ankle plantarflexion moment was coming from tension within the Achilles tendon, and not considering that the FHL, PT and FDL and posterior ankle joint capsule may also be contributing to ankle plantarflexion moment. At best, this study only roughly approximates Achilles tendon tension.
  10. Thanks Kevin I´ll keep that in mind when reading some other stuff I´ve found which I´ll post to see what others think.
  11. some other stuff on loading rates for anyone who´s intersted.

    Attached Files:

  12. Found this as well.

  13. and this. Again by Dixon

  14. So all this begs the Question what are we acheiving with our heel lift.

    1. an increased plantarflexion moment at talocural joint?

    2. Reduced lengthening of Achilles tendon?

    3. Increased stiffness of Triceps surea so therefore functions better?

    4. Change of when the peak force is on the achilles tendon?

    5. Something else Ive not listed ?

    and is this a patient specific treatment outcome the same as with full foot orthotic ?

    any options out there
  15. Michael:

    Clinically, I have consistently seen over the years that adding a heel lift into the shoe of a patient with Achilles tendintis will reduce their pain with walking. Therefore, the heel lift must be doing something mechanically to the Achilles tendon to achieve this pain reduction. I believe that the heel lift decreases the peak tensile stress within the Achilles tendon, since this makes the best mechanical sense to me.

    However, unless direct measurement of Achilles tendon tension is accomplished in live subjects during weightbearing activities with and without heel lifts, we simply won't know for sure what exactly happens with heel lifts. Doing inverse dynamics at the ankle joint can not isolate the plantarflexion moments coming from the Achilles tendon from the plantarflexion moments coming from the flexor digitorum, posterior tibial and flexor hallucis longus muscles, posterior ankle joint capsular ligaments or anterior osseous abutment of the dorsal talar neck onto the distal-anterior tibial plafond. Implantation of a strain gauge or fiberoptic cable into the Achilles tendon in live subjects would be the best way to see what exactly is happening mechanically within the Achilles tendon when we add heel lifts to the individual's shoes. To my knowledge, that study has not been done yet.
  16. Craig Payne

    Craig Payne Moderator

    It could be (5). I got data we will publish on day, that supination resistance goes down by about 12% with a 1cm heel raise ---> that hypothetically means soleus does not need to work as hard to provide a supination moment --> less load in achilles.

    This reduction in load has nothing to do with the nonsense of a heel raise shortening the distance between origin and insertion of the muscle.

    Try this thought experiment: Stand up. Raise up on to your toes. To do this the calf muscles contracted with x amount of load going through the achilles. Now add a heel raise. Raise up on to your toes. Do you think that the calf muscle contracted with same amount in both conditions? Was the load in both conditions the same? Why would the calf muscles contract with less force in the heel raise condition? You bodyweight that they have to overcome is the same in both conditions.

    There i no doubt that heel raises are useful for achilles tendonitis, but its probably not because of the origin-insertion distance being shortened.

    Also foot orthotic massivly reduce the supination or inversion moment --> big reduction in the work needed by soleus --> recution in achilles load (this gets my vote as the probable mechanism)
  17. Craig:

    The difference with the heel lift is probably due to changing the point along the length-tension curve in the passive tensile elements within the gastrocnemius-soleus-Achilles tendon complex at the point of maximum dorsiflexion of the ankle joint during walking and running, not during erect standing where the ankle joint is at 90 degrees. In other words, unless dynamic gait is studied,where ankle joint dorsiflexion is significantly increased versus standing, then I think it is unlikely that heel lifts would have much effect on Achilles tendon tension in most individuals. Yes, the heel lift probably shortens the distance from the origin to insertion of the gastrocnemius-soleus Achilles tendon complex at peak dorsiflexion of the ankle, due to decreased peak ankle joint dorsiflexion angles, which will decrease the length of, and tensile force within, the Achilles tendon. This, in turn, decreases peak tensile stress within the Achilles tendon. Makes very good sense to me.:drinks
  18. Very intersting stuff...... lots to consider....... THE BLACKHOLE OF BIOMECHANICS strikes again, the more you look the more questions you have.
  19. pod29

    pod29 Active Member

    Hi All

    Very interesting topic!

    May I add some thoughts. This may seem like a very simplistic idea, given the level of thought that people are giving this topic. However....

    One of the simplest mechanical changes that a heel raise may induce, is that of shifting the body's centre of mass forward (anterior to the talocrural joint). In some people this may be sufficient enough reduce the net external plantarflexion moment required for forward proplusion. The heel lift may also decrease the resistance to this moment by reducing anterior ankle compression forces. Possibly resulting in a reduced amount of plantarflexion force required from the achilles propel the body forward.

    The concentric phase of Gastroc/soleus contraction is probably not what is causing the damage to the tendon in the first instance, but by reducing the load in propulsion it may decrease tissue stress.

    Inter-subject variablity could be contributed to by a number of factors ie. ankle joint stiffness, sub-talar joint axis position, tibial angle, 1st ray function etc etc. Personally I believe an important one of these may be due to differences in midfoot stiffness.

    Theoretically, a foot that has decreased amounts of mid-foot stiffness may prolong the eccentric phase of Gastroc-soleus (GS) action. Dorsiflexion moments at the mid-foot may increase the load through the achilles and GC by counteracting (or dissipating) the plantar flexion force that the achilles creates. This may be where orthoses are effective in many cases. By increasing the stiffness of the midfoot they may well reduce the eccentric loading time of the achilles and increase the ability of the achilles to transmit it's plantarflexion force into the talo-crural joint to faciltiate forward propulsion. The net result being less muscular work and decreased loading on the tendon itself.

    Just some of my thoughts, look forward to reading more

  20. Hi Luke the bit in red that I´ve highlighted, There also will be an increase in GRF anterior to the talocural joint which would potentially cancel out the +ve.

    Im saying this because of the longer level arm of the GRF force on the talocural joint compaired to the heel lift. ( I maybe wrong in this thought ?)
  21. pod29

    pod29 Active Member

    Hi Michael

    My thought is that the lever arm of the GRF on th TCJ will not change as the distance between the TCJ and metatarsal heads will remain. However, if the achilles action over the foot to create propulsion is considered as a second class lever, shifting the CofM anterior to the TCJ will actually increase the mechanical advantage of the Gastroc-soleus and achilles unit. Again this is assuming that forces are not dissipated through an overly compliant midfoot.

    I will try and attach some dodgy illustrations to improve clarity.

    View attachment 2nd class lever.bmp

    View attachment 2nd class lever heel raise.bmp

    Time for a coffee!
  22. Hi Luke I see what you saying and I´m not sure to be honest.

    As the COM comes forward there must also be an increase in GRF under where the fulcrum is on your picture, there effect of this on the talocural joint I would only really be guessing as there is so many other joints between, so would energy be lost in creating compression, dorsiflexion-plantarflexion moment before it gets to the Talocural joint I´m guessing yes but not really sure.

    A simple heel lift that through patients know helps alot, but we still are not completly understanding the full reasons why..........
  23. pod29

    pod29 Active Member

    Hi Michael

    Think of it as a wheelbarrow. The closer the rocks (load) on the wheel barrow are to your hands, the more effort is required to lift it. If you shift all the rocks closer to the wheel (fulcrum), it will be a lot easier to lift. In our case the fulcrum is the Metarsal heads, the closer our centre of mass is to our mets, the easier it is to propel forward.

    I do agree that this is an overly simplistic model, and that depending on individual joint stiffness in the midfoot, energy will be lost along the way. As I said in my first post I think this is where foot orthoses may become effective, by increasing the dorsiflexion stiffness of these joints.

  24. Hi Luke I think were talking about different things. I get you point about the COM changing, but the GRF will also change due to the change in this COM. To every action there must be and equal and opposite reaction.

    And in you wheelbarrow example of the foot there will be some thing lifting the wheel and your hands becoming the fulcrum.
  25. Athol Thomson

    Athol Thomson Active Member

    Hi All,

    This could be just me talking rot so I am happy to be told so by others!

    I think heel lifts are case specific.

    So far the posts have considered the gastroc/soleus and achilles tendon in terms of concentric contraction or ankle plantarflexion at propulsion.

    However, the gastrocnemius works eccentrically to control the progression of the tibia over the foot during ankle joint dorsiflexion following contact.

    (An exploration of the function of the triceps surae during normal gait using functional electrical stimulation.
    STEWART Caroline ; POSTANS Neil ; SCHWARTZ Michael H. ; ROZUMALSKI Adam ; ROBERTS Andrew
    The results show very different actions for soleus (ankle plantarflexing/knee extending) and gastrocnemius (ankle dorsiflexing/knee flexing) in stance phase. The counterintuitive nature of the action of gastrocnemius suggests that further clinical and biomechanical investigation into this muscle's function is required. The actions of both muscles at the knee confirm published IAA predictions. Gait & posture ISSN 0966-6362
    Source / Source
    2007, vol. 26, no4, pp. 482-488 [7 page(s) (article)])

    This maybe one of the reasons eccentric loading has positive outcomes in achilles tendiopathy as a treatment option? (There is several other reasons as per Maffulli article attached below)

    A forefoot or midfoot runner will initially use eccentric contraction to lower the calcaneus to the suporting surface following forefoot contact and then control the forward progression of the tibia during subsequent ankle joint dorsiflexion. Is it possible that a heel lift simply decreases the duration of eccentric contraction required and therefore tendon loading in this case? If eccentric loading programmes have a beneficial effect on tenocytes and tendon or collagen remodelling during rehab. Could the eccentric not 'concentric' component be more destructive to the tendon during gait especially in an overuse scenario? (Similar to too much weight bearing exercise in bone remodelling)

    My biomechanist and physio friends keep telling me about fascial chains or slings and the spinal engine etc. So if the swing limb helps to generate propulsion via these so-called fascial interactions would this not in some degree aid the gastroc/soleus and achilles tendon during the concentric contraction and ankle joint plantarflexion at heel lift and propulsion? No studies to back thi up of course!

    Just some thoughts,
    Athol Thomson

    How do eccentric exercises work in tendinopathy?
    N. Maffulli1 and U. G. Longo2
    1Department of Trauma and Orthopaedic Surgery, University Hospital of North Staffordshire, Keele University School of Medicine, Stoke on Trent, UK and 2Department of Orthopaedic and Trauma Surgery, Campus Biomedico University, Rome, Italy

    Correspondence to: N. Maffulli, Department of Trauma and Orthopaedic Surgery, Keele University School of Medicine, Thornburrow Drive, Hartshill Stoke on Trent ST4 7QB, UK. E-mail: osa14@keele.ac.uk

    Painful tendon disorders are a major problem in competitive and recreational sports [1, 2]. Tendon injuries are difficult to manage, and current conservative and surgical management options have shown limited and often unpredictable success [3, 4]. Even when early diagnosis of Achilles tendinopathy is combined with appropriate and intensive management, rehabilitation can take several months.

    Conservative management options for tendinopathy of the main body of the Achilles tendon include modified rest, exercise, analgesics, injections, electrotherapy, identification and correction of possible intrinsic and extrinsic causes [4]. This abundance of management modalities has arisen from the lack of consensus as to the cause of tendinopathy [5–8].

    The lack of suitable evidence in support of a given management method does not necessarily imply that it is ineffective. Rather, there may be a lack of adequately powered studies to demonstrate its effectiveness [9].

    Mechanical conditioning can be used as a treatment for enhancing tendon healing [10]. Mechanotransduction is the process of a cell converting mechanical stimuli into biochemical signals. Cells able to sense the mechanical signals are described as being mechanosensitive. Tendon responds to mechanical forces by adapting its metabolism and structural and mechanical properties [11]. Tendons adapt to alterations in the mechanical load being applied by changing their structure and composition. The tenocytes in the tendon are responsible for its adaptive response, and respond to mechanical forces by altering their gene expression patterns, protein synthesis and cell phenotype [12], which can be used to aid the healing process.

    However, the duration, frequency, magnitude and type of mechanical stimulation applied to a tendon greatly affect the outcome of the loading regime. Therefore, the amount of loading necessary to improve and/or accelerate the healing process without causing damage to the healing tissue remains unclear [13, 14].

    There is some evidence that eccentric strengthening programmes may be effective in the management of tendinopathy of the main body of the Achilles tendon [15, 16]. Graded eccentric exercises regimen was proven to be effective in case–control studies and in prospective randomized control trials [15–19]. Stanish et al. [20] introduced the concept of eccentric training in the rehabilitation of tendon injuries in the mid-1980s, and Scandinavian authors popularized it [19] more than a decade later, with some important differences. Stanish et al. [20], for example, recommend that patients should perform the eccentric exercises with no pain, while Scandinavian authors [19] recommend pushing through pain. Though effective in Scandinavian population [17, 18], the results of eccentric exercises observed from other study groups [16, 21] are less convincing than those reported from Scandinavia, with only around 60% of good outcome after a regime of eccentric training both in athletic [15] and sedentary patients [16].

    The best evidence to date does demonstrate that eccentric exercise is likely a useful management for tendinopathy, but this evidence is currently insufficient to suggest it is superior or inferior to other forms of therapeutic exercise [21, 22].

    There is little consensus regarding which variables may influence the outcome of eccentric training, including whether training should be painful, home- vs clinic-based training, the speed of the exercise, the duration of eccentric training and the method of progression. Large randomized controlled trials that consider these parameters and include blinded assessors and extended follow-up periods are required. Three basic principles in an eccentric loading regime have been proposed:

    Length of tendon: if the tendon is pre-stretched, its resting length is increased, and there will be less strain on that tendon during movement.

    Load: by progressively increasing the load exerted on the tendon, there should be a resultant increase in inherent strength of the tendon.

    Speed: by increasing the speed of contraction, a greater force will be developed.

    However, the use of these modalities in the context of an eccentric rehabilitation programme requires confirmation.
    In this issue, Rees et al. [23] examine why eccentric loading should be successful as a therapeutic option for tendinopathy of the main body of the Achilles tendon. They propose that the pattern of tendon loading, with its force fluctuations, rather than the magnitude of the force, is responsible for the therapeutic benefit seen. This parallels evidence from bone remodelling. Although Rees and colleagues propose a potential mechanism for the mechanism for efficacy of eccentric loading [23], they do not provide a definitive explanation to the mechanisms of function of the eccentric exercises. A main problem in the field of tendinopathy is that we do not know where the pain originates from. Four types of nerve endings can normally be identified in tendons: Ruffini corpuscles; free nerve endings; Pacini corpuscles mainly at the tendon site; and the Golgi tendon organs mainly at the muscular site [24]. Classically, pain in tendinopathy has been attributed to inflammatory processes, but, as it has become evident that tendinopathies are not inflammatory conditions, that they present histological evidence of a failed healing response and that even the degenerative paradigm is not really applicable, recently the combination of mechanical and biochemical causes has become more attractive [25]. Microscopic tendon disruption with mechanical breakdown of collagen could theoretically explain the pain mechanism, but clinical and surgical observations challenge this view [25]. The biochemical model has become appealing, as many chemical irritants and neurotransmitters may generate pain in tendinopathy. High concentrations of the neurotransmitter glutamate have been found in patients with Achilles tendinopathy [26]. The tendons in these patients showed no signs of inflammation, as indicated by the normal prostaglandin E2 levels [26]. Substance P and chondroitin sulphate may also be involved in producing pain in tendinopathy [25].

    The commonest form of tendon healing is by scarring, which is inferior to healing by regeneration [27]. Tendons heal by going through inflammatory (1–7 days of injury), proliferative (7–21 days) and remodelling (3 weeks to 1 yr) phases. Despite collagen maturation and remodelling, tendons are biochemically and metabolically less active than bone and muscle [27, 28]. Fibroblasts synthesize collagen type III in the proliferative phase. This will be replaced gradually by collagen type I from day 12–14 with progressive increase in tensile strength [28]. It is still unclear how eccentric exercise may influence this process.

    In conclusion, Rees et al. [23] shed further light on the complex process of the mechanism of eccentric training. Musculoskeletal physicians should be aware of tendon healing processes to optimize their management options. Future research should aim to resolve optimal approaches to conservative management of Achilles tendinopathy. Even though the relevance of eccentric training to the conservative management of Achilles tendinopathy is understood, with accepted and well-recognized less convincing results than those reported from Scandinavia, studies regarding its mechanism are needed as a first step to understand and improve the current management regimens.

    Disclosure statement: The authors have declared no conflicts of interest.


    Ames PR, Longo UG, Denaro V, Maffulli N. Achilles tendon problems: not just an orthopaedic issue. Disabil Rehabil (2008) 6:1–5.
    Maffulli N, Ajis A, Longo UG, Denaro V. Chronic rupture of tendo Achillis. Foot Ankle Clin (2007) 12:583–96.[CrossRef][Medline]
    Longo UG, Ramamurthy C, Denaro V, Maffulli N. Minimally invasive stripping for chronic Achilles tendinopathy. Disabil Rehabil (2008) 19:1–5.
    Maffulli N, Longo UG. Conservative management for tendinopathy: is there enough scientific evidence? Rheumatology (2008) 47:390–1.[Free Full Text]
    Maffulli N, Longo UG, Franceschi F, Rabitti C, Denaro V. Movin and Bonar scores assess the same characteristics of tendon histology. Clin Orthop Relat Res (2008) 466:1605–11.[CrossRef][Web of Science][Medline]
    Longo UG, Franceschi F, Ruzzini L, et al. Characteristics at Haematoxylin and Eosin staining of ruptures of the long head of the biceps tendon. Br J Sports Med. Advance Access published December 10, 2007, doi: 10.1136/bjsm.2007.039016.
    Longo UG, Franceschi F, Ruzzini L, et al. Histopathology of the supraspinatus tendon in rotator cuff tears. Am J Sports Med (2008) 36:533–8.[Abstract/Free Full Text]
    Longo UG, Franceschi F, Ruzzini L, et al. Light microscopic histology of supraspinatus tendon ruptures. Knee Surg Sports Traumatol Arthrosc (2007) 15:1390–4.[CrossRef][Web of Science][Medline]
    Andres BM, Murrell GA. Treatment of tendinopathy: what works, what does not, and what is on the horizon. Clin Orthop Relat Res (2008) 466:1539–54.[CrossRef][Web of Science][Medline]
    Hampson K, Forsyth NR, El Haj A, Maffulli N. Tendon tissue engineering. In:. In: Topics in tissue engineering—Ashammakhi N, Reis R, Chiellini F, eds. (2008) 4:1–21.
    Wang JH. Mechanobiology of tendon. J Biomech (2006) 39:1563–82.[CrossRef][Web of Science][Medline]
    Wang QW, Chen ZL, Piao YJ. Mesenchymal stem cells differentiate into tenocytes by bone morphogenetic protein (BMP) 12 gene transfer. J Biosci Bioeng (2005) 100:418–22.[CrossRef][Web of Science][Medline]
    Steadman JR, Forster RS, Silferskiold JP. Rehabilitation of the knee. Clin Sports Med (1989) 8:605–27.[Web of Science][Medline]
    Zeichen J, van Griensven M, Bosch U. The proliferative response of isolated human tendon fibroblasts to cyclic biaxial mechanical strain. Am J Sports Med (2000) 28:888–92.[Abstract/Free Full Text]
    Maffulli N, Walley G, Sayana MK, Longo UG, Denaro V. Eccentric calf muscle training in athletic patients with Achilles tendinopathy. In: Disabil Rehabil. Advance access published 2008, doi: 10.1080/09638280701786427.
    Sayana MK, Maffulli N. Eccentric calf muscle training in non-athletic patients with Achilles tendinopathy. J Sci Med Sport (2007) 10:52–8.[CrossRef][Web of Science][Medline]
    Mafi N, Lorentzon R, Alfredson H. Superior short-term results with eccentric calf muscle training compared to concentric training in a randomized prospective multicenter study on patients with chronic Achilles tendinosis. Knee Surg Sports Traumatol Arthrosc (2001) 9:42–7.[CrossRef][Web of Science][Medline]
    Roos EM, Engstrom M, Lagerquist A, Soderberg B. Clinical improvement after 6 weeks of eccentric exercise in patients with mid-portion Achilles tendinopathy – a randomized trial with 1-year follow-up. Scand J Med Sci Sports (2004) 14:286–95.[CrossRef][Web of Science][Medline]
    Alfredson H, Pietila T, Jonsson P, Lorentzon R. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. Am J Sports Med (1998) 26:360–6.[Abstract/Free Full Text]
    Stanish WD, Rubinovich RM, Curwin S. Eccentric exercise in chronic tendinitis. Clin Orthop Relat Res (1986) 208:65–8.[Medline]
    Rompe JD, Nafe B, Furia JP, Maffulli N. Eccentric loading, shock-wave treatment, or a wait-and-see policy for tendinopathy of the main body of tendo Achillis: a randomized controlled trial. Am J Sports Med (2007) 35:374–83.[Abstract/Free Full Text]
    Silbernagel KG, Thomee R, Thomee P, Karlsson J. Eccentric overload training for patients with chronic Achilles tendon pain – a randomised controlled study with reliability testing of the evaluation methods. Scand J Med Sci Sports (2001) 11:197–206.[CrossRef][Web of Science][Medline]
    Rees JD, Lichtwark GA, Wolman RL, Wilson AM. The mechanism for efficacy of eccentric loading in Achilles tendon injury; an in vivo study in humans. Rheumatology (2008) 27. doi: 10.1093/rheumatology/ken262.
    Jozsa L, Balint J, Kannus P, Jarvinen M, Lehto M. Mechanoreceptors in human myotendinous junction. Muscle Nerve (1993) 16:453–7.[CrossRef][Web of Science][Medline]
    Khan KM, Cook JL, Maffulli N, Kannus P. Where is the pain coming from in tendinopathy? It may be biochemical, not only structural, in origin. Br J Sports Med (2000) 34:81–3.[Free Full Text]
    Alfredson H, Thorsen K, Lorentzon R. In situ microdialysis in tendon tissue: high levels of glutamate, but not prostaglandin E2 in chronic Achilles tendon pain. Knee Surg Sports Traumatol Arthrosc (1999) 7:378–81.[CrossRef][Web of Science][Medline]
    Leadbetter WB. Cell-matrix response in tendon injury. Clin Sports Med (1992) 11:533–78.[Web of Science][Medline]
    Kader D, Saxena A, Movin T, Maffulli N. Achilles tendinopathy: some aspects of basic science and clinical management. Br J Sports Med (2002) 36:239–49.[Abstract/Free Full Text]
    Accepted 14 July 2008
  26. Griff

    Griff Moderator

  27. Griff

    Griff Moderator


    Attached Files:

  28. How does a muscle lenghten without a contraction force from an agnostic muscle or forces provided by movement of joints that it crosses? For the Gastroc to be a dosiflexor and the Soleus a plantarflexor but the have the same insertion point what happens to the axis of the talocural joint seems to be some pretty funky conclusions being made?

    Or maybe its just me
  29. fatboy

    fatboy Active Member

  30. fatboy

    fatboy Active Member

    So to summarise for those of us less than genius level biomeachanics...

    if the achilles hurts, give it a heel raise. if that doesn't work refer them to someone else.
  31. Hi Simon I´m pretty sure I get the stj axis thing but what about the claims in the paper that Ian put forward that the Gastroc cause a Dorsiflexion moment at the talocural joint It makes no sense to me.

    I get eccentric contraction to slow motion of the Tibia, but a muscle can not push and thats what I´m confused about.
  32. Athol Thomson

    Athol Thomson Active Member

    I think the theory is that while the gastrocnemius eccentrically works to control the progression of the tibia at ankle dosiflexion it has an affect on knee flexion. With limb progression the COm moves forward in relation to the TCJ axis causing ankle dorsiflexion. The power to move forward is generated by the swing leg.

    So even though the muscle activity is eccentric there is a relative flexion of both the knee and the ankle........Possibly???

    Athol Thomson
  33. Here the abstract for those who don´t want to read the whole thing.

  34. Michael:

    The gastrocnemius (gastroc) muscle is definitely an ankle joint plantarflexor in open kinetic chain. However, since the gastroc is also a knee joint flexor, its function during closed kinetic chain is more complex. What these researchers did was to electrically stimulate the gastroc and saw that ankle joint dorsiflexion increased in 4 of 5 subjects. What this means was that the ankle joint dorsiflexion moment increased as a result of increased knee flexion since the body weight was now pushing the tibia harder forward at the knee which, in turn, increased ankle joint dorsiflexion moment. In other words, the increase in ankle joint plantarflexion moment from gastroc contraction pulling on the posterior calcaneus was less than the increase in ankle joint dorsiflexion moment from gastroc contraction that caused the knee to buckle, the tibia to be driven forward, thereby increasing ankle joint dorsiflexion. Whether this is physiological and not simply an experimental artifact of having an important stance phase muscle suddenly shocked by electricity and the individual's central nervous system responding with an unphysiologic response, still remains to be seen.

    I believe that if you look closely at the excellent forward dynamics research by Rick Neptune from over the years, it becomes very clear that the gastroc is an important plantarflexor of the ankle, not the ankle joint dorsiflexor that some authors have hypothesized.
  35. That not what it said in the absract read the line in red above this post. Two different actions of Gastroc and sol.

    It did not say the muscle was working when this action was occuring at this joint a totally different thing.

    Muscles will work to slow the rate of joint movement thru eccentric contraction, but this is not what they stated in the paper.
  36. Thank you Kevin I was starting to get Grumpy Ill go off and read with a smile on my face. They even won an award for that paper.
  37. Michael:

    The important, and very critical, part of this electrical stimulation research was that the researchers did not actually measure moments, they simply measured motion. For all we know, the Achilles tendon could have had increased tension in it when the gastroc was shocked, but it was overcome by the knee buckling force.

    It would much like researchers saying that when landing from a jump in a flexed knee position the gastrocnemius is "causing ankle joint dorsiflexion" without considering the effects of the mass of the body being decelerated by the muscles which resist knee flexion and resist ankle joint dorsiflexion. For all we know, the acceleration of the center of mass downward by the knee flexion caused by shocking the gastroc was the cause of ankle joint dorsiflexion in 4 of 5 subjects. In my experience of watching tens of thousands of people walk over the last quarter century, this would never occur in normal gait unless the patient suddenly experienced a very painful stimulus within their lower extremity that "caused their leg to give out". I think an electrical shock could be such a painful stimulus.
  38. That´s what I was trying to say in my post, but as usual you have explained it much more clearly. Except the bit about the electric shock and knee giving out I had not considered that. Thanks again Kevin.
  39. Please delete my Keyboard has gone mad.

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