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Gastrocnemius: supinator or pronator?

Discussion in 'Biomechanics, Sports and Foot orthoses' started by Simon Spooner, Aug 29, 2008.


  1. Members do not see these Ads. Sign Up.
    Something to consider over the weekend? I found this while looking into the effects of heel lifts on ankle plantarflexor moment in the biomechanical explanation thread

    "Both the lateral gastrocnemius and peroneals are muscles that help eversion of the
    heel."

    Paula D. Henderson, Dr. Stephen J. Piazza: A Biomechanical Evaluation of Standing in High- Heeled Shoes. http://www.gradsch.psu.edu/diversity/mcnair_jrnl/files/25_henderson.pdf

    How can the lateral head of the gastrocnemius be an evertor and presumably by its exclusion, the medial head is then considered to be an invertor, when the muscles action is through the achilles tendon insertion? The achilles position relative to the STJ axis should determine whether the force generated by the muscle results in supination or pronation moment. When I went to school the gastroc/ soleus complex was an invertor except in grossly medially deviated STJ axes. Since these guys were looking at high heel shoes that should have supinated the foot and therefore translated the STJ axis laterally, how does the lateral head act as an evertor?

    Anyone?
     
    Last edited: Aug 30, 2008
  2. admin

    admin Administrator Staff Member

    From the thread on Biomechanical Explanation/Advice needed :
     
  3. admin

    admin Administrator Staff Member

    For completeness, here is the rest from the other thread:
     
  4. efuller

    efuller MVP

    To address the topic of the thread: Achilles tendon supinator or pronator of the STJ.

    The Achilles tendon has a much longer lever arm at the Ankle joint as compared to the STJ. Tension in the tendon will create simultaneous moments at both joints. The plantar flexion moment at the ankle will shift the center of pressure more anterior "faster" than it will shift it laterally. The STJ axis, most of the time is oblique to the foot and an anterior shift of the center of pressure will put the center of pressure more lateral to the location of the STJ axis in the standing foot. So, the anterior shift in the center of pressure, in many feet, will create a greater pronation moment from ground reaction force than the direct supination effect of the tendon about the STJ.

    This does not really address the heel lift question though.

    Cheers,

    Eric Fuller
     
  5. Thanks Eric, I take your point. Why would this relate to the lateral head of gastrocnemius greater than the medial head? Also of note is the lateral shift in orientation of the STJ axis that should occur with supination which should counter this effect.
     
  6. efuller

    efuller MVP

    Hi Simon,

    I agree about the medial/lateral head question. I think it was you that mentioned line of action of force and it's not that much different. It's not different enough to change from supination moment to pronation moment for most feet.

    On the position of the STJ axis shifting with STJ motion. I would agree that it would be important for some feet, but I'm guessing those feet would be rare. I'm trying to recall the range of internal leg/talus rotation seen in gait. It's much smaller than the whole of the range of motion available. So, I maintain that amount of internal rotation motion is small compared to the range of positional variation across people. The change in rotational position that can be achieved with a device under the foot is very small compared to the positional variation across people. Someone who has a medially deviated STJ axis, will not have their axis shift to a position of lateral deviation with a device under the foot.

    So, I'm saying that the positional change with STJ motion is not as important as the amount of medial or lateral position of the STJ axis when assessed in stance.

    Cheers,

    Eric
     
  7. In order to understand the mechanical effect of contractile activity of the gastrocnemius-soleus complex (GSC), one must understand that while the direct effect of the GSC on the subtalar joint (STJ) is to cause a STJ supination moment (due to the medial location of the Achilles tendon relative to the STJ axis), the indirect effect of GSC contractile activity is to increase the ground reaction force (GRF) plantar to the forefoot. This increase in GRF on the plantar forefoot may either cause a STJ supination moment or a STJ pronation moment, depending on the spatial location of the STJ axis and the location of the GRF vectors on the structures of the plantar forefoot. In other words, the internal STJ supination moment exerted by the GSC is always accompanied by a change in external STJ moment due to changes in GRF acting on the plantar foot.

    This mechanical fact explains how the GSC can either cause STJ pronation or STJ supination. Alterations in STJ axis location, in both the rearfoot and forefoot, will have a huge impact on the overall mechanical effect of GSC contractile activity on STJ moments. This is another one of the benefits of gaining a better comprehension of foot function by making an effort to understand the STJ axis location/rotational equilibrium theory of foot function.
     
  8. Got that. but why just the lateral head?
     
  9. Atlas

    Atlas Well-Known Member


    Put your hands on achilles tendon pathology. On some (not most) you will find thickening on the lateral side of the tendon. Whether this is the sheath or paratendon etc..., I don't know. But if the lateral side of the achilles tendon is less supple, thicker, tighter etc..., it follows that the lateral gastroc MAY exert more of an influence than theoretical knowledge suggests.

    IMO, the gastro-soleal role in biomechanics (other than sagittal plane) has been grossly overrated by the podiatry profession for years.


    Ron
    Physiotherapist & Podiatrist
     
  10. Not quite clear on that one either, Simon. Maybe I'll e-mail Steve Piazza to ask him. However, it is cool to see our Marionette system finally being used for some weightbearing STJ axis research.
     
  11. fatboy

    fatboy Active Member

    I've been trying to find the evidence for the 30 -150 degree rotation of the achilles tendon and this book states:

    http://books.google.co.uk/books?id=...onepage&q=the achilles tendon rotates&f=false

    "during their descent the fibres internally rotate... so the inital posterior surface of the soleus attaches on the medial aspect... and the gastrocnemius attaches on the lateral aspect"

    maybe it's the rotation of the achilles tendon fibres that cause the problem.

    A laterally 'attached' tendon (to the Sub-talar joint) would provide an eversion / pronation moment?!

    how you would test the rotation of the achilles clinically in patients i have no idea.

    i wonder if it's too late to take up a career that doesn't make my brain ache, or should i go back to the way i was taught and just add a 2 degree varus rearfoot post to everything.
     
  12. Don't know about the rotation of the fibres being the reason why lateral head of gastroc. should be a pronator. However, I do know that during running the achilles is a "spring", so having spiral orientation of it's fibres makes absolute sense. See Alexanders work.
     
  13. The spiral arrangement of Achilles tendon fibers is the standard anatomical configuration of the Achilles tendon. How many ropes have you seen that are arranged with their fibers parallel and straight, with no braiding or spiral arrangement?

    Achilles tendinitis so commonly occurs probably because of the huge loads this tendon is forced to bear (it is the largest tendon of the body) and the relative lack of blood flow to the narrow section of the Achilles tendon about 3-6 cm superior to the calcaneus.

    To give an approximate estimate of Achilles tendon tensile force, simply multiply the magnitude of ground reaction force acting under the forefoot at late midstance/propulsion by a factor of two, and that will give you a good estimate of the tensile forces within the Achilles tendon. So in running, for a 180 pound individual that is pushing off the ground with 1.5 times body weight of force at the forefoot just before heel off, the Achilles tendon is likely subjected to approximately 500 pounds of force. The force will increase within the Achilles tendon with faster running speeds and increased body mass.

    Now, go find a rope and subject it to a series of sudden 500 pound tugs for 95 times every minute for an hour. You will now have subjected the rope to the equivalent loading forces that the Achilles tendon in subjected to during a 60 minute run. Therefore, it isn't exactly rocket science understanding why Achilles tendon injuries occur. The amazing thing is trying to understand why Achilles tendon injuries don't occur more frequently!!
     
  14. fatboy

    fatboy Active Member

    You've just re-affirmed all the reasons i don't run... and i was about 12 yrs old when i was last 180lbs. :D

    Another factor in achilles tendinopathy is the increase in plantarflexion when having to walk / run uphill.
     
  15. Plantarflexion or dorsiflexion uphill?

    Kevin, I am interested in braids versus spirals- are the fibres braided, i.e. plaited at that level of microscopy- woven between each other, or spiralled around each other?
     
  16. Simon:

    Collagen fibrils are wavy, or "crimped", and then straightened out under lower loads thus creating the "toe-portion" of the stress-strain curve. The organization of the collagen fibrils, to fibers, to primary fiber bundle (subfascicle), to secondary fiber bundle (fascicle), to tertiary fiber bundle to tendon is generally a parallel fiber arrangement. To my knowledge, no tendon is braided and only the Achilles tendon has a spiral arrangement of all the tendons in the human body. Fascinating to imagine why that is, isn't it?:drinks
     

    Attached Files:

  17. fatboy

    fatboy Active Member

    Plantarflexion, as the foot is more dorsiflexed when going uphill.

    it was either that that caused my achilles 'sprain', or trying to run up the Great Orm in flip-flops...
     
  18. How does spiralling influence the biomechanical properties of the tendon?
     
  19. I would love to see what these authors had to say about it.
     
  20. Kent

    Kent Active Member

    There is still some debate as to whether or not the mid-portion is an area of relative avascularity. Different authors have implicated the origin, the mid-portion and the insertion as all being areas of relative avascularity over the years. I've attached a nice review paper on the anatomy and vascularisation of the Achilles tendon. It also describes the spiral arrangement of the tendon.

    Cheers,
    Kent
     

    Attached Files:

  21. I´m guessing that you would like to see the whole paper ?

    Here for your reading pleasure.
     

    Attached Files:

  22. I´m not sure who has read the full paper that Kevin suggested.
    I posted it above.

    It got me thinking, Could the reason that people get overuse injuries of the Achilles be more related to the amount of torsion of the achilles rather that length etc.

    So the people who don´t get this overuse activity are people who have a good balance between achilles torsion and load.

    and by fitting a heel lift we are increasing the amount of torsion of the achilles? but then if that is so, why does eccentric training have +ve effects ? Same thing in reverse ?

    and then if that is correct is it possible to utrasound the achilles to be able too measure the amount of torsion ?
    If it can it may be a way to determine which treatment path would have the best result.

    ie pt low torsion - heel lift
    pt high torsion- stretching and eccentric training

    Kind of asking questions/thinking out loud
    But not shouting out load
     
  23. fatboy

    fatboy Active Member

    *prepares to get shot down in flames*

    Doesn't the heel raise ease the torsion?

    I haven't read the new paper you have kindly posted; but if the TA rotates internally up to 90 degres and you lift the heel, won't the calcanues invert and 'unwind' therfore reducing the torsion?

    and wouldn't the eccentric loading help prepare the TA for the increase in load from a lengthened position, mimicking the action when the knee is flexed during walking?

    Now i am off to read the paper.
     
  24. I´m not sure I see the Achilles as a spring in my head so the more we push with our heel lift the tighter the coil, but I could be wrong. Hopefully those with more knowledge can set us straight.

    EDIT I am seeing it as a spring now with all the reading Ive done in the last few weeks, and I think Simon mention the spring in energy return which is probably where I got the idea from I guess
     
  25. Attached Files:

  26. Found this in my travels talks about the catapult effect of the Achilles rather than an spring. Thought it might be of interst ?
     

    Attached Files:

  27. BrentD

    BrentD Welcome New Poster

    I don't know whether I am allowed to dig up an almost five-year old, but as far as I am concerned still very exciting, thread to reformulate the question asked by Simon, the OP, but: is the the jury still out regarding the relative LG/MG activity with inversion/eversion moments? The spiral arrangement of Achilles' tendon fibers could explain this by the twist of some of the fibers and the attachment on opposite aspects of the calcaneus. But on the other hand, from an evolutionary point of view, it would more or less defeat the obvious function of a rotating Achilles' tendon, which is to equalize the asymmetry between eversion and inversion shearing forces... or would it not?

    But, either way, it would contradict the quote brought up by Simon Spooner that:

    "Both the lateral gastrocnemius and peroneals are muscles that help eversion of the heel."

    I, too, was taught (as I suspect we all were, here) that the gastrocnemius as a whole acts as a supinator exclusively (period!) But whatever the truth, I suppose that, given the structure, the movement about the inversion/eversion axis would be insignificant "except in grossly medially deviated STJ axes", as Simon puts it.

    I have never read any paper on differential activation of LG vs MG secondarily to eversion/inversion stance patterns (at least since those appalling magazines, thirty years ago, which used to "teach" an unsuspecting crowd of kids like myself that hand and foot spacing had an influence on biceps and quadriceps recruitment and "turning the toes out" (sic!) would "work out the inner calf". But, of course, those weren't peer-reviewed... :D )

    But more seriously: any new insight on this topic?
     
  28. Andrew Bull

    Andrew Bull Member


    Hi,

    Agree with Simon Spooner.

    Been searching the web like crazy but haven't been able to find much on this topic. Most sites/papers lump lateral and medial gastrocs into the same action.

    I'm a clinician (27yrs mostly sports), not really an academic, but here's my 2 cents worth. Suggestions appreciated.

    Apologies for being so late to the party, but I've been lecturing on this a lot for the last 2 years.

    The role of hypermobility in a lot of foot problems is understated I think. At last years SMA Conference in Langkawi, I didn't hear anyone say "hypermobility" once ( and not just syndromes like Ehlers-Danlos, as a mild amount can still wreck feet). It's ridiculously common in females, asians, indians, polynesians and apparently africans but I haven't treated many. Simon Bartold's research a few year back showed how for females it becomes more pronounced with oestrogen levels at times and how that affects ligament and tendon elasticity.

    I spoke with John Orchard a long time ago when consulting to the Swans and we discussed how it was the "flexible" ( but probably just more hypermobile) athletes who usually got injured more, not the ones who couldn't touch their toes.

    I'm pretty convinced the lateral and medial heads of gastrocs work quite differently and the lateral head everts the calc/pronates the foot ( in a normal foot structure) and is responsible for a whole lot of secondary problems through the entire foot, and frequently this lateral gastroc tightness is secondary to hypermobility in the feet. This lateral gastroc tightness is probably why so many people don't tolerate an effective orthotic, leading to heel raises or "placebo-thotics" being prescribed (soft eva/2mm poly etc).

    You can frequently see the foot everted in the swing phase as the antagonists (especially TA and TP, but effectively anything that wants to dorsiflex the foot/toes) struggle to resupinate the foot before strike, and sometimes they are so tight in the lateral gastroc and soleus they will land in an everted position, possibly leading to a shock related problem in a pronated foot type due to an increase rate of pronation and decreased time of pronation, plus a smashed 1+2 in propulsion ( plus sesamoiditis, p.fasciitis, medial calc. nerve pinch, lis franc strains,FHL,HAV etc) because of early heel lift.

    Effectively, if you're hypermobile and you have over-pronated feet, your muscles get use to pronating, then they force you to pronate with velocity. It's like a whip crack effect and your lateral calves, lateral hamstrings, hip interal rotators and hip flexors are all trying to "whip crack" the foot into pronation.... and fight against an orthotic block.


    A quick stretch we've been teaching patients for years with a lot of success is a minor variation on the gastroc stretch. Basically, lean against wall on elbows, feet parallel, hips centred (don't twist pelvis, or drop to side), front knee bent, back knee straight, SUPINATE THE BACK FOOT/TUCK HALLUX DOWN and PUSH THE BACK HEEL DOWN HARD ON FLOOR. The problem with this stretch is the 5% compliance rate.

    This stretch doesn't fix hypermobility and as soon as the patient stops it they immediately begin to lose range, because if the foot can bend in the middle it will. Then the calves, especially laterals start to tighten again. We stress that PART A = Stretch, PART B = orthotics if needed. If they don't want to do these stretches we tell them orthotics are a waste of money. .....Getting brutal in my old age......

    An easier way ( that reduces cheating and makes it easier with a visual prompt when the patient sees it!) is to stand on a calf stretch board ( 25ish degrees) with your back against a wall, feet parallel and positioned so heels"just" touch the board. Then supinate both feet. Watch the patients eyes light up and frequently heels lift off the board if they're not a regular stretcher ( yoga, pilates).

    Most hypermobile patients ( and others with tight calves/standing jobs) struggle to keep their heels on the floor (even Wallabies, Sevens players, especially polynesians due to hypermobility being extremely common) as their feet will flex in the middle which we call "second ankle syndrome". If you get down while these patients do this lateral gastroc stretch you can frequently slide your finger (or even fist for one Wallaby!) under their calcaneus.

    You can also frequently see a calloused styloid process as this becomes the "heel " mid-way through propulsion. Another sign is a sharp palpation along the dorsal cuboid/4/5 joint line due to this midfoot bind and dorsal impingement. sometimes pain along lateral met shafts from " springboarding" in early lift.

    I strongly believe this lack of lateral gastroc range due to/combined with second ankle syndrome frequently explains most cuboid friction and binding problems and a vast majority of mid and forefoot problems.

    Hope this isn't too random/rant. Had two coffees!

    Happy to discuss.

    Cheers,

    Andy Bull
    Sydney Sports Podiatry
     
  29. Hi Andrew.

    Couple of thoughts. Latest research is indicating that there us 3 separate tendons within the Achilles throw in the plantaris and we have 4. We know through Jill Cooks work that these separate tendon bundles will be active at different times.

    The Achilles rather than being a spring like structure it acts more like a catapult.

    Terms like hyper mobile and hyper pronation should never be used, ever. By using them we must have a normal and a scientific and repeatable method of measuring, we don't.

    N=1 every individual will have there own physiological window. If you get pushed out of the physiological window at the higher end of loads you will get breakdown of tissue due to loads.

    The idea that individuals with lower soft tissue stiffness are more likely to get injured playing AFL is interesting
     
  30. Andrew Bull

    Andrew Bull Member

    Thanks Mike, I'll check out Jill's work.

    Will have to admit that not using the term hyper-mobile is bizarre, but I understand your scientific reasoning about hard to measure. So what do we call hyper-mobility syndromes now? It exists even though you can't measure it accurately, and it's the main reason most of our patients have over-pronation related injuries.

    I had a hyper-mobile ultra runner just leave. He runs about 100km per week and is certainly not weak, and yet he has pronation related problems due to something I can't call hyper-mobility due to ligament laxity anymore?

    So am I correct in saying a patient has lower soft tissue stiffness causing an increased joint range of motion? Seems same-same.

    I'm also pretty sure Dr Tim Hewett used the term hyper-pronation as part of the mechanism of non-contact ACL rupture in his SMA lecture in 2016.

    On another note, was chatting to an orthopod who used to be a physio a few years ago about most of our patients having a degree of ligament laxity and he mentioned how many patients with ligament laxity also had cartilage that didn't stick very well to their joints.
     
  31. Same same but different

    By discussing force ie how much force to move a object we get more accurate info that leads to better orthotic prescription or orthotic dosing .
     
  32. Andrew Bull

    Andrew Bull Member

    Hi Mike,

    I think we are talking essentially about the same thing. We discuss loads/10% increase rule in training/technique/ cross training/surface/shoes/gradients etc

    Where I was heading is that many patients have always overpronated due to lax ligaments since childhood, so their muscles get used to over-pronating ( resulting in the tight lateral gastrocs) and then force the foot to pronate with velocity, overloading everything trying to decelerate pronation.

    Do you have any links to Jill Cook's work on the multiple bundles of the achilles to soleus/latera/ gastroc/medial gastroc and plantaris please? I've been searching but can't find.

    thanks in advance
     
  33. Andrew Jill Cook' s wrote about Achilles compression we discussed it here I will see if I can find the thread.

    Maybe we are talking the same thing but terminology is important .

    You keep saying over Or hyper there are no such things it is the key to treating patients imho. N=1 what causes tissue breakdown in one will not always in another
     
  34. Andrew Bull

    Andrew Bull Member

    Thanks Mike. Interesting links.

    Agree about tissue breakdown and strength and

    The question I have then is what do you call increased joint range of motion due to increased ligament laxity. There is no doubt in my mind that patients with ligament laxity are far more likely to have problems from running sports than those with tight ligaments.

    What do you call hypermobility syndromes like Ehlers Danlos? People who have it still call it hypermobility, as does every study I've read by prominent researchers.

    I question that just because you can't measure it, doesn't mean it doesn't exist.

    One of the main causes of calf group tightness ( especially lateral gastrocs) is increased mobility in the midfoot due to what I apparently can't call hyper-mobility anymore. Most of these patients get at least a 6/9 Beighton's test score.

    So what should we call it?

    P.S: Have you tried that stretch yet?
     
  35. efuller

    efuller MVP

    Are you familiar with subtalar joint rotational equilibrium theory? It may be able to better explain what you are seeing. For example, a foot with a lot of eversion available, may or may not, have a very stiff end of range of motion. However, this eversion will move the foot lateral to the STJ axis and this will increase the pronation moment from the ground. In other words, the ground will pronate the foot with the more medially positioned axis (relative to the foot) harder than a foot with its STJ axis in an average position.
     
  36. efuller

    efuller MVP

    I agree with a lot of what you said. However, I have to disagree with the lateral and medial heads of the gastroc having a markedly different effect. The way you can tell what a muscle does is look at the line of action of force relative the joint axis in question. If you look in the sagittal plane you can obviously see that pull from the Achilles is upward on the posterior aspect of the calcaneus and this line of action obviously causes a plantar flexion moment at the ankle joint. To visualize the three dimensional relationship between the line of pull of the Achilles and the subtalar joint axis it is easiest to look in the transverse plane. In the transverse plane the pull of the achilles, when looking from above is directly toward you. For most feet, the pull of the Achilles will be medial to the STJ axis and cause a direct supination moment. Now, back to the frontal plane and look at the difference in line of pull of the medial head versus lateral head of gastroc. The line of action of the lateral head would point farther from the STJ axis than the medial head. Not by much, but if anything the lateral head will be a better supinator than the medial head.

    Eric
     
  37. Andrew Bull

    Andrew Bull Member

    Hi Eric,
    Yes, very aware of the STJ axis and also it's effect on creating functional ligament laxity/forefoot supinatus and high load to the tibialis muscles and FHL.

    Here's a quick stretch that I mentioned earlier that I think shows the lateral gastroc, having tightness secondary to a pronated foot type, due to a lateral axis or ligamentous laxity, will act as a pronation accelerator, as do the lateral hamstrings ( and frequently hip flexors and internal rotators) for the same reason:

    Place 25 degree calf incline/decline board in the incline position from wall
    Stand on board with 7/10 discomfort and feet parallel, knees straight (full gastroc stretch), heels JUST touching board, bum and back on wall.
    Feel calf stretch pain in resting dorsiflexion
    SUPINATE both feet in this position ( tuck toes under) and feel lateral gastroc light up and patients eyes light up.

    I'm a logical person. It seems clear that if it hurts more to supinate the feet with a straight knee, then the lateral gastroc's have a pronation increasing/accelerating moment and are far more of an antagonist to the tibialis muscles in a straight or almost straight knee position (i.e: walking and running) than the peroneals usually would. We've noticed for years that patients with tight lateral gastrocs frequently have significant eversion of the calcaneus during swing and on contact as their tibialis muscles can't fight a tight lateral gastroc, yet after two weeks of this stretch can easily resupinate and land with a mild calcaneal inversion allowing a longer time in pronation and a more effective windlass.

    Watch his everted calcaneal position just before contact. His shins weren't weak, but weren't strong enough to fight his pronation accelerating lateral gastrocs. You can also see his feet fold in the middle with early heel lift while the styloid becomes a "second heel" through propulsion. We see a lot of cuboid dorsal impingements at the cuboid/4/5 that is incorrectly called cuboid/peroneal friction syndrome I believe ( and occasionally 4/5 met shaft stress).

    Cool link here but can't post until 10 posts apparently to prevent spam. youtube dot com/watch?v=Tw_EilN4u54

    We've found that unless the lateral gastroc is specifically targeted with this stretch, orthotics can be "pissing into the wind". This leads to many contemporary's prescribing super-flexy "placebo-thotics" that do very little, or just adding heel lifts, which makes the problems worse long term and the patient unable to go without orthotics with an even worse equinus.

    These patients need to do this stretch for the rest of their life because as soon as they stop, they start losing lateral gastroc range, because if their feet can fold in the middle, they will, and their calves will become tighter.

    As I mentioned earlier, one polynesian Wallaby had such severe second ankle syndrome (midfoot flex) that during his straight knee calf stretch, I could put my entire fist underneath his heel when his styloid was still comfortably on the floor. He couldn't even get his heels to the ground at 90 degrees dorsiflexion in a straight knee stretch. He certainly couldn't supinate in this position ( lateral gastroc resistance) This is not uncommon.

    Your thoughts?
     
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