Does the Stance Leg Push or Does the Swing Leg Pull?

Bruce,

I hope things are OK for you.
Your point of view will be missed.

Regards,

Stanley

 

Eric,
Thanks for the incredible insights you bring to this discussion.
Regarding figure 8, please look the title associated with this. I took the liberty of accentuating the key point of this:
“Fig. 8. Mean electromyograph vs. applied external force relative to normal walking for the medial gastrocnemius and the soleus during the THIRD QUARTER OF STANCE. Values are means ± SD. *P < 0.01. P < 0.0001 from normal walking”.

What exactly are the plantar flexors doing at this time? I figured the Neptune article would be a good place to look. Neptune shows that stance is 60% of the gait cycle (see fig 1 page 1389) therefore the third quarter would be 30%-45% of the gait cycle.
Neptune says ”Both SOL and GAS provided trunk vertical support throughout single-leg stance and pre-swing (Fig. 4). Since the trunk is moving downward from mid single leg stance through pre-swing as SOL and GAS act to accelerate the trunk upward, these muscles decelerate the trunk and cause trunk power in the vertical direction to be negative (Fig. 5: 30–55% gait cycle, dashed lines are negative). (2nd paragraph under results page 1391)
So these muscles are decelerating the body and therefore acting eccentrically at this time. Eccentric contractions are the most efficient, and the body tries to function efficiently. The muscle power is decelerating the body and storing this as spring energy in the tendons. (The idea of storing the decelerating energy and using it later for acceleration is the principle in Hybrid cars).
Remember that the Neptune model is just that, a model. Unless you model correctly, the results will not be accurate. His model had to have some push off to take the place of the spring of the tendons. (http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=4415).

Gottschall says:
“Ground reaction force. The GRF and impulse results established the biomechanical effects of our external force devices. The external force devices affected both braking and propulsive horizontal GRF peaks and impulses compared with normal walking (Fig. 3B). Compared with normal walking, with 3% ESA only, the braking force peak increased by an insignificant 8% (P = 0.29), whereas the propulsive peak decreased by 17% (P = 0.0005). Thus the ESA alone inadvertently aided forward propulsion, and we accounted for this aiding force by incorporating the AHF device. The AHF alone caused the horizontal braking forces to increase by 92% and the propulsive forces to decrease to just 28% of normal. When we combined the 10% AHF and the 3% ESA, the braking force increased by 95% and the propulsive force decreased to 31% of the values for normal walking. Thus the similarity of the changes of these horizontal GRF variables allowed us to fairly compare the differences in metabolic cost and muscle activity between AHF only with AHF and ESA combined conditions.” (First paragraph under results)

The horizontal ground reactive force with the ESA confirms that the swing leg can provide propulsion. When the AHF is applied, it appears that the body is trying to slow down by increasing braking forces and decreasing propulsion forces. I don’t see where the article mentions the timing of the horizontal ground reactive force in relation to the gastroc activity. Where did you see it?

Regards,

Stanley

 

The question comes down to how long conditioning lasts. It could also be related to how well the person remembers what motions hurt. Have you ever injured yourself and in your convalescent phase forgotten you were injured and tried to move only to be reminded by the pain that you were injured. This is analogous to what we are talking about here.

Ok, it may not be pain, but some other efferent mechanism.

I chuckle at the "inadvertent" statement. They were intentionally altering the gait. The brain has to alter muscle output to remain balanced with the strings attached. From this statement you could conclude that there was forward propulsion during normal walking without the ESA and the ESA removed it. This evidence is backed up by the decrease in medial gastroc EMG.

good points.

Yes you will see EMG activity before you see motion in two senses of the term. It is probably possible to cause depolarization without causing motion. The other sense is the electro mechanical delay that Kevin mentioned earlier. There is a 100 ms lag between the onset of EMG activity and force development. There is also development of force after EMG stops.

The electro mechanical delay would mean that force is still being produced by the soleus and medial gastroc up untill the point where swing begins.

My statement that the amount of EMG would be too small to see in that I was referring to the change in EMG where the gastroc and soleus are supporting body weight versus when they are supporting body weight and causing forward acceleration of the swing leg (4-5% of body weight) This is different from the amount of EMG you would see at no contraction versus some contraction.

The above argument is made moot by examining the medial gastroc data which show that it is significantly reduced.

I'm sorry that I'm unable to post copies of the Winter articles. I'll look up the ones that I've sited and post the list. Maybe you can get them through inter-library loan.

Regards,
Eric

 

If you look at their figure 6 and timing of the EMG activity of the gastroc and soleus. Stance phase is 62% of the total gait cycle. My calculations of 3/4 of 62% put the timing of data where you see decreased medial gastroc at about 45-6% of the whole cycle. This is the time at which the EMG signal of the gastroc and soleus are shutting down or the very tail end of their activity. When you take into account the electrochemical delay this is very significant for our discussion. Without the ESA he medial gastroc is much more active at the time when it should be for providing propulsion and it is significantly less active with the ESA.

Nice argument except for the fact of the electro mechanical delay. Force is being developed by the muscle after the EMG shuts down. If the ankle is plantar flexing at this time it is providing propulsion.

Man, this is a badly written article.
"The AHF alone caused the horizontal braking forces to increase by 92% and the propulsive forces to decrease to just 28% of normal."
You should never switch back and forth between one way of measuring and another. It would help if they it increased to 192% of normal to make number comparisons easier.

Regardless, the EMG data support the notion that the Medial gastroc is providing force that could initiate swing.

See figure 3B. It shows horizontal force curves.

Regards,

Eric

 

Hi Eric,

Eric, I see your point and it is well taken.:good: I wondered how much this 100msec delay in the gait cycle meant in relation to the gait cycle, so I did some calculations.
If we had stride rate, the calculations would be easy. From the stride rate we get strides/second. Each stride is 100%, so we would be able to determine what percentage of the gait cycle occurs/second. Then we can calculate what percentage of the gait cycle occurs in 100msec.
As you say, “Man, this is a badly written article”. I guess this is a good thing, because if he could write, he would have been an English major. :dizzy: He only mentions stride rate of 1.25m/sec, but does not mention stride rate except they kept it constant.
I looked up what normal stride rate is and I hope this is accurate enough. I found this summary of an article:
http://jeb.biologists.org/cgi/content/abstract/210/18/3255
in which he mentions “preferred stride rate (54.3 strides min–1)”.
54.3 Strides/minute = .905 strides/sec. In 100msec (.1 sec) 9.05% of the gait cycle transpires. Add this to the 45-46% that you already calculated and you end up with 54-5%.
To double check, I calculated it was looking at Fig.1 of the Neptune article, they show gait cycle duration was 1.1 sec at a speed of 1.5 m/sec. Gottschall used a speed of 1.25 m/sec, so it was 83.33% as fast. That means that the cycle duration was 1.1 sec X .833, which equals .917 strides/sec. Using the above calculations, we arrive at basically the same thing.
This means that the gastroc is not firing 7% of the gait cycle earlier than it should.

I also wanted to see if the nice round number of 100msec is accurate.
Neptune says: Although excitation in both muscles has ceased by mid pre-swing, both muscles produce force throughout pre-swing because muscle deactivation (e.g., Ca2+ uptake by the sarcoplasmic reticulum) is not instantaneous. Since both muscles are shortening then, they produce positive power (Fig. 6, SOL, GAS: solid lines are positive).
He doesn’t give a number.
I looked on the net, and I found this article:
http://www.sciencedirect.com/scienc...serid=10&md5=eaf3e954160a3b82f4a8f106465510da
and although it was using guinea pig papillary muscles, it found “The total activation time (TAT) of the papillary muscles (calculated from the delay between the end of the stimulus and the activation of the last photodiode) was increased from 10.2 to 11.5ms at 3Hz, but was only slightly prolonged at the lower frequency (from 10.9 to 11.1ms at 1Hz).” This study found the electrochemical delay to be 10.2-10.9 msec depending on the frequency.

This other study which was done on humans:
http://cat.inist.fr/?aModele=afficheN&cpsidt=3388241
shows the “The major finding of this study was that EMD of the involuntary contractions [e.g. mean 22.1 (SEM 1.32) ms in TR 90[o]; mean 17.2 (SEM 0.62) ms in ES 150 V] was significantly shorter than that of the voluntary contractions [e.g. mean 38.7 (SEM 1.18) ms in MVC, P<0.05].”
This shows two things: First the electromechanical delay is 22.1msec, and secondly that the muscle reacts quicker with involuntary contractions.
If we use these numbers, at .905 strides/seconds X 22.1 ms becomes 1.99%. Add this to the 45-46% that you already calculated and you end up with 47-8%. Using these numbers, this means that the gastroc is not firing 14% of the gait cycle earlier than it should..

I realize you found that the delay was 100msec. Could you give a reference for this?

I see the curves, I don’t understand the point.

Regards,

Stanley

 

The studies you quote look at the onset of force relative to the EMG. The value we need is the difference in time from when the EMG stops to when the force decreases.

Also, when are you thinking the the EMG should be active for the the muscle to contribute to active swing. It has to contribute the force before toe off, which is at 60% of the gait cycle. From looking at the Gotschall article figure 3B regarding horizontal force

(http://jap.physiology.org/cgi/content/full/99/1/23)

You can measure that peak horizontal force occurs roughly at 85-8% of stance phase. So, stance phase is 60% of stride cycle, so peak horizontal force comes at approximately 52% of stride cycle. The EMG data show shut off of EMG at 50% of stride cycle.

Using your number of .917 sec per stride, we get 1.09 stides /sec. Or 1% a stride is equal to approximately 10 ms. So, if the difference in time between EMG drop off and force reduction were 20ms it would exactly coincide with the horizontal force peak. If it were longer than 20ms then ithe muscle is providing force at a time when horizontal push is occurring.

In a quick search I found these graphs that show the relative time of EMG on and of and muscle force. It appears that the force can persist longer after EMG is off than the time of gap between onset of EMG and muscle force.

http://jeb.biologists.org/cgi/content/figsonly/206/17/2941

figure 3

http://www.springerlink.com/content/jwl76p7r56064v52/

The site mentions literature review of between 30 and 100ms and found around 50ms for various conditions.

Originally Posted by Stanley View Post


The horizontal ground reactive force with the ESA confirms that the swing leg can provide propulsion. When the AHF is applied, it appears that the body is trying to slow down by increasing braking forces and decreasing propulsion forces. I don’t see where the article mentions the timing of the horizontal ground reactive force in relation to the gastroc activity. Where did you see it?[/INDENT]​

I'm sorry Stanley, I did not complete the thought. You have to compare figure 3B to the figure that shows the timing of EMG.

Contrary, to their conclusion, their data supports the notion the gastroc supplies power for swing. When there is an external swing assist, there is a decrease in gastroc activity and a decrease in horizontal force.

Regards,

Eric​

 

Hi Eric,

When we finish this discussion, we will really know something.

I agree, I appreciate you taking the time to find the Peter Cavanagh article that shows this down below.

Eric, I reread the article several times and I cannot find where it says that the peak horizontal force comes at 85-88% of stance. Where did you see it? He does say that the stance phase is 62% of the stride cycle, and he is basing this on the GRF.
“The GRF data showed that the average stance phase comprised 0–62%” (page 26).

I agree with your calculations that 1% of a stride is 10ms. I see that you are saying that the horizontal push is greatest when there is maximum contraction of the medical gastroc at 50% of the gait cycle + the delay of the muscle contraction. That sounds reasonable.

Great article, it makes a lot of excellent points and is a classic for learning muscle morphology and function.
For instance it raises the questions,
“Do limb muscles accommodate changes in locomotor performance through a collective shift in muscle performance, or through muscles specialized for a particular mechanical role? If a muscle is specialized for a particular mechanical role, how is this reflected in its architecture?”
It talks about some of the points I raised earlier:
“Many limb muscles might contract under near isometric conditions, performing relatively little work during steady terrestrial locomotion (Taylor, 1994), because force generation to support the body incurs most
of the animal’s metabolic cost (Kram and Taylor, 1990). Isometric muscle contractions generate force more economically than shortening ones, which probably reduces the cost of locomotion (Kram and Taylor, 1990; Roberts et al., 1997, 1998; Biewener and Roberts, 2000).”
“These differences in mechanical roles between proximal and distal limb muscles may relate to muscle–tendon morphology. Proximal muscles generally have long parallel muscle fibers with little or no free tendon, suggesting the capacity to shorten or stretch over relatively long distances, which may favor a role in work modulation. Distal muscles tend to have short, pennate fibers that transmit force via long free tendons, an architecture that favors force generating capacity per unit mass, and storage and release of elastic energy in the tendon”

The human gastrocnemius being a distal pinnate muscle has an architecture that favors storage and release of elastic energy in the tendon.

If you look at the curves on p.2946 (Fig.2), you will see the same thing that happens in humans in that the gastroc is not active for the final quarter of stance phase. I see that comparing the EMG to the force generated that the loss of force is slower than the development of the force, as you astutely noticed. If you look closely at these same graphs, you will notice that the maximum force is developed before 50% of the stance cycle. You will also notice that there is minimal force generated at the end of stance.

The most amazing thing in this article is Table 2 on page 2947. Just look at the amount of work performed by the tendon. Daley on page 2950 says “DF-IV tendon energy recovery reached 21.1±8.8•J•kg–1, greatly exceeding DF-IV muscle shortening work”
Is the delay that we see initially from the time the EMG shows contraction to the generation of force due to the stretch of the tendon; and the delay we see at the end from the termination of muscle contraction to the termination of force a result of the tendon returning the energy? It would appear so.

It says “The mean value for the delay under eccentric condition, 49.5 ms, was significantly different (p<0.05) from the delays during isometric (53.9 ms) and concentric activity (55.5 ms). It is suggested that the time required to stretch the series elastic component (SEC) represents the major portion of the measured delay and that during eccentric muscle activity the SEC is in a more favorable condition for rapid force development.”
This goes along with what I have been saying, that the eccentric contraction is the preferred method. This just confirms another reason-speed of response.
Using these numbers, the calculations are: 50% of the gait cycle + the delay of the muscle contraction. The gastroc is functioning eccentrically at midstance, so we will use 49.5 ms delay. You calculated 1% of a stride is 10ms, so 4.95% (we can say 5%) of the gait cycle has elapsed because of delay. 50% + 5%= 55%. This is still 7% prior to the end of stance. This reminds me of what Howard said way back in post #36: “Inman, in his test "Human Walking" recognized that peak muscular contraction did not match the peaks in thrust. Something else in contributing”

P26 see results: I put the pertinent sentences in capital letters.
RESULTS
“Ground reaction force. The GRF and impulse results established the biomechanical effects of our external force devices. The external force devices affected both braking and propulsive horizontal GRF peaks and impulses compared with normal walking (Fig. 3B). Compared with normal walking, with 3% ESA only, the braking force peak increased by an insignificant 8% (P _ 0.29), whereas the propulsive peak decreased by 17% (P _ 0.0005). THUS THE ESA ALONE INADVERTENTLY AIDED FORWARD PROPULSION, and we accounted for this aiding force by incorporating the AHF device. THE AHF ALONE CAUSED THE HORIZONTAL BRAKING FORCES TO INCREASE BY 92% AND THE PROPULSIVE FORCES TO DECREASE TO JUST 28% OF NORMAL. When we combined the 10% AHF and the 3% ESA, the braking force increased by 95% and the propulsive force decreased to 31% of the values for normal
walking. Thus the similarity of the changes of these horizontal GRF variables allowed us to fairly compare the differences in metabolic cost and muscle activity between AHF only with AHF and ESA combined conditions”.

Eric, you have much more skill at reading graphs than I do. How can you tell when in the gait cycle these things are occurring? I don't see the percentage of the gait cycle listed on the figure 3B.

Eric, Gottschall states During the ESA conditions, neither the MG mEMG nor the Sol mEMG was significantly affected by the ESA forces. The key word is significantly.
Contrary to your conclusion, the author and the data support the notion that the gastroc does not supply power for swing. When looking at the big picture, maybe Howard was right.

Regards,

Stanley​

 

Hi Stanley,

http://jap.physiology.org/cgi/content/full/99/1/23
figure 3

The force curve starts at heel contact and the force curve ends at toe off. The entire length of the curve is the entire stance phase. The propulsive force peak occurs 7/8ths of the way through stance phase.

Stanley, I have never said that the push has to occur at the end of stance. The push has to occur when there is sufficient vertical force to allow for the friction needed for the push. The push will come around the horizontal force peak at about 50% of entire gait cycle which agrees with the EMG data showing that the gastroc and soleus can produce the force.

If there is force at one end of a tendon there has to be force at the other end of the tendon if the tendon is not accelerating relative to the ends. So the tendon cannot produce force without the muscle producing force.

See comment above about how the push does not occur at the end of stance but before the end of stance. The Gottschall data combined with the knowledge of electro mechanical delay show that the horizontal force peak occurs during a time of gastroc and soleus contraction.

EMG is the wrong tool to answer the question we are debating. Whether or not power is added to the trailing leg (in the period of time before toe off) depends on whether or not the ankle plantar flexes. (Power = joint moment x joint angular velocity) To answer the question you have to look at joint power. The data from the Gotschall EMG are consistent with the joint power calculations of Winter and Neptune.

Horrible writing... "decreased to 28% of normal" right next to "decreased by 17%".

They give no reason or support for the contention that the ESA alone aided forward propulsion. It could have just as easily aided swing. Aiding swing is more likely because of where the force is applied.

There is no reason to believe that these gait perturbations should be additive in their effects.

The force curve starts at heel contact and the force curve ends at toe off. The entire length of the curve is the entire stance phase. The propulsive force peak occurs 7/8ths of the way through stance phase. From enlarging the graph and measuring it.

From the Gottshall results (not conclusion)

As we have reported previously (10), during the AHF-only trials, the MG mEMG was lower during the propulsive phase of stance; however, the Sol mEMG did not change compared with the normal walking trials (Fig. 8). With 10% AHF only, the MG mEMG was 55% lower than the normal walking magnitude (P < 0.0001), but the Sol mEMG did not differ compared with normal walking (P = 0.16). Moreover, when ESA was combined with AHF, the mEMG of neither the MG nor the Sol differed from the AHF-only trial.

P<.0001 is significant. I don't know how the reviewer let their conclusion through with this in their data.
The medial gastroc was significantly different

Additionally, with the ESA alone there was a significant decrease in propulsive force peak. The ESA eliminates the need for the gastroc to add to swing.

Stanley, I have tried convincing you with data that we both have. I have put forth a good argument using this data. In a court of Law we could send it to the jury now. However, you have not seen the best evidence for my side of the case. I will rest until you have read Winter's work.


Regards,

Eric


His Text has just about everything including some very good stuff on EMG

Winter, D. A. Biomechanics and motor Control of Human Movement 2nd ed. 1990 John Wiley & Sons, Inc. New York


Articles that relate to what we’ve been talking about.
MacKinnon CD. Winter DA. Control of whole body balance in the frontal plane during human walking. Journal of Biomechanics. 26(6):633﷓44, 1993 Jun.

Winter DA. Overall principle of lower limb support during stance phase of gait. Journal of Biomechanics. 13(11):923﷓7, 1980.

Winter, DA Kinematic and Kinetic Patterns in Human Gait: Variability and Compensating Effects. Human Movement Science 3 p. 51-76 1984


Winter, DA Sagittal Plane Balance and Posture in Human Walking. IEEE Engineering in Medicine and Biology Magazine. Sept. 1987


Other good ones
Arsenault AB. Winter DA. Marteniuk RG. Is there a 'normal' profile of EMG activity in gait?. Medical & Biological Engineering & Computing. 24(4):337﷓43, 1986 Jul

Olney SJ. Winter DA. Predictions of knee and ankle moments of force in walking from EMG and kinematic data. Journal of Biomechanics. 18(1):9﷓20, 1985.

Scott SH. Winter DA. Internal forces of chronic running injury sites. Medicine & Science in Sports & Exercise. 22(3):357﷓69, 1990 Jun.

Scott SH. Winter DA. Talocrural and talocalcaneal joint kinematics and kinetics during the stance phase of walking. Journal of Biomechanics. 24(8):743﷓52, 1991.

Winter DA. Patla AE. Frank JS. Assessment of balance control in humans. Medical Progress through Technology. 16(1﷓2):31﷓51, 1990 May.

Winter, DA Concerning the scientific basis for the diagnosis of pathological gait and for reahbilitation protocols Pysiotherapy Canada vol. 37 No. 4 p245-252 1985

Winter DA. Bishop PJ. Lower extremity injury. Biomechanical factors associated with chronic injury to the lower extremity. Sports Medicine. 14(3):149﷓56, 1992 Sep.

Winter DA. Foot trajectory in human gait: a precise and multifactorial motor control task. Physical Therapy. 72(1):45﷓53; discussion 54﷓6, 1992 Jan.

Winter DA. Patla AE. Frank JS. Walt SE. Biomechanical walking pattern changes in the fit and healthy elderly. Physical Therapy. 70(6):340﷓7, 1990 Jun.


Winter, DA Biomechanics of Normal and Pathological Gait: Implications for Understanding Human Locomotor Control. Journal of Motor Behavior Vol. 21 No. 4 337-355 1989

 

Hi Eric,

Thanks for showing me how to analyze articles better. It is a lifelong tool that will help me in my endeavors.

Thanks, now I see where you got it. In the article Gottschall says that the stance phase is 62% of the stride cycle, and he is basing this on the GRF. I measured the parallel GRF with 0 AHF and 0 ESA, and I enlarged it. I found your measurements to be close to accurate. I found 6/7 which is 85% and you said 7/8 which works out to 87.5%. If we multiply this by 62% we come up with 52.7%-54.25%, which is a little less than the EMG + delay that I calculated at 55%. In the case of EMG + delay this is 7% less than the end of stance. In your calculations you find it to be 7.75%-9.3% less than the end of stance.
Now with the tools you taught me, I was reviewing the Neptune article, and in fig. 3, there was some data from Winter. I know you hold him in high regard so I looked closely at it. Interestingly, it was EMG data of muscles firing in gait. So I measured it as you taught me, and I found that the highest amount of EMG force was at 47% of stride after which it drops off rather rapidly. Adding the 5% for muscle delay, we get 52% of the stride cycle, which is 10% less than the end of stance. Looking at this data made me wonder, why would the gastroc not follow through? Any time you push something, you push up until the time it is released. You wouldn’t throw a ball and stop when your arm is inline with your nose? Why would the gastroc be different in its approach to propulsion? I have no answer except that it can. This takes me back to the guinea fowl article you found, which talks about the stored energy in the tendon. Looking at the curves, the peak force from the muscles occured before 50% of stance. If you store the energy prior to the push, then you wouldn’t have to use the follow through. I figured that we need an example in real life, so I thought of something that would propel the body, a pole. So if we look at the construction of the poles used in pole vaulting, we see how the science has changed in the last 40 years. 40 years ago, rigid poles were used, which required extreme amounts of energy all the way through the vault. Now with the fiberglass poles, the energy is stored in the pole, and the energy is returned to the vaulter for a greater propulsion.

Do you mean that late is not the end, and the push is supposed to be at a time when it is not optimal?

I agree, but let’s go one step further. Is the muscle producing the force in the tendon concentrically or eccentrically, and when? If it is eccentrically, then the muscle is just utilizing the energy from somewhere else. If it is concentrically, then it is the muscle that is supplying the energy. This is why it is important to know when the tension is developed. Before heel off, there is definitely eccentric contraction of the muscle. After heel off there might be eccentric contraction of the gastrocs for the first part, as the knee is extending.

We agree that the peak of horizontal force is not at the end of stance, and as you said in post 115 "It is middle and late propulsion when the angle of the foot to the ground, and the position of the foot relative to the rest of the body, is more optimal for providing push".

If EMG is such a bad tool, then why did Neptune quote Winter’s EMG work? The question is where is the energy coming from to make the ankle plantarflex? As I have said the eccentric contraction stores energy in the tendon that is released when the COM is over the first metatarsal head. This is the same principle as the abductory twist. The EMG data from both Gotschell and Winter confirm this, and from what you have told me that Winter found does not dispute this.

This is the third time I am posting this (see posts 157 and 167)He said on P 26 of the results section “Compared with normal walking, with 3% ESA only, the braking force peak increased by an insignificant 8% (P _ 0.29), whereas the propulsive peak decreased by 17% (P _ 0.0005). Thus the ESA alone inadvertently aided forward propulsion”. I guess there is something here that you don’t understand. I will try to explain it. If the propulsion peak decreases by a statistically significant number, and the person is walking at the same speed, and the only parameter that has changed is the ESA, then the thing that is substituting for propulsion is the ESA.

Then what mathematical function would you propose that we should use? My idea is if the units (N) are the same, either you add or subtract. If you multiply you would get N squared.

Eric, in the section you quoted, it does not discuss the ESA only results. In the conclusion he expands on this by saying “During the ESA conditions, neither the MG mEMG nor the Sol mEMG was significantly affected by the ESA forces.
During the AHF conditions, we found that the MG mEMG decreased during AHF-only trials but that the Sol mEMG did not change (10). Similar to previous studies (24, 29), our temporal results for normal walking showed that, on average, neither the MG nor the Sol was active past 52% of the stride. It is possible that the force generated by these ankle extensors at the end of the first half of stance phase can produce forward acceleration of the limb. But, our results suggest that neither the MG nor Sol directly initiates or propagates leg swing.”

He is concerned about the timing, as I am which I discussed above.

Eric, I agree with that you have tried to convince me and you put forth a good argument. However, I am not convinced and I have given valid reasons as to why. I wonder how long this discussion will take to complete if we are to discuss all the references you gave me, as it has taken 16 posts to discuss the 5 ½ page Modica article, and the only reason we stopped on that one was the Gotschall article was more applicable. So with 3 posts/page, 100 pages are 300 posts. I am willing if you are, as if you haven’t figured it out with Howard after 10 years. It would be to everyone’s benefit if we could come to some consensus.
The main article you have been basing your discussion on is the Winter article on inverse dynamics. To expedite this process, you could fax me the Winter article or E-mail me a scanned copy. Let me know what you want to do.


Regards,

Stanley

 

Hello Stanley,

Stanley, why do you insist that the very end is optimal? It can't happen then because there is not enough frictional force. The concept is impulse, which is force times time. Impulse is change in momentum. A small force applied for a long time can provide the same impulse as a large force applied for a short time. The ankle push would have to occur over a time when the muscle is producing force and near when the horizontal force peak occurs, around 54%. Where did you get your 5% number for time difference from end of EMG signal to time of end of production of muscle force? Even the article that I sited earlier had differences in this time. The problem here is we are trying to establish muscle force from EMG output which is fraught with errors. We could look at the results of force motion. Would you choose EMG over body part accelerations?

Look again at the EMG actiity versus condition graphs. There is about a 1/3 drop off between the 3% ESA and no strings. The reason for this drop off not being statistically significant must be a huge variation in the signal. As I've said before not every step has a push off. There is intra and inter subject variability in push off. If half of the subjects did not have push off before the ESA and did not have it after the ESA then these subjects would mask a significant change in those subjects who did exhibit propulsion before the ESA.

I agree with your last sentence. The ESA decreases the need for propulsion so, those subjects who are using their gastroc for propulsion will use it less. There is a trend in their data that supports this.

Yes, it suggests that, but does not use the best measure to prove that. Stanley, when you've watched people walk, have you seen some people who walk without ankle plantar flexion and some people who walk with ankle plantar flexion just before the initiation of swing.

It would be nice to come to a consensus. Why don't you just admit that I'm right? I'm not going to even question your patriotism for disagreeing with me.

I'm sorry Stanley, I can't get you the articles, only the references.

Regards,

Eric

 

To expand on your analogy to illustrate what I said ealier. Suppose the pole vaulting poll is planted on a device that allows the pole to sink down another foot when a release is triggered. So, the pole vaulter is up in the air heading toward the bar, the release is triggered and there is a sudden decrease in the upward force at the bottom of the pole. The vaulter will no longer continue to have any upward acceleration from the pole. (As he is going up there is upward force from the pole and downward force from gravity. So when the release is triggered there will be no more upward force from the pole.)

The analogy applies here because just as we have to look at both ends of the pole we have to look at both ends of the tendon. Yes, you can store elastic energy in the tendon, but there has to be force in the muscle for that elastic energy to be converted to usefull motion of the body.

So, if you see an EMG cut off at one point in time and you see ankle plantar flexion and upward acceleration of the body part with ankle plantar flexion, at the same time you have a force that could cause that acceleration, at a time after the EMG is turned off, wouldn't conclude that the muscles produced the force that caused the motion?

If we don't know how long after the EMG stops that the muscle produces force then the only way we could figure it out is to measure the force, or the effects of the force. This is why I've been saying that using EMG data is the wrong tool to answer the question of whether or not ankle push occurs.

Regards,

Eric

 

Hi Eric,

I am going on vacation, and that means no computer or internet. So I want to wish you and yours a Merry Christmas and a Happy New Year. :santa:

Eric, I can see why you forgot this, we discussed it a long time ago, See below:

Are you saying that push off is a small force for a long period of time or a large force for a short period of time?

The problem is the gastroc provides its maximum contraction at43-46% (Neptune P1393) or 33%-44% (Gottschall Fig 5); add the muscle delay of 5% and you get 48-51% (Neptune) or 38%-49% (Gottschall). This is earlier than the 54% you mention.

The 5% was discussed 3 posts ago in post #167.

If something is statistically significant, then it is. If it is not statistically significant in the study then it isn’t. You are saying something should have been statistically significant so that it could fit into your theory; and therefore something has to be wrong with the study. I didn’t realize that statistical significance is arguable, I thought that just the interpretation of the data was arguable, not the statistics.

In the conclusion section it says, “ During the ESA conditions, neither the MG mEMG nor the Sol mEMG was significantly affected by the ESA forces”. So are you saying that something that is not significant is a trend?

Do you mean some people walk with sagittal plane dysfunction and some without?

Eric, if what you said made sense, I would agree. But on every post there are some areas of some major leaps. For instance, just in your last post you expect me to believe that statistical insignificance equates to statistical significance.igs: Then there is the muscles having the greatest effect after the time they can have an effect. igs: Then there is the fact that you say the tendons do not store energy,igs: even though the archeologists say it was required for us, and the article on Guinea Fowl show that their gait is dependent on this effect.

Don’t you have just the article on inverse dynamics to fax me?

When exactly does the Achilles tendon lose tension?
Using your knowledge of elastic energy, explain how DF IV tendon in the Guinea fowl article you showed, did more work than the muscle, and exactly how this differs from the human model.

Not if it is after the delay time. I would say close but no cigar. Why would you think that a muscle would move a joint at a time when it is not firing? Wouldn’t you look for other causes?

Check post 167, this has been calculated.

Regards:santa2:,

Stanley

 

Just goes to show you: the stance limb does push against the ground throughout the stance phase of gait! (i.e. if it didn't push, then there would be no ground reaction force!!):santa:Merry Christmas!:santa:

 

Stanley,

Thanks for the Christmas wishes. Have a good vacation and a Merry Christmas.:santa:

The push off, when it occurs could be short or long, but it would occur over a period of time between heel off and toe off, also known as the propulsive phase of gait. As the vertical force decreases, because of incrased weight bearing by the contralateral foot, there will be less friction so there is less ability to propulse.

I keep forgetting how literal you are. Yes, I can see how you thought I meant at the instant of toe off from my posts. However, to get my meaning you could insert in the time period between heel off and toe off in all the statements you quoted.

The 5% number I pulled out of thin air to make my calculations exact. If you look at the article figure 3

http://jeb.biologists.org/cgi/content/figsonly/206/17/2941

You can see that there is force in the bird gastroc 200 ms after the EMG is off. That translates to aproximately 20% of the entire period of gait. If humans are close to similar to birds e.g. 10% of entire period of gait, then the timing is consistant with propulsion.

I'll add some to explain my point further. In statistics you can have an error in your collection of data that will produce erroneous conclusions from your data. You can have random error and systematic error. Random error is addressed in the P value.

A systemic error can occur if your sample is not random or not homogeneous. In this case I am theorizing that the author combined subjects who do not walk with ankle plantar flexion and subjects who do walk with ankle plantar flexion. (Winter showed that there is inter individual and intra individual differences in ankle power) You probably have seen this your self in observing gait. Some people have a heel off after the opposite foot contacts and some people exhibit ankle plantar flexion after heel off. The latter individuals are likely to use their gastroc to produce this motion.

My point is that those individuals who don't use their gastroc before the ESA will probably have no change in their gastroc after the ESA. Those subjects who did use their gastroc before the ESA will use their gastroc less after the ESA. So if you take these different groups and average them together you will get a smaller, and possibly not statistically significant result when you measure the magnitude of the difference before and after the ESA. Statistics books give this example and recommend using a method of statistics that compares how often an individual showed a difference. From my reading of the article this was not done. If you look at figure 8

http://jap.physiology.org/cgi/content/full/99/1/23

You see a 25% drop in gastroc with the 3% ESA only and if you look at the variation of the measurement and apply an equal variation to the normal they are very close to not overlapping. Interesingly they did not report the p value that they did get for this conclusion. Whereas they did report a not significant p value for some other measure.

Yes. Some have called it normal and abnormal. Others have called it propulsive and apropulsive gait.

I'll give you that I may have been a little short on my explanation of systematic error the first time. But I did not say what you said I did regarding statistical significance.

I disagree with your calculations on when muscles can have an effect.

I never said that tendons do not store energy.

No, I could not find it. You can get it from the library as easily as I can. Maybe you can find his textbook on Amazon. It is very good and clearly written.

My point was that the Achilles tendon will lose tension when the muscle loses tension. You are confusing work with force. Work = Force x distance. With the elastic stretch in the tendon there will be more distance moved when they have approximately the same force.

I made those calculations without looking for data and was making assumptions. The 5% assumption is way off when you look at the 200 ms delay between EMG turning off and force dropping to zero. Your earlier measurements were looking at peak force. The force should drop off because the weight is transferred gradually to the other foot. The 200ms delay was explained above.

Let's step back and see if our calculations make sense. If there is no tension in the muscle then there should be no tension in the tendon during the last bit of propulsion then there would be zero plantar flexion moment. If there was zero plantar flexion moment from the muscle and there is upward force from the ground then you would see dorsiflexion of the ankle. How often do you see dorsiflexion of the ankle before toe off. Would you call this normal? I would say that it might happen in an extreme apropulsive gait.

Regards, :santa2:

Eric

 

Hi Eric,

I hope you had a nice time while I was away. :drinks

Most of the force of the muscles is used to support body weight. How do you calculate the amount is used for propulsion?

Eric, I didn’t realize that we could pull numbers out of thin air to make our arguments work. I prefer to look at the facts and allow this to tell me what is going on.

The calculations I came up with match the ones you based on numbers “pulled out of thin air”, and now you say are in error.

Fig. 3 refers to a bird RUNNING at 1.3m/s and on a 16° incline. The last line on p2956 states “By operating at a longer length, a muscle exhibits slower force relaxation (Josephson and Stokes, 1989) and achieves more prolonged lengthening force enhancement (Edman et al. 1978)" It is precisely this prolonged lengthening force that allows for the tension to be maintained in the Achilles tendon in humans to allow for the release of energy which was stored in it.

Thank you so much for the lesson on systemic (systematic) error.
So you are saying that there was a drop that was insignificant because some subjects do not fire their gastroc (because they do not walk with plantarflexion) whether there is an ESA or not. You also have said many times that a subject could walk with either hip flexion or ankle plantar flexion. Using your logic and applying it to hip flexion, we should see some systemic error with the subjects who are just using ankle plantar flexion to power their swing, which should result in insignificant changes in the EMG of these muscles. Fig. 7B shows the Iliopsoas and Femoris, and it also shows significant decreases for both these muscles.

At the time I wrote this, I based in on the numbers you pulled out of thin air. On Post #165 I shared some data on animals that showed the delay was 10.2-10.9 msec in guinea pigs and 22.1 msec in humans. Subsequently, you came up with Peter Cavanagh’s article which showed 49.5 msec. Now you want to use a chart that shows guinea fowl running or going uphill to be the determinant of this number in human walking. I think the 49.5 msec that you found makes the most sense for human walking, even if it doesn’t go along with what you would like to see.

Your calculations would negate any possible effects from the Achilles tendon, so in this specific instance you negate the effect of the Achilles tendon storing energy.

I thought there was one article you were basing things on. Which article should I get on joint power?

Regarding work vs. tension, with 0 tension there will be 0 work. You have been trying to say that there is enough tension in the Achilles from a concentric contraction of the gastroc to power swing. Now you are saying there is no force in the muscle to convert the elastic energy to useful motion of the body. You still haven’t explained how DF IV tendon in the Guinea fowl article you showed, did more work than the muscle.

You were the one that brought up Peter Cavanagh’s article.
http://www.springerlink.com/content/jwl76p7r56064v52/
Are you now saying it is invalid?

Looking at the article that Guinea fowl article you found, shows quite clearly that the tendons perform work at propulsion. On P.2941 it says: "the isometric contractions generate force more economically than shortening ones which probably reduces the cost of locomotion". Also on p.2941 it says: “These differences in mechanical roles between proximal and distal limb muscles may relate to muscle–tendon morphology. Proximal muscles generally have long parallel muscle fibers with little or no free tendon, suggesting the capacity to shorten or stretch over relatively long distances, which may favor a role in work modulation. Distal muscles tend to have short, pennate fibers that transmit force via long free tendons, an architecture that favors force generating capacity per unit mass, and storage and release of elastic energy in the tendon.”
So it seems that it would be favorable to have an isometric contraction at propulsion so the muscle is not doing the work, but rather the tendon.

Regards,

Stanley

 

Just goes to show you: the stance SHOE does push against the ground throughout the stance phase of gait! (i.e. if it didn't push, then there would be no ground reaction force!!

 

Stanley:

When a shoe weighs approximately one pound and the person wearing the shoe weighs 200 pounds, and the force plate measuring the ground reaction force exerted by the shoe registers 200 pounds in late midstance of walking, how much of this force from the "stance SHOE", as you say, is coming from the shoe and how much of it is coming from the individual's limb pushing the shoe into the force plate?

 

Hi Stanley, It was a merry Christmas and a Happy new year. I hope you enjoyed your vacation.:drinks

Through inverse dynamics. Joint power = joint moment x joint velocity. Power = change in energy. When propulsion occurs energy is added. So, you would have to see ankle plantar flexion prior to toe off for there to be propulsion from the ankle. It occurs some of the time.

Agreed. This supports my point.

I was making guesses on data that we don't have to explain how a 25% drop in gastroc activity could be statistically insignificant. The data that we do have from Winter is that ankle push trades off with hip pull. There is between day variation within a subject and between subject variation in the ratio of hip pull/ ankle push. What data we do not have is that what percentage of people use what ratio of hip pull / ankle push. Let's say a third of the people used more ankle push and 2/3 of the people used more hip pull. That would fit the data perfectly. Those that did not use ankle push would not show a decrease in gastroc activity. When those who do not show a decrease are averaged with those that do you would not see a significant change. However, when you look at hip pull muscles you would always see a significant change if 2/3 of the people had more hip pull. So, I disagree with your point above.

Stanley, maybe we could have stopped the discussion a long time ago if I had said this. Not everyone uses ankle push. From looking at people walk over the years, I would say that a small percentage of people exhibit ankle plantar flexion with walking. It's possible to use ankle push, but few use it.

Stanley, That 49 ms was for time between start of EMG and start of muscle force. What we are talking about is the time between end of EMG and end of muscle force.

Could you explain your assertion further? Also, why is it important to separate the tendon from the muscle. I will concede that it is possible for the muscle to have isometric tension that allows elastic energy stored in the tendon to add energy to the trailing leg. However, for there to be force in the tendon there has to be force in the muscle.

If you want to read one thing, I would recommend the book. However, there are bits of information in the articles that are not in the book.


Biomechanics and Motor Control of Human Movement by David A. Winter

Regards,

Eric Fuller

 

Hi Eric,

I understand that you are saying some of the time. And further down you say a small percentage. If we are talking about ankle push not being the preferential method, then we can agree. Inverse dynamics measures what is going on at a joint, but doesn’t necessarily tell what is powering the joint (muscle or tendon).

One point about “achieves more prolonged lengthening force enhancement” which means that there is an eccentric contraction. In humans this equates to the eccentric contraction of the soleus and gastroc storing energy in the Achilles tendon.

I looked at the charts again, and found the Rectus femoris and the Medial gastroc both have a 20% drop, which would seem to invalidate the 1/3-2/3 numbers you were theorizing with, as we should see a greater percentage of drop in the Rectus femoris. I would assume that the reason why one is significant and the other isn’t is because there was a greater fluctuation of the gastroc data than that of the Rectus femoris.

Agreed.

As I said much earlier in our discussion, I felt that in the preferred situation, it didn't make sense for the body to use concentric contraction (as it is inefficiencient) , except in certain necessary circumstances (for example: accelerating to get prey; or to get away from becoming prey). Therefore, what would make sense preferentially is the swing leg powering gait, and the momentum from the body being used by the gastroc and soleus to store the energy in the Achilles tendon for propulsion. At that time the gastrocs and soleus are isometrically firing to allow the tendon to utilize its energy.
I never would have figured this out without your help. :drinks

Regards,

Stanley

 

Kevin,

The answer is not obtained by the force plate. What if someone is sitting in a chair on a force plate, and he raises his hands quickly over his head? The force plate will read an increase in ground reactive force. Using your logic, it is his butt that pushes against the ground, (or is it the chair?). So what is really causing the increase in the GRF?

 

Eric:

While I agree that not everyone uses "ankle push", I can't agree with you that only a "small percentage of people exhibit ankle plantarflexion with walking. It's possible to use ankle push, but few use it." Ankle plantarflexion during propulsion is not only common but is one of the characteristics of normal walking kinematics.

In other words, I would say that normal walking entails concentric ankle joint plantarflexion during propulsion while abnormal walking involves no concentric ankle joint plantarflexion during propulsion. We call this abnormal gait style, with no concentric ankle joint plantarflexion, an "apropulsive gait". Normal ankle joint plantarflexion during propulsion is the hallmark of a "propulsive gait".

Here is a quote from Winter regarding his data on human walking:

In other words, ankle plantarflexion during propulsion is normal and occurs nearly always in those individuals determined to exhibit normal gait kinematics during walking. In addition, as David Winter clearly states, this ankle push is where most of the "new" energy is put back into the body.

 

Stanley:

On the contrary, the force plate does give us the real answers to our questions. The force plate tells us that it is not the shoe (as you stated above) that is causing the ground reaction force vectors during walking. Rather, it is the segmental accelerations of the body that are causing the characteristic ground reaction force vector locations, magnitudes and temporal patterns acting on the plantar foot.......the summation of which all of which involve a push on the ground, not a pull!

 

Here is another reference that supports my contention that concentric ankle plantarflexion is a normal part of human walking during propulsion.

 

Your logic would be true if the only activity of the rectus femorus were to swing the leg forward. However, part of the activity is lifting the leg and this still has to be done even if you have the ESA attached.

To me it does not make sense for the body to use eccentric contrations to move. Concentric contractions cause motion, eccentric contractions limit motion. Yes you could have an eccentric contraction of the muscle unit that could concievably help you store energy in a tendon, but you would need data on the distance the tendon stretches and movement of the joint. You have to use energy to move around.

For the swing leg to power gait, something has to power the swing leg. So, saying the swing leg powers gait is not a complete anlaysis of the situation.

Other than those points directly above we are much closer to consensus. :drinks

Regards,

Eric

 

Kevin,

You're right. I did not write exactly what I was thinking. There are very few individuals who are using 100% ankle push, but I would guess that a large majority would use some ankle push. My sense is that the majority of people use more hip pull as opposed to ankle push, especially as age increases and the foot is not as strong as it used to be. I also agree that a preferred walking style is to have ankle push.

Regards,

Eric

 

Eric:

Agreed......phew, I thought either you or I were going crazy there for awhile.:drinks

 

Kevin,

How exactly can you tell from a force plate measuring GRF that the force is coming from where you imagine it to be from?

 

Hi Eric,

Eric, I agree that part of the function of the Rectus Femoris can be to raise the leg, and the part to raise the leg will not be affected by the ESA. The ESA will substitute for the part that causes swinging of the leg and result in less of an EMG contraction. That being said since lifting the leg is not being substituted for, there will be less of a decrease in contraction of the Rectus femoris because of this. So there is an unnaturally higher contraction (less of a diminution) of the Rectus femoris seen in the data. This is what you are saying, and it is excellent reasoning. :good: There is no way to know for sure if your premise is correct with these subjects.

I agree that the analysis is not complete, so let me say that the all the muscles that lift the leg power swing.
Eric, I would like you to look at this article to see what you think. It would be fun to dissect this and see what it really means.
http://www.rvc.ac.uk/SML/People/documents/LichtwarkJEB2006Achillestendon.pdf

To give you a taste of what it says, the introduction starts with:
The mechanics and energetics of both walking and running have been well documented in the past. In both gait types, elastic energy is thought to be stored within the elastic tissues of the muscle–tendon units that support the body and propel it upwards during the stance phase (Alexander, 1988; Ker et al., 1987; Fukunaga et al., 2001). To achieve versatility, however, the amount of energy stored in the elastic tissues must be modulated by muscular contraction. Here we investigate how the muscle fascicles of the gastrocnemius medialis (GM) interact with the elastic Achilles tendon (AT) to achieve this versatility under different locomotion conditions.

It also talks about the concentric contraction of the gastrocs, so there is a little of everthing in it.

We have both made major changes in our positions, which helps us both explain the data we see.

Regards,

Stanley

 

Stanley:

The force plate measures the center of pressure and three-dimensional location, direction and orientation of the force vector from the object acting on it. What does this physical fact have to do with either my or your imagination??

Now, I have a question for you, Stanley. When a person walks barefoot over a force plate, will it measure a pushing force (toward the force plate) or a pulling force (away from the force plate) from the foot?

 

Kevin;

How exactly do you differentiate between an active push from the foot as opposed to a stabilization of the foot due to forward motion of the CoF with force plate data?

What differentiates a stored energy return response in the foot as opposed to a push from a first step initiation of gait?

Data is data and always open to interpretation. :deadhorse:

Bruce

 

What if someone is sitting in a chair on a force plate, and he raises his hands quickly over his head? The force plate will read an increase in ground reactive force. Using your logic, it is his butt that pushes against the ground, (or is it the chair?). So what is really causing the increase in the GRF?

 

For every action there is an equal and opposite reaction. Force = mass x acceleration. To raise the hands up in the air there has to be a force from the shoulder accelerating the arms upward. The equal and opposite reaction is a downward force from the arm on to the shoulder. You can continue the process through the vertebra and other anatomical structures down to the butt on the chair. If you put a force plate on the chair and one under the chair the difference between the two will essentially be the weight of legs not supported by the chair and the weight of the chair. Both the force platform on the chair and under the chair will register an increase in force when the hands are raised.

Is your point is that if you just look at the platform chair interface then you cannot know what is happening above? It is perfectly reasonable to assume that if you see a force increase under the chair you would see a force increase on top of the chair at the butt chair interface. Both are "caused" by the upward acceleration of the arms. Why would the forces be different. Maybe if your chair was an ejector seat.

In the case of the shoe force platform interface. I was once at a presentation at a conference where they were trying to show that the forces were different between the top of sole of the shoe and the sole of the shoe versus ground interface by using an in-shoe sensor and a force platform. There was a difference between the two, but the consensus in the audience was that it measurement error from the different force measuring systems and not a significant difference in force caused by something happening in the shoe.

If your force platform registers 200 lbs and your shoe weighs one pound, it is a pretty good assumption that the foot is applying 199 lbs to the shoe.

Regards,

Eric Fuller

 

I've said this at least twice on this thread already. Inverse dynamics. If you see an acceleration then a force or moment caused it. If there is upward acceleration of the leg and there is ankle plantar flexion and the ground reaction force is high enough that it should dorsiflex the ankle then it safe to assume that ankle push occured. :deadhorse:

I don't know what you mean by stored energy return resposne. Are you talking about elastic energy in the Achilles tendon?

Regards.

Eric

 

Hi Eric,

Thanks for your input. Everything you said I agree with. But let’s go back to what this is about.

Kevin Post 174: Just goes to show you: the stance limb does push against the ground throughout the stance phase of gait! (i.e. if it didn't push, then there would be no ground reaction force!!)

GROUND REACTION FORCE. The way you can measure this is with a force plate that is set up to measure the vertical force or the Z axis (In other words, a scale). Adding extra force plates to measure butt to chair forces is an extra measuring device that is measuring something in addition to Ground reactive force. By the way, force plates can also be used to measure forces in the XY axis and anterior/posterior and medial/lateral shearing forces, all of which are beyond the scope of the premise of this discussion.

I agree, as this is the key point. If you raise your arms you will register an increase in ground reactive force. Using the same reasoning, if you raise your leg, you will get an increase in ground reactive force.
To say that an increase in ground reactive force is coming from one part or another without additional information is impossible. It may as well be the shoe or the opposite leg as easily as it is the foot, or wherever you imagine it to be.

Regards,

Stanley

 

I disagree, if the point of the discussion is to demonstrate that the stance leg is pushing the body forward (or not), then the anterior posterior shear is quintessential, as it demonstrates whether the stance leg is acting to accelerate or decelerate.

For example, the work of Pollard et al. (don't have full reference to hand) demonstrated that the 5th MTPJ is not involved in propulsion by measuring shear forces beneath the MTPJ's.

 

Simon,

I apologize that I didn't make myself clear as to which discussion I was referring to.
I was referring to the discussion that Kevin started in post 174 where he said:

In a force plate anterior/posterior shear is a different measurement than the Z axis, and furthermore Kevin did not even reference force plate in that post.

Regards,

Stanley

 

How??

 

Kevin was talking purely force plate in his reference Eric. That does not include kinematics which is necessary with the force plate to derive inverse dynamics.

I think Stanley has done an excellent job in your discussions to differentiate whether or not your statement is completely true on upward accelerations of the leg with AJ PFion.

In your comments you feel few if any patients have true ankle push anyway so doesn't that make your comment moot?

Finally, when I refer to a stored energy response I am talking about an energy return from all the foot plantarflexors, or any muscle tendon unit that crosses the AJ and can or will store and then release energy after AJ Dfion.

Bruce

 

Simon,

I am not an expert on force plates, as my experience with them is over 20 years ago, but the way I understand it, the Z axis is perpendicular to the transverse plane, so this would be vertical force (weight).
A/P shear is perpendicular to the frontal plane and would occur in the X axis.
You obviously have more experience in this area, so what do you think?

Regards,

Stanley