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Gastrocnemius: supinator or pronator?

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

  1. Andrew Bull

    Andrew Bull Member

    Edit. more medially positioned axis.
  2. Lateral Gastroc resistance sounds like what are describing is supination resistance.

    The higher the pronatory forces the higher the supination resistance

    In feet with extremely medial STJ axis and with a high amount of Navicular drop. The talus position changes which affecteds the talo-cural joint. I believe affected the ability of the tibia to move past 90 degrees without heel lift.

    Add a medial skiv/wedge under the heel and I see the tibia able to move past 90degrees. The force required to dorsiflex the ankle is reduced in these feet the less medial the STJ axis is
  3. efuller

    efuller MVP

    Another explanation of your observation is that the weight bearing motion of supination causes dorsiflexion of the ankle. This is known looking at radiographs of the foot with the STJ pronated and STJ relatively supinated.

    The tendon excursion (distance the tendon travels) is dependent on the lever arm the tendon has on the joint. The Achilles has a much larger lever arm on the ankle joint as compared to the STJ. So, a small amount of dorsiflexion of the ankle (with STJ supination) could be the cause of the increase in tension in the gastroc muscle.

    What did you think of my explanation of why the lateral head of the gasroc should make it a better supinator of the STJ than the medial head?

    An alternate explanation to yours is with the equinus shifts the weight to the forefoot. (heel not touching floor). In most feet the location of the STJ axis is much farther medial to the forefoot than it is to the heel. This increases the leverage that ground reaction force has to cause a pronation moment at the STJ. I believe it is this increased pronation moment from the ground that resists supination of the STJ in the position that you described.

    The Achilles tendon is a direct supinator of the STJ (most of the time) and a direct plantar flexor of the ankle. It has much better leverage at the ankle than it does at the STJ. So, when the Achilles plantar flexes the ankle, it make the ground pronate the STJ harder (with greater moment) than the direct effect the tendon has to supinate the STJ. You add the moments from both sources and the bigger one wins. This is how an equinus deformity can create pronation of the STJ, even though the tendon is a direct supinator of the STJ.

  4. Andrew Bull

    Andrew Bull Member

    Hey Eric and Mike,
    Agree with the medial STJ axis placement, but my observations of walking to running gait seem to contradict what you are proposing:

    There's also the latest research about the achilles having three tightly bound separate "bundles acting independently". Four if plantaris is included. This is seeming to suggest independent function. Eric: If this theory proves correct, then possibly the lateral gastroc has more pull on the lateral achilles and more of a pronatory effect in plantarflexion, and resistance to supination in dorsiflexion? And hence the medial gastroc having more pull on the medial achilles? Ask an athlete to stand on tip toes in maximum plantarflexion, then move into inversion and eversion of the calc in this position (shift from weight on 1st to weight outside 5th). Watch the lateral and medial gastrocs work very differently. Palpate in these positions and feel how much their rigidity changes in inversion and eversion of the calc. They really don't seem to work together at all.

    We see a lot of patients who have a relatively vertical RCSP, and this looks fine in midstance when walking, then completely bottoms out when running (usually due to ligament laxity- not weakness as it happens in extremely strong and fit athletes, who obviously don't have a medially deviated STJ axis. Frequently a midfoot flex or "Second Ankle Sydnrome" is prominent running when negligible walking. (I went to a prominent PA members lecture a while ago who stated he didn't bother filming patients running because it didn't change his prescription. I was flabbergasted.)

    Patients walking have an everted calc in swing due to tight calves and increased dorsiflexion required. Tibialis mms unable to resupinate easily against laterals. Yet in running the same patient with increased ground clearance ( and less dorsiflexion of ankle required for ground clearance) has no issue inverting the calc in swing phase.

    You keep mentioning supination resistance. By what? Is it neural? Fascial? If it is only peroneals then why does a bent knee supinated foot calf stretch offer little resistance for a patient and then they say their discomfort doubles ( and point directly at their lateral gastrocnemius) to straighten the knee with a supinated calf stretch? Not sure how it could be anything other than lateral gastroc? How could the lateral gastroc be considered a supinator when supinating makes the laterals tighter? Bend the knee and pain disappears so unlikely to be peroneals. They also find it a whole lot easier to supinate with a bent knee.

    And patients who are having issues with an orthotic then do this straight supinated knee calf stretch suddenly find their orthotics far more comfortable and effective- without sticking heel raises on.

    Most importantly, ligament laxity frequently causes this chain of tightness and events. I have plenty of high end sports patients who are not weak, do not have a medially deviated STJ axis and still pronate badly due to ligament laxity that everyone else calls hypermobility, but apparently we can't. You could apply the same logic to achilles/gastroc range ( pronated/supinated/STJ position/ankle position/midfoot collapse). Can't measure consistently so doesn't exist.

    Have you tried the stretch? Nobody has said YES yet....... Seriously, with most problem feet it's a game changer. Remove the pronation accelerator and every structure trying to decelerate pronation doesn't have to work as hard.
  5. efuller

    efuller MVP

    I am skeptical of that research. When I was at the California College of Podiatric Medicine, I did a fair amount of cadaver work. That included looking at Achilles tendons. If different portions of the tendon are sliding relative to each other, then you should be able to see some evidence of that. For example, you would expect to see a bursa between those fibers. True if you cut partially across the tendon you can create some sliding, but it's not easy. Yes, the lateral gastroc, may have more pull on the lateral side of the Achilles, but that pull on the lateral side of the Achilles still creates a direct supination moment. Why do you think that pull from the lateral gastroc will cause pronation? The way to figure out the moment created by a tendon is to look at the line of action of force relative to the axis in question.

    Where the position of the foot sits, in swing, is a subconscious choice of the central nervous system. It is dependent on the relative activation and tension in muscles. I disagree with the idea that the calcaneus is everted in swing because of tight calves. Try this experiment, non weight bearing contract gastroc and soleus and plantarflex your ankle. You can quite easily supinate and pronate your STJ while there is tension in the Achilles tendon. This tells us that the Achilles is not a very strong direct supinator or pronator of the STJ because much smaller muscles are able to overcome the moments created by the Achilles at the STJ.

    On the other hand, you have to relax the muscles attached to the Achilles for the anterior tibial muscle to have any effect at the ankle. You can maximally contrct your anterior tibial muscle and dorsiflex your ankle, non weight bear, and easily supinate and pronate your STJ. So the anterior tibial muscle doesn't have as much leverage at the STJ as the other muscles.

    So, the CNS chooses (subconsciously) the position of the STJ in swing.

    Supinating the STJ raises the arch and this creates dorsiflexion at the ankle and this will make the Achilles tighter. This is an alternate explanation to your observation of the muscle becoming tighter.

    Supination resistance is a test done with the foot in relaxed stance. The hand is placed in the medial arch and an upward force is applied. Some feet supinate easily with the applied force and some feet resist this force and don't supinate. The amount of resistance has been correlated with STJ axis position. More medially deviated STJ axis feet tend to have a higher resistance to supination. Or to explain that mechancially, there is a higher pronation moment from the ground in feet with a more medially deviated STJ axis foot.

  6. Andrew Bull

    Andrew Bull Member

    Thanks Eric

    Think we're just going to have to agree to disagree on this.

    Firstly, you are Dorsiflexing not plantarflexing the ankle to clear the ground in swing phase. This brings the tight laterals into play against the tibialis mms. This is why the same patient will evert in walking but invert running because they don't need to dorsiflex as much when running because of increased ground clearance and less dorsiflexion required.

    Next, not sure how a lateral muscle (gastrocs) pulling on a lateral calcaneus could do anything other than increase lateral pull and tip calcaneus into eversion not inversion. Patients with tight calves nearly always evert unless they have a severely lateral STJ axis/ rigid cavus foot type.

    Some patients have such ridiculously tight gastrocs that their Achilles is in some tension in resting stance. It's normally more gastroc than soleus because they can touch heels to floor when they bend their knees as we both know.

    We've also seen patients have an immediate reduction in supination resistance after 5 minutes of lateral gastroc stretches. This would be an interesting study to do. Get a bunch of patients with tight calves and measure their supination resistance with Craig Paynes device then again after a month of lateral gastroc and lateral soleus calf board stretches.

    Have you tried that stretch yet? You haven't mentioned it in several posts.

    We've discussed the medially deviated STJ axis enough and agree that it increases supination resistance, logically (I use the "shift the pivot" on a see-saw analogy with patients) .

    This is not the only thing causing supination resistance, but increases it.
    It's chicken and egg: Your foot pronates more and faster due to ligament laxity and/or a medically deviated STJ axis, and everything above this getting used to this pronated position. Since childhood your muscles get used to this pronated foot position, then your tight pronation accelerating muscles want your floor to pronates, and with velocity.

    "It's not falling that kills you, it's the sudden stop at the end"

    Pronation velocity has long been considered a bigger problem than how much.

    Every part of the body that gets used to a foot being in a more pronated position, (and isn't stretched frequently) will tighten to this position and act as a pronation accelerator, including the lateral gastrocs. These act like a whip on the foot, big toe being the tip of the whip (sesamoiditis, FHL)

    Have you tried that stretch yet?

    Sticking any orthotic under a foot with hip rotators, lateral hamstrings and calf muscles and personals that want to accelerate pronation is "pissing into the wind" . If you don't address the tightness of the antagonists, it won't work.

    Have you tried that stretch yet?

    Supination resistance = (sometimes, but not always) medially deviated STJ axis + every tight muscle, tendon, nerve, fascia that is used to a pronated foot position, probably since childhood and has never been stretched because the foot is never in an inverted, dorsiflexed position with a straight knee unless you specifically do this stretch. Try it on a patient. Some can't even straighten their knees in an inverted dorsiflexed position.

    I think lax ligaments (which we can't call hypermobility even though everyone else does) is frequently confused for medially deviated STJ, especially if the foot collapses through a weak spring ligament.

    Have you tried that stretch yet? Works better on a calf board for accuracy and compliance from patients.

    Apologies for typos: On phone and old man eyes!

    Last edited: Jul 13, 2018 at 4:13 AM
  7. Andrew Bull

    Andrew Bull Member

  8. Andrew Bull

    Andrew Bull Member

  9. efuller

    efuller MVP

    I believe you are replying to my example of the ability to pronate and supinate the STJ even though the Achilles has tension in it. My example was to non weight bearing forcibly contract the muscles attached to the Achilles tendon and then attempt to pronate and supinate the STJ. It can be done easily.
    There is no difference between the plantar flexed position and the dorsiflexed position of the ankle. The laterals are "tight" in both positions. The muscle belly shortens when it contracts and there is tension in the tendon, even though the ankle is plantar flexed.

    So, the position of the foot in swing is determined by the relative activation of the peroneals and the tibialis posterior muscle.

    Take a teeter totter and and attach two ropes on the same side of the fulcrum, one rope farther from the fulcrum than the other. Upward pull on both ropes will cause the same direction of motion. What do you think is the fulcrum for the subtalar joint? It's the subtalar joint axis. The Lateral muscles still attach to the medial side of the axis and an upward pull will still cause STJ supination.

    I agree that knee flexion can increase ankle dorsiflexion.

    Are you saying that if you walk around pronated, you will never be able to relax your peroneal muscles?

    Have you read Talliard's article on Sinus tarsi syndrome. The activity of the peroneals decreases in sinus tarsi syndrome. The peroneals are relaxed in a pronated foot.

    When the foot "collapses" there is often further abduction of the forefoot on the rearfoot and this will make the STJ axis more medial as the Axis is determined by the facets of the talocalcaneal joint. You should measure the position of the stj axis in the position the foot is in at rest. So, a foot with lax ligaments will tend to have a more medially deviated STJ axis.

    I'm still not accepting the idea that tight lateral structures cause eversion. Yes, active contraction of the peroneal muscles will cause eversion, but they just don't stay tight all the time (whether or not they are stretched)


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