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After copy & pasting 42 A4 pages from PA including sections of quoted articles, have I got it right,
If my pt wants to "burn fat" I get her to run on jelly rather than eat it,
but if a runner with stress #'s of the long bones of their leg wants advice I tell him to join the barefooters, preferably on concrete,
mark
if a runner with stress #'s of the long bones of their leg wants advice I tell him to join the barefooters, preferably on concrete,
mark
Hey Mark,
As Simon said we've been talking about this on the phone recently. Here's where I'm currently at with my understanding (courtesy of him):
The CNS will modulate the stiffness of the leg 'spring' (kleg) in tune with the surface stiffness (surface encompassing the ground, footwear and orthoses).
It does this to minimise any significant excursion of the Centre of Mass (CoM)
It is fair to assume that there may be a zone of optimal leg stiffness (Spooners ZOOLS) for a given individual performing a given activity. (Where performance is maximised, and injury risk is minimised - although it should be said that these 2 variables may essentially have differing kleg values)
Several factors can and will change the kleg (e.g. Foot type, running technique, running speed, change of surface stuffness etc)
Generally speaking the injury profile seen with increased stiffness will be bone injury, and with decreased stiffness will be soft tissue injury
As a rule - running on a stiffer surface, such as concrete, (or removing cushioned shoes) will result in the CNS modulating the kleg to become less stiff (more compliant). It seems intuitive therefore that this may be beneficial for those with bone injury (e.g. Tibial stress reactions).
However,
If a runner presents with exercise induced leg pain which turns out to be a stress fracture, our assumption is that there may have been an inability (or failure) of the CNS to effectively modify the leg stiffness, and therefore an approrpiate 'net stiffness' has not been achieved - in essence the leg is too stiff for the environment, and cannot change.
Therefore,
If we introduce cushioned footwear, or advise them to run on softer surfaces, we actually re-tune the net stiffness to be more appropriate. So we soften the surface to bring it in line with the kleg.
I rang Spooner about this as it was bothering me also. The above is what we all do clinically on a daily basis (and we know it works) but taking the leg stiffness concepts to the letter it immediately makes you assume that to lower leg stiffness we need to increase surface stiffness. I think the key here is whether or not the leg stiffness can be modulated by the CNS.
Hope that makes sense and reads ok - apologies if not - I'm typing it on my Blackberry whilst sitting in a conference.
The Following 6 Users Say Thank You to Ian G For This Useful Post:
Excellent summary mate! So how can we determine the ability (or inability) of the CNS to regulate leg stiffness?
Cheers
If there is lower limb overuse injury, this might be an indicator. Another method might be to look at metabolic cost. I think the key may lie in identifying left / right asymmetries in leg stiffness. Early days. If only I had a well equipped lab to play in........
If there is lower limb overuse injury, this might be an indicator. Another method might be to look at metabolic cost. I think the key may lie in identifying left / right asymmetries in leg stiffness. Early days. If only I had a well equipped lab to play in........
Lower limb injury could be an indicator, but you might suggest that the horse has already bolted? left/right asymmetries seem like a good place to start in a clinical setting.
In a lab setting... How about if we could manipuate the CNS / spinal reflexes in some way in order to determine if/where there is some "breakdown" in stiffness regulation? Maybe by using a nerve block? I've also seen 90Hz vibration used successfully to manipulate stretch reflex responses in the gastroc-soleus during running. Could we use techniques like this to manipulate the pathway?
Lower limb injury could be an indicator, but you might suggest that the horse has already bolted? left/right asymmetries seem like a good place to start in a clinical setting.
In a lab setting... How about if we could manipuate the CNS / spinal reflexes in some way in order to determine if/where there is some "breakdown" in stiffness regulation? Maybe by using a nerve block? I've also seen 90Hz vibration used successfully to manipulate stretch reflex responses in the gastroc-soleus during running. Could we use techniques like this to manipulate the pathway?
I think breakdown in stiffness regulation can be due to far simpler factors like joint ROM. The CNS can be functioning just fine, but if the range of motion isn't available...
Are you familiar with the work on Soleus H-reflex stimulation and the phase of gait dependent motor responses which have been obtained? I talked about these studies some years ago on here and on the old Podiatry Mailbase- see if you can find them. If not I'll have a look later.
It does this to minimise any significant excursion of the Centre of Mass (CoM)
Not necessarily minimise the excursion, more to maintain a constant displacement cycle. Also, its about minimising eye shake too.
Quote:
Originally Posted by Ian G
If a runner presents with exercise induced leg pain which turns out to be a stress fracture, our assumption is that there may have been an inability (or failure) of the CNS to effectively modify the leg stiffness, and therefore an approrpiate 'net stiffness' has not been achieved - in essence the leg is too stiff for the environment, and cannot change.
Therefore,
If we introduce cushioned footwear, or advise them to run on softer surfaces, we actually re-tune the net stiffness to be more appropriate. So we soften the surface to bring it in line with the kleg.
To reiterate, injury occurs because the leg has failed to successfully modulate stiffness to meet the environmental demands and in attempting to maintain a fairly constant net system stiffness (Knet= Kleg + Ksurface) the leg has been outside of it's Zone Of Optimal Leg Stiffness (ZOOLS). In this situation we can either: match the Kleg to the Ksurf by altering stride parameters, or we can match the Ksurf to the Kleg by altering the surface stiffness; or both.
Something like that.
BTW this is really just an extension of Niggs preferred movement pathway paradigm- I'm just saying it's the movement path of the CoM which is key and this is what the locomotor apparatus is trying to maintain in the face of variation in terrain.
BTW this is really just an extension of Niggs preferred movement pathway paradigm- I'm just saying it's the movement path of the CoM which is key and this is what the locomotor apparatus is trying to maintain in the face of variation in terrain.
After reading this stiffness thread, there seems to be a lot of theorizing going on, with little research evidence to back up the theory. As you all know, I enjoy theorizing also, but I'm not so certain I can agree with all of the statements that have been made so far.
First of all, I'm not so sure that the key for the body is to maintain its CoM in a certain path as Simon says above. Rather I believe that the main driving force is for the body to minimize metabolic energy for running over a given surface stiffness by changing the kinetics and kinematics of the lower extremity, which will, in turn, cause the CoM to move in a certain prescribed path. In other words, is the driving force to change leg stiffness when encountering surfaces of different stiffnesses while running to make the CoM move in a certain path or is the driving force to change leg stiffness when encountering surfaces of different stiffnesses while running to optimize metabolic efficiency of running?
I vote that the central nervous system chooses the most metabolically efficient leg stiffness for each surface of different running stiffness rather than choosing the leg stiffness that will make the CoM move a certain path.
Secondly, in Ian's posting, he alludes to the theory that "Generally speaking the injury profile seen with increased stiffness will be bone injury, and with decreased stiffness will be soft tissue injury". Do we have any evidence for this generalization, or is this pure speculation? It seems, to me, to be a gross over-simplification, just as the barefoot runners like to focus on impact shock as the cause of all running injuries, to only focus on leg stiffness variations causing injury. What happened to such injury mechanisms such as increased magnitudes of subtalar pronation moments, increased tibial bending moments due to eccentric bending loads on the tibia, etc when you are discussing your hypothesis that increased stiffness causes bone injury and decreased stiffness causes soft tissue injury?
Third, how do we measure or evaluate leg stiffness in our practices or whether our patients are properly altering their leg stiffness for the different surfaces they are running on? How do we use this theory that leg stiffness may be important in injury production to better treat our patients or to improve our patient's running performance? And finally, do we have any good research evidence that high leg stiffness in a runner causes any more or different injuries than in a runner that has low leg stiffness?
Just some thoughts that popped out when I read some of the interesting statements made on this thread.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
First of all, I'm not so sure that the key for the body is to maintain its CoM in a certain path as Simon says above. Rather I believe that the main driving force is for the body to minimize metabolic energy for running over a given surface stiffness by changing the kinetics and kinematics of the lower extremity, which will, in turn, cause the CoM to move in a certain prescribed path. In other words, is the driving force to change leg stiffness when encountering surfaces of different stiffnesses while running to make the CoM move in a certain path or is the driving force to change leg stiffness when encountering surfaces of different stiffnesses while running to optimize metabolic efficiency of running?
I vote that the central nervous system chooses the most metabolically efficient leg stiffness for each surface of different running stiffness rather than choosing the leg stiffness that will make the CoM move a certain path.
Kevin, no disagreement from me. And as the CoM pathway and the metabolic cost are so obviously linked then I believe we are just saying the same thing in a different way. The specific CoM movement pathway I spoke about above which the body wants to maintain, is the CoM movement pathway which is most metabolically efficient for the given locomotor task. See also the work of Gordon: http://www-personal.umich.edu/~artku...rdonPoster.pdf and the .pdf attached; Ortega http://jap.physiology.org/content/99/6/2099.long etc
This is the reason I corrected Ian: it's not about minimising the excursion of the centre of mass (as this will actually increase metabolic cost), it's about maintaining a steady, metabolically optimised, CoM displacement cycle for a given locomotor task. Viz. the preferred movement pathway for the CoM.
However, things like pain avoidance may also trigger a change in the CoM pathway. But again, a steady state cycle would seem desirable.
Quote:
Originally Posted by Kevin Kirby
Secondly, in Ian's posting, he alludes to the theory that "Generally speaking the injury profile seen with increased stiffness will be bone injury, and with decreased stiffness will be soft tissue injury". Do we have any evidence for this generalization, or is this pure speculation? It seems, to me, to be a gross over-simplification, just as the barefoot runners like to focus on impact shock as the cause of all running injuries, to only focus on leg stiffness variations causing injury. What happened to such injury mechanisms such as increased magnitudes of subtalar pronation moments, increased tibial bending moments due to eccentric bending loads on the tibia, etc when you are discussing your hypothesis that increased stiffness causes bone injury and decreased stiffness causes soft tissue injury?
Third, how do we measure or evaluate leg stiffness in our practices or whether our patients are properly altering their leg stiffness for the different surfaces they are running on? How do we use this theory that leg stiffness may be important in injury production to better treat our patients or to improve our patient's running performance?
Clinically, Daryl Phillips F-scan module is probably the best way to determine leg stiffness without a force plate. I use a treadmill and camera and look at contact times and step frequency- it's crude, but gives a rough idea/ estimate. Failing that, a single leg hopping test. As I intimated previously, I tend to look for left to right asymmetries see http://www.ncbi.nlm.nih.gov/pubmed/22117105 and obviously the presence of pathology. In terms of treatment I use the information to modify stride parameters and orthoses stiffness characteristics. Early days as I said.
Quote:
Originally Posted by Kevin Kirby
And finally, do we have any good research evidence that high leg stiffness in a runner causes any more or different injuries than in a runner that has low leg stiffness?
Kevin, no disagreement from me. And as the CoM pathway and the metabolic cost are so obviously linked then I believe we are just saying the same thing in a different way. The specific CoM movement pathway I spoke about above which the body wants to maintain, is the CoM movement pathway which is most metabolically efficient for the given locomotor task. See also the work of Gordon: http://www-personal.umich.edu/~artku...rdonPoster.pdf and the .pdf attached; Ortega http://jap.physiology.org/content/99/6/2099.long etc
This is the reason I corrected Ian: it's not about minimising the excursion of the centre of mass (as this will actually increase metabolic cost), it's about maintaining a steady, metabolically optimised, CoM displacement cycle for a given locomotor task. Viz. the preferred movement pathway for the CoM. However, things like pain avoidance may also trigger a change in the CoM pathway. But again, a steady state cycle would seem desirable.
That sounds better now. I believe it is important to remember that the central nervous system (CNS) is driving the near instantaneous changes in leg stiffness that are occurring during running in different shoes and different surfaces. In fact, as far as we know currently, the key driving factors behind why the CNS chooses a certain kinematic pattern of running is to reduce the metabolic cost of running and to avoid pain and injury during running, not to make the center of mass move in a certain path during running.
However, I am not so convinced by the paper provided that we can be so certain that lower stiffness lower extremities will always tend to develop soft tissue injuries and higher stiffness lower extremities will always tend to develop bony injuries. Again, I think those that truly believe this are placing way too much emphasis on lower extremity stiffness during running as the key factor in running injury production.
For example, what if I have a high school female distance runner who is just beginning to run longer distances, has relatively low leg stiffness and then develops a tibial or metatarsal stress fracture more due to their low bone density and narrow diameter bones (i.e. decreased moment area of inertia) than due to whether their legs were more or less stiff.
I have seen countless stress fractures in the metatarsals and tibias in young female runners much more so than in their male counterparts. And, typically, the male runners have much more stiff legs than do their female counterparts, but have far fewer stress fractures (stiffness being determined by how little time the runners feet spend on the ground for a given running speed).
Certainly, lower extremity stiffness is one factor to consider and it is fun to talk about and theorize about. However, I am not convinced that it is the most important or even in one of the most important factors that tend to produce injuries in runners from what I have seen in the 27 years I have been treating injuries in runners.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
If we introduce cushioned footwear, or advise them to run on softer surfaces, we actually re-tune the net stiffness to be more appropriate. So we soften the surface to bring it in line with the kleg.
The key is to match the leg stiffness to the surface stiffness so that they share the same resonant frequency. That way the transfer between kinetic and potential energy of the leg and the surface stay in phase. That way the surface isn't trying to transfer kinetic energy into the leg when the leg is trying to lose its kinetic energy to the surface. Too much energy in a tissue = tissue injury. This is what Tom Mcmahon realised.
The key is to match the leg stiffness to the surface stiffness so that they share the same resonant frequency. That way the transfer between kinetic and potential energy of the leg and the surface stay in phase. That way the surface isn't trying to transfer kinetic energy into the leg when the leg is trying to lose its kinetic energy to the surface. Too much energy in a tissue = tissue injury. This is what Tom Mcmahon realised.
Energy is the new stiffness this season.
This is a great post Simon!
Energy storage seems to be important with respect to connective tissue regeneration and repair.
A bit off topic so you might respond with a so?
A book I have been reading about connective tissue regeneration says something along the lines of;
The mechanism in which elastic energy is stored in connective tissue during locomotion brings about fibroblast stimulation in these tissues that directly effects gene expression and the regulation of cellular protein synthesis at the extracellular matrix.(via process called mechnochemical transduction).
A link to the book is below with a nice summary on page 40:
Energy storage seems to be important with respect to connective tissue regeneration and repair.
A bit off topic so you might respond with a so?
A book I have been reading about connective tissue regeneration says something along the lines of;
The mechanism in which elastic energy is stored in connective tissue during locomotion brings about fibroblast stimulation in these tissues that directly effects gene expression and the regulation of cellular protein synthesis at the extracellular matrix.(via process called mechnochemical transduction).
So? Seriously, explain your thinking Mr Thomson...
So? Seriously, explain your thinking Mr Thomson...
Again from the book.....I wish I could say it was my thoughts.
Forces generated by muscle are stored as elastic strain energy during tendon deformation, then transferred to bone to allow for joint movement.
Some of this energy goes into moving the joint and some of the energy is transduced into cellular changes via a process called Mechanochemical transduction.
This dictates how cellular activity will respond to the forces and ultimately lead to changes in the mechanical properties and composition of the connective tissue.
Stored energy drives mechanochemical transduction during locomotion so I was thinking that leg stiffness/surface stiffness will have a part to play. Especially when the practitioner is attempting to accelerate connective tissue repair after injury. Maybe as the patient returns to straight line running.
After copy & pasting 42 A4 pages from PA including sections of quoted articles, have I got it right,
If my pt wants to "burn fat" I get her to run on jelly rather than eat it,
but if a runner with stress #'s of the long bones of their leg wants advice I tell him to join the barefooters, preferably on concrete,
mark
Btw what the kerdock paper showed was that if you want to burn more calories you should run on a hard surface.
Ian and Simon thank you, I was completely lost on the previous stiffness threads and your posts really cleared it up for me. Epiphany moment!
__________________
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." - Orville Wright
Ian and Simon thank you, I was completely lost on the previous stiffness threads and your posts really cleared it up for me.
Agreed- nice summary. Saves reading the whole other thread again...
So...
How does foot function have in influence?
Does the stiffness of the foot help modulate total leg stiffness directly?
Or does the stiffness of the foot have an influence on how effectively extrinsic muscles can regulate stiffness?
Interesting stuff.
__________________
Craig Tanner
Podiatrist ASPETAR-
Qatar Orthopaedic and Sports Medicine Hospital
Doha
QATAR http://www.aspetar.com/
Agreed- nice summary. Saves reading the whole other thread again...
So...
How does foot function have in influence?
Does the stiffness of the foot help modulate total leg stiffness directly?
Or does the stiffness of the foot have an influence on how effectively extrinsic muscles can regulate stiffness?
Interesting stuff.
Yes, the foot will be a spring in the series of springs ( muscles) which make up the lower extremity, and if the effectiveness of one spring is reduced that `load`must be taken up by the other springs to maintain kleg , so we have individual muscle stiffness added together to give us net lower extremity stiffness or Kleg. Measuring muscle stiffness
All of the theroy behind this is based around Hookes law - Hooks law
Agreed- nice summary. Saves reading the whole other thread again...
So...
How does foot function have in influence?
Does the stiffness of the foot help modulate total leg stiffness directly?
Or does the stiffness of the foot have an influence on how effectively extrinsic muscles can regulate stiffness?
Interesting stuff.
Craig, I've attached this paper for you (I'm trying to avoid turning this into an attachment fest has occurred with the leg stiffness thread).
Robbin, precisely. Which is why Janda's muscle imbalance theory may be significant.
I'll come back to Kevin's post a little later when I find time.
Is there an app for the I-phone that would allow it to be used as a Accelerometer?
If so, could we assess vertical and possibly horizontal displacement over, for example, the duration of a run?
Could we then compare initial in-shoe pressure measurements e.g a force/time curve verses the same measures at the end of the run.
Would an change in CoM correlate to increase foot pressures and consequently an decrease in the body to regulate stiffness?
Is there an app for the I-phone that would allow it to be used as a Accelerometer?
If so, could we assess vertical and possibly horizontal displacement over, for example, the duration of a run?
Could we then compare initial in-shoe pressure measurements e.g a force/time curve verses the same measures at the end of the run.
Would an change in CoM correlate to increase foot pressures and consequently an decrease in the body to regulate stiffness?
Stiffness
Hybrid Mode
