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[log in to unmask]" type="cite">Kevin,

If shoes with heels increases  resupination, I would think this would mean that the center of mass is being moved anteriorly, decreasing the stress on the Achilles and thereby decreasing the moments to lower the arch (and thereby allowing for resupination). A simpler way to look at this, and I always look at things simply, is the heel of the shoe is negating the equinus. Also isn't late stance pronation more a finding of FnHL? You confused me with the last sentence. How does STJ supination make the dorsal and plantar thickness of the foot increase?

Regards,

Stanley


Kevin Kirby wrote:

Stanley and Colleagues:

The foot may resupinate at the STJ in late midstance but not commonly during barefoot walking, more commonly in shoes with heels.  If STJ supination occurs, then this would tend to stiffen the midfoot/midtarsal joint due to the increased dorsal and plantar thickness of the foot.

Sincerely,
 
Kevin
 
****************************************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
 
Private Practice:
107 Scripps Drive, Suite 200
Sacramento, CA  95825  USA
 
Voice:  (916) 925-8111     Fax:  (916) 925-8136
****************************************************************************


Stanley Beekman wrote:

Kevin,

I replied in/ Blue and italics and slightly larger. /

Kevin Kirby wrote:

Stanley and Colleagues:

Stanley wrote:

<<You propose an interesting theory, but some things are not that clear.

I think you are saying that when the midfoot and midtarsal joints (LisFranc's and Choparts joints) are not loaded (dorsiflexed),  the metatarsals are allowed to dorsiflex. When the midfoot and midtarsal joints are loaded, the joints are "locked" due to joint compression forces,and the metatarsals cannot dorsiflex further.>>

Kevin replies:

That is not exactly what I said.  First of all, definitions are in order.  When I say "midtarsal joint" I mean the combination of the talo-navicular joint and calcaneo-cuboid joints.  When I say "midfoot joints" I mean the combination of the naviculo-cuneiform joints and LisFranc's joint (i.e. cuneiform-metatarsal joints and cuboid-metatarsal joints).Dorsiflexion of the forefoot on the rearfoot (i.e. including the midfoot and midtarsal joints) will tend to elongate the passive tensile load-bearing elements of the plantar foot.  These passive tensile load-bearing elements of the plantar foot include the plantar ligaments (too numerous to name) and the plantar aponeurosis (i.e. medial, central and lateral components).  Upon progressive elongation of these structures, they will exert a progressive increase in tensile force on their origins and insertions on the osseous structures of the plantar foot. As the elongation of these passive tensile load-bearing elements increase, their tensile force also increases since they are now being elongated further along their respective stress-strain curves.  The increase in tensile force in these passive tensile load-bearing elements will not only cause an increase in dorsiflexion stiffness of the forefoot as a whole relative to the rearfoot, but will also cause an increase in dorsiflexion stiffness of each of the individual metatarsal rays.

Here is where I disagree specifically with your above statement.  First of all, loading of the midfoot and midtarsal joints can not occur passively without these tensile load-bearing elements also increasing their tensile loading forces.  As the passive tensile load-bearing elements increase their tensile forces, their reaction forces on their origins and insertions on the plantar osseous structures will cause a reactive increase joint compression forces.  If all these passive tensile load-bearing elements are sectioned or cut, loading of the midfoot and midtarsal joints can not occur with loading of the metatarsal heads by ground reaction force (GRF) except by contractile activity of the extrinsic muscles of the plantar foot including the posterior tibial, flexor digitorum longus, flexor hallucis longus and peroneus longus and the little plantar intrinsics.

I/_'m sorry I oversimplified what you are trying to say. I understood about the plantar ligaments counteracting the pull of the dorsiflexion of the metatarsals, and the combined force is increased joint compression forces (As I statedfurther in the posting) Your key statement was: _/ _*because the midfoot and midtarsal joints have increased  resultant interosseous compression forces, the joints will be more stiff to forefoot dorsiflexion moments*_"
_/Since you stated the cause and effect, I followed suit in my summarizing of your theory./_

Secondly, the joints are definitely not "locked" and the metatarsals can always dorsiflex further with sufficient magnitudes of GRF acting on the forefoot.  The longitudinal arch of the foot is more like a leaf-spring that can always flatten further if sufficient loads are placed on it.  The longitudinal arch does not "lock" and is not like a ratcheting mechanism that "locks" at intermediate steps in its rotation about its axis. 

/I used the term locked in parentheses to show it was not an exact term. I am familiar with the spring formula(F=KX) You said:/
*the forefoot as a whole will tend to resist any further increases in forefoot dorsiflexion with further increases in forefoot dorsiflexion moments caused by increasing GRF
*/This is a relative "locking", as it is more than just a linear spring effect. By the way "lock" is not an absolute term. If you "lock" your car, it doesn't mean it cannot be stolen, just more difficult (in a more than linear function//)  /:)*
*

A ratcheting mechanism of the longitudinal arch would not be advantageous for our body since it would prevent the foot being able to deform smoothly with increasing loads.  The longitudinal arch is a variable stiffness leaf spring that becomes stiffer under increasing loads and becomes more compliant under decreasing loads

/Variable springs will change their stiffness with changes in displacement not loads. It is true that an increased load will cause an increased displacement that will result in an increase in stiffness, but if we are talking about a moment in time (ds/dt s being stiffness and t being time), then you would be inaccurate./

so that sudden increases in GRF on the plantar foot are not transmitted as sudden vertical accelerations into the tibia and human locomotor apparatus (i.e. otherwise known as shock).

Stanley continues:

<<What confuses me is
You are proposing that GRF will increase joint compression. Wouldn't GRF cause dorsiflexion which is matched (as this dorsiflexion progresses) by the resistance of the plantar ligaments, the combined vector being compression? If this is the case, and the ligaments are passive, then wouldn't it be dorsiflexion that causes "locking"?
Since dorsiflexion is a component of pronation, aren't you really saying that pronation of the midtarsal joint is causing locking of the foot?>>

Kevin replies:

Again, I wouldn't say "locking", I would say "stiffening".  Since the midtarsal joints are not necessarily pronation-supination axes, then we can no longer accurately use that terminology of "midtarsal joint pronation" or "midtarsal joint supination" to describe the kinematics of the midtarsal joint.

Stanley continues:

<<As far as the Triceps surae and the force it puts on the forefoot, doesn't the foot act as a second class lever (the Achilles tendon being on one side, the fulcrum (1ST MPJ) on the other side, and the weight in the middle)? Isn't the weight (center of gravity) over the fulcrum (1ST MPJ) at the moment the calcaneus comes off the ground which causes 0 tension in the Achilles as a result of the superimposed body weight [Obviously, in equinus this does not occur, as the center of gravity is pulled posteriorly by the tension in the Achilles tendon. (unless there is compensation for the equinus which brings the center of gravity anteriorly)]?

Could you clear up my confusion?>>

Kevin replies:

I prefer to use the combination of the GRF vector relative to the center of mass (CoM) to discuss these types of concepts since it is more accurate and less confusing.  When the calcaneus comes off the ground the Achilles tendon is at it's peak tensile force ( Erdimir A, Hamel AJ, Fauth AR, Piazza SJ, Sharkey NA:  Dynamic loading of the plantar aponeurosis in walking.  JBJS, 86A:546-552, 2004), not at zero.

_/I said it would be 0 as a result of superimposed body weight. The additional force would be related to propulsive forces accelerating the body. I am not familiar with the article, but it would not be relevant if there was an equinus in the subjects. /_

By the way, Achilles tendon tension does not "pull the center of gravity posteriorly" but it does decelerate the anterior movement of the CoM body when the CoM is posterior to the forefoot by increasing GRF on the forefoot. 

_/I guess my terminology is not accurate as I am not an engineer, but pulling would decelerate something, and if something is decelerated it would be tardy getting to where it should be. That should make it posterior if it is decelerating something going anteriorly, shouldn't it? Also isn't position the first derivative of velocity, so isn't it really the same thing?/_

However, if the triceps surae increase GRF on the forefoot when the CoM is anterior to the forefoot, this will accelerate the anterior movement of the CoM during walking.  Therefore, unless you know the precise location of the CoM relative to the point of action and line of action of the GRF vector, then you can not possibly know its exact effect on the CoM of the body.

_/I thought we were talking from early stance phase to late stance phase, so the Center of Mass is posterior to the forefoot. If the calcaneus  is not raising up, then the force would have to cause a deceleration of the center of mass, so the center of mass would be posterior to where it should be barring compensations.

Kevin, I have one more question. You talk about the dorsiflexion of the forefoot on the rearfoot from early stance to late stance. Doesn't the foot resupinate at the subtalar joint during this time which results in the arch raising (I didn't use the term supinating or pronating of the midtarsal joint), which would result in the metatarsals plantar flexing relative to the rearfoot?

I am still confused!

Regards,

Stanley
/_

Good discussion!!
Sincerely,
 
Kevin
 
****************************************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
 
Private Practice:
107 Scripps Drive, Suite 200
Sacramento, CA  95825  USA
 
Voice:  (916) 925-8111     Fax:  (916) 925-8136
****************************************************************************


Stanley Beekman wrote:

Kevin,

You propose an interesting theory, but some things are not that clear.

I think you are saying that when the midfoot and midtarsal joints (LisFranc's and Choparts joints) are not loaded (dorsiflexed),  the metatarsals are allowed to dorsiflex. When the midfoot and midtarsal joints are loaded, the joints are "locked" due to joint compression forces,and the metatarsals cannot dorsiflex further.

What confuses me is
You are proposing that GRF will increase joint compression. Wouldn't GRF cause dorsiflexion which is matched (as this dorsiflexion progresses) by the resistance of the plantar ligaments, the combined vector being compression? If this is the case, and the ligaments are passive, then wouldn't it be dorsiflexion that causes "locking"?
Since dorsiflexion is a component of pronation, aren't you really saying that pronation of the midtarsal joint is causing locking of the foot?

As far as the Triceps surae and the force it puts on the forefoot, doesn't the foot act as a second class lever (the Achilles tendon being on one side, the fulcrum (1ST MPJ) on the other side, and the weight in the middle)? Isn't the weight (center of gravity) over the fulcrum (1ST MPJ) at the moment the calcaneus comes off the ground which causes 0 tension in the Achilles as a result of the superimposed body weight [Obviously, in equinus this does not occur, as the center of gravity is pulled posteriorly by the tension in the Achilles tendon. (unless there is compensation for the equinus which brings the center of gravity anteriorly)]?

Could you clear up my confusion?

Stanley


Kevin Kirby wrote:

The point I was trying to make was that the rotational position of the subtalar joint (i.e. if the STJ is supinated, pronated, neutral or in a position somewhere between these values) is not the only factor that determines the natural ability of the foot to be a mobile adapter (i.e. be more compliant) in early stance phase and a rigid lever (i.e. to be more stiff) in late stance phase.  The natural arrangement of the two most powerful muscles of the leg, the gastrocnemius and soleus muscles, attaching to the calcaneus via the Achilles tendon posterior to the ankle joint combined with their ability to cause large ankle joint plantarflexion moments with their contractile activity will tend to cause progressively increasing GRF plantar to the forefoot as midstance progresses.  The GRF plantar to the forefoot caused by the increasing contractile activity of the posteriorly located gastrocnemius and soleus will cause a natural increase in tension of the passive tensile load-bearing elements of the plantar foot and longitudinal arch (i.e. plantar ligaments and plantar aponeurosis) as these tensile load-bearing elements are progressively elongated by the resultant dorsiflexion of the forefoot on the rearfoot [caused by GRF on the forefoot].
With low GRF loads on the plantar forefoot in early stance phase, the passive tensile load-bearing elements of the plantar arch are placed under less tension and because the midfoot and midtarsal joints have less resultant interosseous compression forces, the joints will be more compliant to forefoot dorsiflexion moments (i.e. the individual metatarsal rays will be able to move more easily relative to each other to accommodate for uneven ground surfaces).  However, with high GRF loads on the plantar forefoot in late stance phase, the passive tensile load-bearing elements of the plantar arch are placed under increased tensile loads and because the midfoot and midtarsal joints have increased  resultant interosseous compression forces, the joints will be more stiff to forefoot dorsiflexion moments (i.e. the individual metatarsal rays will be able to move less easily relative to each other to accommodate for uneven ground surfaces and the forefoot as a whole will tend to resist any further increases in forefoot dorsiflexion with further increases in forefoot dorsiflexion moments caused by increasing GRF).

This passive midtarsal/midfoot stiffening effect can be demonstrated not only with a cadaver foot, without any muscular action available, but can also be demonstrated with the wooden models of the foot that I have demonstrated at previous PFOLA workshops.  This passive midtarsal/midfoot stiffening mechanism will occur regardless of whether the foot undergoes normal STJ rotational motions or the STJ  is maximally pronated throughout stance phase.  And finally, the passive midtarsal/midfoot stiffening mechanism is of great importance for the human species in that it allows us to greatly improve our ability to avoid injury, to walk on uneven surfaces and, possibly most importantly, improves our bipedal locomotor efficiency by allowing us to expend a minimum amount of muscular effort for longitudinal arch support or longitudinal arch stiffening during walking activities.  This passive midtarsal/midfoot stiffening mechanism will be one of the topics of my lecture or workshop at the PFOLA meeting in November in San Diego this year.

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