The Short Foot Exercise

Here it is, in all its glory...Our version of the short foot exercise. Love it or hate it, say it “doesn’t translate”, we find it a useful training tool for both the patient/client as well as the clinician. It awakens and creates awareness of the sometimes dormant muscles in the user and offers a window to monitor progression for them, as well as the observer.

Remember that the foot intrinsics are supposed to be active from midstance through terminal stance/pre swing. Having the person “walk with their toes up” to avoid overusing the long flexors is a cue that works well for us. This can be a useful adjunct to your other exercises on the road to better foot intrinsic function.


Dr Ivo Waerlop, one of The Gait Guys

Sulowska I, Mika A, Oleksy Ł, Stolarczyk A. The Influence of Plantar Short Foot Muscle Exercises on the Lower Extremity Muscle Strength and Power in Proximal Segments of the Kinematic Chain in Long-Distance Runners Biomed Res Int. 2019 Jan 2;2019:6947273. doi: 10.1155/2019/6947273. eCollection 2019

Okamura K, Kanai S, Hasegawa M, Otsuka A, Oki S. Effect of electromyographic biofeedback on learning the short foot exercise. J Back Musculoskelet Rehabil. 2019 Jan 4. doi: 10.3233/BMR-181155. [Epub ahead of print]

McKeon PO, Hertel J, Bramble D, et al. the foot core system: a new paradigm for understanding intrinsic foot muscle function Br J Sports Med March 2014 doi:10.1136/bjsports-2013- 092690

Dugan S, Bhat K: Biomechanics and Analysis of Running Gait Phys Med Rehabil Clin N Am 16 (2005) 603–621

Bahram J: Evaluation and Retraining of the Intrinsic Foot Muscles for Pain Syndromes Related to Abnormal Control of Pronation http://www.aptei.ca/wp-content/uploads/Intrinsic-Muscles-of-the-Foot-Retraining-Jan-29-05.pdf


#shortfootexercise #footexercises #footrehab #thegaitguys #gaitanalysis #gaitrehab #toesupwalking



https://vimeo.com/342800960

The QP....What's the deal?

tumblr_mau352bxll1qhko2so1_540.png

Possibly heard of, rarely implicated and not often treated, this is one muscle you should consider taking a look at.

The quadratus plantae is generally considered to arise from two heads of differing and variable  fiber type composition, with the lateral head having slightly more Type 1 endurance fibers (1) The two heads are separated from each other by the long plantar ligament, though it can arise from from one (somewhat more common)  to 3 heads (very rare).  The attachments can be variable, The medial head is larger and more muscular, attached to the medial calcaneus, lateral aspect of the long plantar ligament and often from the plantar calcaneocuboid ligament (2);  the lateral head is smaller and more tendinous, attaching to the lateral border of the inferior surface of the calcaneus and the long plantar ligament.  The two portions join and end in a flattened band which inserts into the lateral, upper and under surfaces of the muscles, tendons or aponeurosis of predominantly the flexor digitorum longus and usually of the second and third, and sometimes fourth toes (2,3). 

Its action can be equally as variable. In addition to augmenting the pull of the long flexor tendons along the long axis of the foot and so that the 3rd and 4th toes do not curl under the foot, the tendinous slips of the FHL may distribute the load of the great toe to the second toe to the third or fourth toe in the forefoot, especially during toe-off (3).

look at the 4th and 5th digits trying to "crawl under the foot"

look at the 4th and 5th digits trying to "crawl under the foot"

The main attachment of the QP to the tendinous slips of the FHL may provide more efficient control of the long flexor tendons in comparison with that of the QP to the tendon of the FDL (3). EMG studies suggest it resists extension of the toes during the stance phase of locomotion, which serves to increase the stability of the foot. Additional EMG studies suggest it actually acts as a primary toe flexor in voluntary movements, being preferentially recruited over flexor digitorum longus and from comparative anatomical considerations it also seems likely that quadratus plantae may be an intrinsic evertor of the foot (4).

This muscle is a major player in gait and rehabilitation of this muscle should not be overlooked. I could only find one study looking at exercise activation of the QP (5) . It was examined along with the abductor hallucis, flexor digitorum brevis, abductor digiti minimi, flexor digiti minimi, adductor hallucis oblique, flexor hallucis brevis, interossei and lumbricals during rehabilitative the short-foot exercise, toes spread out, first-toe extension, second- to fifth-toes extension.

So, what else can you do?

  • you could ignore the muscle and hope it gets better. (in all likelihood it will worsen)
  • you could give them long flexor, toe scrunching towel-curling, marble-grasping exercises, like you see all over the internet…and give the flexor digitorum longus even more of a mechanical advantage, and make the problem worse
  • you could give them exercises to increase the function of the long extensors, which would increase the mechanical advantage of the quadratus plantae. like the shuffle walk; lift, spread and reach and tripod standing exercises
  • look north of the foot to see what might be causing the problem (loss of ankle rocker, insufficient gluteal activity, loss of internal rotation of the hip, etc) 

Check out the QP on your next foot pain patient, or whenever you see the toes trying to crawl under the foot. You may be surprised at your results. 

 

1. Schroeder KL, Rosser BW, Kim SY. Fiber type composition of the human quadratus plantae muscle: a comparison of the lateral and medial heads. J Foot Ankle Res. 2014 Dec 13;7(1):54. doi: 10.1186/s13047-014-0054-5. eCollection 2014.

2. Pretterklieber B1. Morphological characteristics and variations of the human quadratus plantae muscle. Ann Anat. 2017 Nov 21;216:9-22. doi: 10.1016/j.aanat.2017.10.006. [Epub ahead of print]

3. Hur MS, Kim JH, Woo JS, Choi BY, Kim HJ, Lee KS. An anatomic study of the quadratus plantae in relation to tendinous slips of the flexor hallucis longus for gait analysis. Clin Anat. 2011 Sep;24(6):768-73. doi: 10.1002/ca.21170.

4. Sooriakumaran P, Sivananthan S. Why does man have a quadratus plantae? A review of its comparative anatomy. Croat Med J. 2005 Feb;46(1):30-5.

5. Gooding TM, Feger MA, Hart JM, Hertel J. ntrinsic Foot Muscle Activation During Specific Exercises: A T2 Time Magnetic Resonance Imaging Study. J Athl Train. 2016 Aug;51(8):644-650. Epub 2016 Oct 3.

Which foot exercises activate the intrinsics?

So, your goal is to strengthen the intrinsics. What exercise is best? Probably the most specific one, right? Well....maybe. These 4 exercises seem to all hit them.

This study looked at the muscle activation of the abductor hallucis, flexor digitorum brevis, abductor digiti minimi, quadratus plantae, flexor digiti minimi, adductor hallucis oblique, flexor hallucis brevis, and interossei and lumbricals with the short foot, toe spreading, big toe extension and lesser toes extension exercises with T2 weighted MRI post exercises (perhaps not the best way to look at it) and shows they all work to varying degrees.

"All muscles showed increased activation after all exercises. The mean percentage increase in activation ranged from 16.7% to 34.9% for the short-foot exercise, 17.3% to 35.2% for toes spread out, 13.1% to 18.1% for first-toe extension, and 8.9% to 22.5% for second- to fifth-toes extension."

Gooding TM, Feger MA, Hart JM, Hertel J. Intrinsic Foot Muscle Activation During Specific Exercises: A T2 Time Magnetic Resonance Imaging Study. Journal of Athletic Training. 2016;51(8):644-650. doi:10.4085/1062-6050-51.10.07.

link to full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5094843/

The Power of Triangles

 

We talk about triangles a lot. Think about triangles. Hey Pythaogoras did! They are powerful distributors of force. Here we will talk about 3 of them.

There are 4 layers of muscles in the foot. The 1st triangle occurs in the 1st layer. Think of the abductor hallucis and the abductor digiti minimi. Proximally they both attach to the calcaneus and distally to the 1st and 5th proximal phalanges. Now think about the transverse metatarsal ligament that runs between the disal metatarsal heads. Wow, a triangle! this one is superficial.

Now think about the adductor hallicus. It has a transverse and oblique head. think about that transverse metatarsal ligament again. Wow, another triangle!

What about the flexor hallicus brevis and flexor digiti minimi? The former originates from the cuboid, lateral cunieform andd portion of the tib posterior tendon; the latter from the proximal 5th metatarsal. They both go forward and insert into the respective proximal phalynx (with the sesamoids intervening in the case of the FHB). and what connects these? The deep transverse metatarsal ligament of course! And this triangle surrounds the adductor triangle, with both occurring the 3rd layer of the 4 layers of foot muscles.

Triangles… and you thought geometry was boring!

Remaining triangular when we need to (because of our pointy heads)…

Yay for the lift, spread and reach exercise!   Toe spreads and squeezes are aimed at strengthening specific intrinsic foot muscles—the dorsal and plantar interrosei, according to Irene S. Davis, PhD, PT, director of the Spaulding National Running Center and a professor in the Department of Physical Medicine and Rehabilitation at Harvard Medical School in Boston. Doming or foot shortening exercises contract most of the muscles on the plantar side of the foot, and help to strengthen the abductor hallucis muscle   see our post here:  https://tmblr.co/ZrRYjx1iuSYMM   Goo YM, Heo HJ, An DH. EMG activity of the abductor hallucis muscle during foot arch exercises using different weight bearing postures. J Phys Ther Sci 2014;26(10):1635-1636.

Yay for the lift, spread and reach exercise!

Toe spreads and squeezes are aimed at strengthening specific intrinsic foot muscles—the dorsal and plantar interrosei, according to Irene S. Davis, PhD, PT, director of the Spaulding National Running Center and a professor in the Department of Physical Medicine and Rehabilitation at Harvard Medical School in Boston. Doming or foot shortening exercises contract most of the muscles on the plantar side of the foot, and help to strengthen the abductor hallucis muscle

see our post here: https://tmblr.co/ZrRYjx1iuSYMM

Goo YM, Heo HJ, An DH. EMG activity of the abductor hallucis muscle during foot arch exercises using different weight bearing postures. J Phys Ther Sci 2014;26(10):1635-1636.

Treat the paraspinals in addition to the peripheral muscle   As people who treat a wide variety of gait related disorders we often emphasize needling the paraspinal muscles associated with the segemental innervation of the peripheral muscle you are treating. For example, you may facilitate or needle the L2-L4 paraspinals (ie: femoral nerve distribution) along with the quads, or perhaps the C5-C6 PPD’s along with the shoulder muscles for the deltiods or rotator cuff for arm swiing. We do this to get more temporal and spacial summation at a spinal cord level, to hopefully get better clinical results.  White and Panjabi described clinical instability as the loss of the ability of the spine, under physiologic loads, to maintain relationships between vertebrae in such a way that there is neither damage nor subsequent irritation to the spinal cord or nerve roots, and, in addition there is no development of incapacitating deformity or pain due to structural changes.  Increased movement between vertebrae (antero or retrolisthesis) of > 3.5 mm (or 25% of the saggital body diameter) during flexion and/or extension suggests clinical instability. This often leads to intersegmental dysfunction and subsequent neurological sequelae which could be explained through the following mechanisms:  Recall that the spinal nerve, formed from the union of the ventral (motor) and dorsal (sensory) rami, when exiting the IVF splits into an anterior and posterior division, supplying the structures anterior and posterior to the IVF respectively. The posterior division has 3 branches: a lateral branch that supplies the axial muscles such as the iliocostalis and quadratus; an intermediate branch, which innervates the medial muscles, such as the longissimus, spinalis and semispinalis; and a medial branch, which innervates the segmental muscles, (multifidus and rotatores) as well as the joint capsule. Inappropriate intersegmental motion has 2 probable neurological sequelae: I) alteration of afferentation from that level having segmental (reflexogenic muscle spasm or vasoconstrictive/vasodilatory changes from excitation of primary afferents and gamma motoneurons) and suprasegmental (less cerebellar afferentation, less cortical stimulation) effects and II) compression or traction of the medial branch of the PPD, causing,  over time, demyelination and resultant denervation, of the intrinsic muscles, resulting in impaired motor control both segmentally and suprasegmentally. The segmental effects are directly measurable with needle EMG. This is a form of paraspinal mapping, which has also been explored by Haig et al. So, in short, instability can lead to denervation and denervation can lead to instability.   We often see clinically that treating a trigger point (needling, dry needling, acupuncture, manual pressure) can alter the function of the associated muscle . Improvements in muscle strength and changes in proprioception are not uncommon. Needling also seems to increase fibroblastic activty through the local inflammation it causes. Wouldn’t better muscle function and some scar tissue be a beneficial thing to someone with instability?  The next time you have a patient with instability, make sure to include the paraspinals in your quest for better outcomes.

Treat the paraspinals in addition to the peripheral muscle

As people who treat a wide variety of gait related disorders we often emphasize needling the paraspinal muscles associated with the segemental innervation of the peripheral muscle you are treating. For example, you may facilitate or needle the L2-L4 paraspinals (ie: femoral nerve distribution) along with the quads, or perhaps the C5-C6 PPD’s along with the shoulder muscles for the deltiods or rotator cuff for arm swiing. We do this to get more temporal and spacial summation at a spinal cord level, to hopefully get better clinical results.

White and Panjabi described clinical instability as the loss of the ability of the spine, under physiologic loads, to maintain relationships between vertebrae in such a way that there is neither damage nor subsequent irritation to the spinal cord or nerve roots, and, in addition there is no development of incapacitating deformity or pain due to structural changes.

Increased movement between vertebrae (antero or retrolisthesis) of > 3.5 mm (or 25% of the saggital body diameter) during flexion and/or extension suggests clinical instability. This often leads to intersegmental dysfunction and subsequent neurological sequelae which could be explained through the following mechanisms:

Recall that the spinal nerve, formed from the union of the ventral (motor) and dorsal (sensory) rami, when exiting the IVF splits into an anterior and posterior division, supplying the structures anterior and posterior to the IVF respectively. The posterior division has 3 branches: a lateral branch that supplies the axial muscles such as the iliocostalis and quadratus; an intermediate branch, which innervates the medial muscles, such as the longissimus, spinalis and semispinalis; and a medial branch, which innervates the segmental muscles, (multifidus and rotatores) as well as the joint capsule. Inappropriate intersegmental motion has 2 probable neurological sequelae: I) alteration of afferentation from that level having segmental (reflexogenic muscle spasm or vasoconstrictive/vasodilatory changes from excitation of primary afferents and gamma motoneurons) and suprasegmental (less cerebellar afferentation, less cortical stimulation) effects and II) compression or traction of the medial branch of the PPD, causing,  over time, demyelination and resultant denervation, of the intrinsic muscles, resulting in impaired motor control both segmentally and suprasegmentally. The segmental effects are directly measurable with needle EMG. This is a form of paraspinal mapping, which has also been explored by Haig et al. So, in short, instability can lead to denervation and denervation can lead to instability.

We often see clinically that treating a trigger point (needling, dry needling, acupuncture, manual pressure) can alter the function of the associated muscle . Improvements in muscle strength and changes in proprioception are not uncommon. Needling also seems to increase fibroblastic activty through the local inflammation it causes. Wouldn’t better muscle function and some scar tissue be a beneficial thing to someone with instability?

The next time you have a patient with instability, make sure to include the paraspinals in your quest for better outcomes.

Muscle activity

Does variability in muscle activity reflect a preferred way of moving or just reflect what they’ve always done? In this study it was found that there isn’t always this tight relationship between activity in the muscles and the movement we’re seeing.
“Clearly, locomotion is not as simple as we thought it was,” Foster said. “This decoupling – big changes in movement without corresponding changes in muscle activity – suggests there are other important factors going on and we need to better understand them if we want to reproduce these movements in prosthetics or robotics.”
Hmmmm. thoughts. this makes everything more interesting doesn’t it ?!

http://esciencenews.com/articles/2014/03/14/motion.and.muscles.dont.always.work.lockstep.researchers.find.surprising.new.study

Muscle activity and movement

“We expected to see a one-to-one correlation between the muscle activity and movements because motion is generally driven by muscles,” Higham said, “but as we changed the structure of their habitat and they changed their motions, we were surprised to find very few accompanying changes in muscle activity.”

Context-dependent changes in motor control and kinematics during locomotion: modulation and decoupling. Foster and Higham
http://www.ncbi.nlm.nih.gov/pubmed/24621949

Functional Ankle Instability and the Peroneals    
     
  Lots of links available here with today’s blog post. please make sure to take your time and check out each one (underlined below)    
 As you remember, the peroneii (3 heads) are on the outside of the lower leg (in a nice, easy to remember order of longus, brevis and tertius, from top to bottom) and  help to stabilize the lateral ankle . The peroneus brevis and tertius dorsiflex and evert the foot while the peroneus longus plantarflexes and everts the foot. We discuss the peroneii more in depth  here in this post . It then is probably no surprise to you that people with ankle issues, probably have some degree of peroneal dysfunction. Over the years the literature has supported notable peroneal dysfunction following even a single inversion sprain event.  
  Functional ankle instability  (FAI) is defined as “ the subjective feeling of ankle instability or recurrent, symptomatic ankle sprains (or both) due to proprioceptive and neuromuscular deficits."  
 Arthrogenic muscle inhibition (AMI) is a neurological phenomenon where the muscles crossing a joint become "inhibited”, sometimes due to effusion (swelling) of the joint (as seen  here ) and that may or may not be the case with the ankle (see  here ), or it could be due to nociceptive input  altering spindle output  or possibly  higher centers  causing the decreased muscle activity.  
 This paper (see abstract below) merely exemplifies both the peroneals and FAI as well as AMI. 
   Take home message?   
 Keep the peroneals strong with lots of balance work! 
  The Gait Guys: bringing you the meat, without the filler!                                                                           

   Am J Sports Med.  2009 May;37(5):982-8. doi: 10.1177/0363546508330147. Epub 2009 Mar 6.  
  Peroneal activation deficits in persons with functional ankle instability.  
   Palmieri-Smith RM ,  Hopkins JT ,  Brown TN .  
 
  Source  
  School of Kinesiology, University of Michigan, 401 Washtenaw Avenue, Ann Arbor, MI 48109, USA. riannp@umich.edu  
 
 
  Abstract  
  BACKGROUND:   
  Functional ankle instability (FAI) may be prevalent in as many as 40% of patients after acute lateral ankle sprain. Altered afference resulting from damaged mechanoreceptors after an ankle sprain may lead to reflex inhibition of surrounding joint musculature. This activation deficit, referred to as arthrogenic muscle inhibition (AMI), may be the underlying cause of FAI. Incomplete activation could prevent adequate control of the ankle joint, leading to repeated episodes of instability.  
  HYPOTHESIS:   
  Arthrogenic muscle inhibition is present in the peroneal musculature of functionally unstable ankles and is related to dynamic peroneal muscle activity.  
  STUDY DESIGN:   
  Cross-sectional study; Level of evidence, 3.  
  METHODS:   
  Twenty-one (18 female, 3 male) patients with unilateral FAI and 21 (18 female, 3 male) uninjured, matched controls participated in this study. Peroneal maximum H-reflexes and M-waves were recorded bilaterally to establish the presence or absence of AMI, while electromyography (EMG) recorded as patients underwent a sudden ankle inversion perturbation during walking was used to quantify dynamic activation. The H:M ratio and average EMG amplitudes were calculated and used in data analyses. Two-way analyses of variance were used to compare limbs and groups. A regression analysis was conducted to examine the association between the H:M ratio and the EMG amplitudes.  
  RESULTS:   
  The FAI patients had larger peroneal H:M ratios in their nonpathological ankle (0.399 +/- 0.185) than in their pathological ankle (0.323 +/- 0.161) (P = .036), while no differences were noted between the ankles of the controls (0.442 +/- 0.176 and 0.425 +/- 0.180). The FAI patients also exhibited lower EMG after inversion perturbation in their pathological ankle (1.7 +/- 1.3) than in their uninjured ankle (EMG, 3.3 +/- 3.1) (P < .001), while no differences between legs were noted for controls (P > .05). No significant relationship was found between the peroneal H:M ratio and peroneal EMG (P > .05).  
  CONCLUSION:   
  Arthrogenic muscle inhibition is present in the peroneal musculature of persons with FAI but is not related to dynamic muscle activation as measured by peroneal EMG amplitude. Reversing AMI may not assist in protecting the ankle from further episodes of instability; however dynamic muscle activation (as measured by peroneal EMG amplitude) should be restored to maximize ankle stabilization. Dynamic peroneal activity is impaired in functionally unstable ankles, which may contribute to recurrent joint instability and may leave the ankle vulnerable to injurious loads.  
 
   all material (except for the study); copyright 2013 The Gait Guys/ The Homunculus Group. All rights reserved. Please ask before you lift our stuff. If you are nice and give us credit, we will probably let you use it!

Functional Ankle Instability and the Peroneals 


Lots of links available here with today’s blog post. please make sure to take your time and check out each one (underlined below) 

As you remember, the peroneii (3 heads) are on the outside of the lower leg (in a nice, easy to remember order of longus, brevis and tertius, from top to bottom) and help to stabilize the lateral ankle. The peroneus brevis and tertius dorsiflex and evert the foot while the peroneus longus plantarflexes and everts the foot. We discuss the peroneii more in depth here in this post. It then is probably no surprise to you that people with ankle issues, probably have some degree of peroneal dysfunction. Over the years the literature has supported notable peroneal dysfunction following even a single inversion sprain event. 

Functional ankle instability (FAI) is defined as “ the subjective feeling of ankle instability or recurrent, symptomatic ankle sprains (or both) due to proprioceptive and neuromuscular deficits." 

Arthrogenic muscle inhibition (AMI) is a neurological phenomenon where the muscles crossing a joint become "inhibited”, sometimes due to effusion (swelling) of the joint (as seen here) and that may or may not be the case with the ankle (see here), or it could be due to nociceptive input altering spindle output or possibly higher centers causing the decreased muscle activity. 

This paper (see abstract below) merely exemplifies both the peroneals and FAI as well as AMI.

Take home message?

Keep the peroneals strong with lots of balance work!

The Gait Guys: bringing you the meat, without the filler!                                                                         

Am J Sports Med. 2009 May;37(5):982-8. doi: 10.1177/0363546508330147. Epub 2009 Mar 6.

Peroneal activation deficits in persons with functional ankle instability.

Source

School of Kinesiology, University of Michigan, 401 Washtenaw Avenue, Ann Arbor, MI 48109, USA. riannp@umich.edu

Abstract

BACKGROUND:

Functional ankle instability (FAI) may be prevalent in as many as 40% of patients after acute lateral ankle sprain. Altered afference resulting from damaged mechanoreceptors after an ankle sprain may lead to reflex inhibition of surrounding joint musculature. This activation deficit, referred to as arthrogenic muscle inhibition (AMI), may be the underlying cause of FAI. Incomplete activation could prevent adequate control of the ankle joint, leading to repeated episodes of instability.

HYPOTHESIS:

Arthrogenic muscle inhibition is present in the peroneal musculature of functionally unstable ankles and is related to dynamic peroneal muscle activity.

STUDY DESIGN:

Cross-sectional study; Level of evidence, 3.

METHODS:

Twenty-one (18 female, 3 male) patients with unilateral FAI and 21 (18 female, 3 male) uninjured, matched controls participated in this study. Peroneal maximum H-reflexes and M-waves were recorded bilaterally to establish the presence or absence of AMI, while electromyography (EMG) recorded as patients underwent a sudden ankle inversion perturbation during walking was used to quantify dynamic activation. The H:M ratio and average EMG amplitudes were calculated and used in data analyses. Two-way analyses of variance were used to compare limbs and groups. A regression analysis was conducted to examine the association between the H:M ratio and the EMG amplitudes.

RESULTS:

The FAI patients had larger peroneal H:M ratios in their nonpathological ankle (0.399 +/- 0.185) than in their pathological ankle (0.323 +/- 0.161) (P = .036), while no differences were noted between the ankles of the controls (0.442 +/- 0.176 and 0.425 +/- 0.180). The FAI patients also exhibited lower EMG after inversion perturbation in their pathological ankle (1.7 +/- 1.3) than in their uninjured ankle (EMG, 3.3 +/- 3.1) (P < .001), while no differences between legs were noted for controls (P > .05). No significant relationship was found between the peroneal H:M ratio and peroneal EMG (P > .05).

CONCLUSION:

Arthrogenic muscle inhibition is present in the peroneal musculature of persons with FAI but is not related to dynamic muscle activation as measured by peroneal EMG amplitude. Reversing AMI may not assist in protecting the ankle from further episodes of instability; however dynamic muscle activation (as measured by peroneal EMG amplitude) should be restored to maximize ankle stabilization. Dynamic peroneal activity is impaired in functionally unstable ankles, which may contribute to recurrent joint instability and may leave the ankle vulnerable to injurious loads.

all material (except for the study); copyright 2013 The Gait Guys/ The Homunculus Group. All rights reserved. Please ask before you lift our stuff. If you are nice and give us credit, we will probably let you use it!

tumblr_m2j60zuBR31qhko2so1_1280.jpg
tumblr_m2j60zuBR31qhko2so2_r2_1280.jpg

Neuromechanics Weekly: PART 2:

Stretching increases strength in contralateral muscles?

Lots of cool links in this post. please try and find time to check them out.

Figure it out?  Ever wonder about some of the magic behind some of those manual therapy techniques that are out there ? Sometimes it is not magic at all !

There are 2 related reasons we can think of to cause this seemingly odd length-strength phenomenon (OK, there are more, but this is what we are going to cover today):

  • Reciprocal Inhibition
  • Crossed extensor reflexes/responses

We remember reciprocal inhibition (as demonstrated in LEFT picture above) is when we activate or stimulate a muscle, the Ia afferent from that muscle stimulates that same muscle to contract (this is how a simple reflex arc works) and, through an inhibitory interneuron, inhibits the antagonist muscle on the opposite side of the joint.

Remember, that Ia afferents go to muscle spindles (don’t remember? look here); they respond to LENGTH changes. Wouldn’t you say stretching affects length? If we were talking about the R tricep surae group, we would be inhibiting the R anterior compartment.

But wait, the article said it affects the opposite side….Of course, there is more…

The picture on the right shows the crossed extensor response or reflex (don’t remember? look here). In a nutshell, when you FIRE the flexors on one side, you INHIBIT the extensors on the same side (sound like reciprocal inhibition? It should… it is : ) You also FIRE the extensors on the opposite side while INHIBITING the flexors on the opposite side. (Yes, the opposite side extensors will inhibit the opposite side flexors as well. Yes, this is also reciprocal inhibition).

But wait, that means the opposite calf would be weaker, not stronger, right?

It would be weaker if being called upon to be used at that moment in time, BUT in the study, stretching increased ROM of the stretched calf 8%, with a 1% loss of ROM of the opposite calf (study summary).

Hmm… sounds like shortening to me. That would mean that those spindles (ie the opposite calf)  would be MORE RESPONSIVE to stretch (ie a change in length; and coincidentally, the Golgi’s more responsive to the tension change) . And what happens when we preload a neuronal pool? The likelihood of firing is increased (like doing a Jendrassik maneuver to increase a reflex). The rest is neural adaptation (strength gains initially are due to increased efficiency of the nervous system. For a review to see our video on this, click here)

Interesting that one of the comments on the article was “I don’t have the full text of the paper but a summary prepared by Chris Beardsley and Bret Contreras states that one of the mechanisms for crossover in the case of unilateral strength training is thought to be modulation at the spinal cord level.”   Could they be talking about reciprocal inhibition and crossed extensor responses?

Wow! Very cool! And to think, you knew the answer. We are proud of you!

Ivo and Shawn…Neuro Geeks too!  And applying it to gait, running and motor patterns of all types !

Need more muscle activation? How about a crouched gait?

Muscle contributions to support and progression during single-limb stance in crouch gait

J Biomech. 2010 Aug 10;43(11):2099-105. Epub 2010 May 20.


You have heard us talk about crouch gait as a rehabilitative exercise (see another post here). Here is some proof that you are working harder

“The results of this analysis indicate that children walking in crouch gait have less passive skeletal support of body weight and utilize substantially higher muscle forces to walk than unimpaired individuals.”

and

“… during crouch gait, these muscles are active throughout single-limb stance, in contrast to the modulation of muscle forces seen during single-limb stance in an unimpaired gait.”

...and working the right muscles

“Crouch gait relies on the same muscles as unimpaired gait to accelerate the mass center upward, including the soleus, vasti, gastrocnemius, gluteus medius, rectus femoris, and gluteus maximus.”

and

“Subjects walking in crouch gait rely more on proximal muscles, including the gluteus medius and hamstrings, to accelerate the mass center forward during single-limb stance than subjects with an unimpaired gait.”

Yup, crouched gait gives you more bang for the buck. Try it….You’ll like it!

Yes, we are the Geeks of Gait…. sifting through and synthesizing the research so you don’t have to


J Biomech. 2010 Aug 10;43(11):2099-105. Epub 2010 May 20.

Source

Departments of Mechanical Engineering, Clark Center, Stanford University, Stanford, CA 94305-5450, United States. ksteele@stanford.edu

Abstract

Pathological movement patterns like crouch gait are characterized by abnormal kinematics and muscle activations that alter how muscles support the body weight during walking. Individual muscles are often the target of interventions to improve crouch gait, yet the roles of individual muscles during crouch gait remain unknown. The goal of this study was to examine how muscles contribute to mass center accelerations and joint angular accelerations during single-limb stance in crouch gait, and compare these contributions to unimpaired gait. Subject-specific dynamic simulations were created for ten children who walked in a mild crouch gait and had no previous surgeries. The simulations were analyzed to determine the acceleration of the mass center and angular accelerations of the hip, knee, and ankle generated by individual muscles.

The results of this analysis indicate that children walking in crouch gait have less passive skeletal support of body weight and utilize substantially higher muscle forces to walk than unimpaired individuals.  

Crouch gait relies on the same muscles as unimpaired gait to accelerate the mass center upward, including the soleus, vasti, gastrocnemius, gluteus medius, rectus femoris, and gluteus maximus.

However, during crouch gait, these muscles are active throughout single-limb stance, in contrast to the modulation of muscle forces seen during single-limb stance in an unimpaired gait. Subjects walking in crouch gait rely more on proximal muscles, including the gluteus medius and hamstrings, to accelerate the mass center forward during single-limb stance than subjects with an unimpaired gait.

Copyright 2010 Elsevier Ltd. All rights reserved.

Its a great day to be a neuro geek  
 So if the receptors on the bottom of the foot aren&rsquo;t involved aren&rsquo;t involved in 2 joint muscles staying coordinated (like the hamstring and rectus femoris in this study), how do we determine the appropriate muscle length and ratios? How about our built in muscle length receptors? Lets hear it for muscle spindles! Hooray for Ia and type II afferents! 
 Sifting through the science so you don&rsquo;t have to. We are The Gait Guys&hellip; 
  Exp Brain Res.  1998 Jun;120(4):479-86. 
 Coordination of two-joint rectus femoris and hamstrings during the swing phase of human walking and running. 
  Prilutsky BI ,  Gregor RJ ,  Ryan MM . 
 Source 
 Department  of Health and Performance Sciences, Center for Human Movement Studies,  The Georgia Institute of Technology, Atlanta 30332-0110, USA. 
 Abstract 
 It  has been hypothesized previously that because a strong correlation was  found between the difference in electromyographic activity (EMG) of  rectus femoris (RF) and hamstrings (HA; EMG(RF)-EMG(HA)) and the  difference in the resultant moments at the knee and hip (Mk-Mh) during  exertion of external forces on the ground by the leg, input from skin  receptors of the foot may play an important role in the control of the  distribution of the resultant moments between the knee and hip by  modulating activation of the two-joint RF and HA. In the present study,  we examined the coordination of RF and HA during the swing phase of  walking and running at different speeds, where activity of foot  mechanoreceptors is not modulated by an external force. Four subjects  walked at speeds of 1.8 m/s and 2.7 m/s and ran at speeds of 2.7 m/s and  3.6 m/s on a motor-driven treadmill. Surface EMG of RF, semimembranosus  (SM), and long head of biceps femoris (BF) and coordinates of the four  leg joints were recorded. An inverse dynamics analysis was used to  calculate the resultant moments at the ankle, knee, and hip during the  swing phase. EMG signals were rectified and low-pass filtered to obtain  linear envelopes and then shifted in time to account for  electromechanical delay between EMG and joint moments. During walking  and running at all studied speeds, mean EMG envelope values of RF were  statistically (P&lt;0.05) higher in the first half of the swing (or at  hip flexion/knee extension combinations of joint moments) than in the  second half (or at hip extension/knee flexion combinations of joint  moments). Mean EMG values of BF and SM were higher (P&lt;0.05) in the  second half of the swing than in the first half. EMG and joint moment  peaks were substantially higher (P&lt;0.05) in the swing phase of  walking at 2.7 m/s than during the swing phase of running at the same  speed. Correlation coefficients calculated between the differences  (EMG(RF)-EMG(HA)) and (Mk-Mh), taken every 1% of the swing phase, were  higher than 0.90 for all speeds of walking and running. Since the close  relationship between EMG and joint moments was obtained in the absence  of an external force applied to the foot, it was suggested that the  observed coordination of RF and HA can be regulated without a  stance-specific modulation of cutaneous afferent input from the foot.  The functional role of the observed coordination of RF and HA was  suggested to reduce muscle fatigue.

Its a great day to be a neuro geek

So if the receptors on the bottom of the foot aren’t involved aren’t involved in 2 joint muscles staying coordinated (like the hamstring and rectus femoris in this study), how do we determine the appropriate muscle length and ratios? How about our built in muscle length receptors? Lets hear it for muscle spindles! Hooray for Ia and type II afferents!

Sifting through the science so you don’t have to. We are The Gait Guys…

Exp Brain Res. 1998 Jun;120(4):479-86.

Coordination of two-joint rectus femoris and hamstrings during the swing phase of human walking and running.

Prilutsky BI, Gregor RJ, Ryan MM.

Source

Department of Health and Performance Sciences, Center for Human Movement Studies, The Georgia Institute of Technology, Atlanta 30332-0110, USA.

Abstract

It has been hypothesized previously that because a strong correlation was found between the difference in electromyographic activity (EMG) of rectus femoris (RF) and hamstrings (HA; EMG(RF)-EMG(HA)) and the difference in the resultant moments at the knee and hip (Mk-Mh) during exertion of external forces on the ground by the leg, input from skin receptors of the foot may play an important role in the control of the distribution of the resultant moments between the knee and hip by modulating activation of the two-joint RF and HA. In the present study, we examined the coordination of RF and HA during the swing phase of walking and running at different speeds, where activity of foot mechanoreceptors is not modulated by an external force. Four subjects walked at speeds of 1.8 m/s and 2.7 m/s and ran at speeds of 2.7 m/s and 3.6 m/s on a motor-driven treadmill. Surface EMG of RF, semimembranosus (SM), and long head of biceps femoris (BF) and coordinates of the four leg joints were recorded. An inverse dynamics analysis was used to calculate the resultant moments at the ankle, knee, and hip during the swing phase. EMG signals were rectified and low-pass filtered to obtain linear envelopes and then shifted in time to account for electromechanical delay between EMG and joint moments. During walking and running at all studied speeds, mean EMG envelope values of RF were statistically (P<0.05) higher in the first half of the swing (or at hip flexion/knee extension combinations of joint moments) than in the second half (or at hip extension/knee flexion combinations of joint moments). Mean EMG values of BF and SM were higher (P<0.05) in the second half of the swing than in the first half. EMG and joint moment peaks were substantially higher (P<0.05) in the swing phase of walking at 2.7 m/s than during the swing phase of running at the same speed. Correlation coefficients calculated between the differences (EMG(RF)-EMG(HA)) and (Mk-Mh), taken every 1% of the swing phase, were higher than 0.90 for all speeds of walking and running. Since the close relationship between EMG and joint moments was obtained in the absence of an external force applied to the foot, it was suggested that the observed coordination of RF and HA can be regulated without a stance-specific modulation of cutaneous afferent input from the foot. The functional role of the observed coordination of RF and HA was suggested to reduce muscle fatigue.

A brief gait review from a youtube clip we found:

at :03 notice the shrugged shoulders and trapezius activation, forcing respirations to the upper lung fields. This also facilitates the scalene muscles in the neck (which is probably one of the reasons they flex their neck). Breathing from here is shallow and inefficient. This action (shrugging the shoulders) activates the upper trap and deactivates the lats (which are the functional link between the upper and lower extremities)

at 05: they begin to flex the lumbar spine

at :06 they flex at the waist as well as the neck. This rounds the spine and puts the glutes at a mechanical disadvantage for extending the hips and limiting some of the driving power. They then become hamstring dependent, which isn’t as efficient. Dropping the head defacilitates the extensor muscles neurologically, so they will have some power loss (as well as stiffness loss) as well. They keep their neck flexed till :07, where they really begin to pick up more speed. The torso remains flexed at the waist through most of the footage.

it appears at :07 that the left foot strikes the ground in eversion bottom of foot pointing away from camera) indicating some degree of forefoot pronation. A shot from behind would be helpful to confirm this

The arm swing appears asymmetrical from left to right, right being greater both forward and especially backward. I would wonder what they are hiding (biomechanically) there (so are they increased on the right or less on the left?. Here is where foot age from behind would be instructional).

Ok folks. Hope you enjoyed the ride!

we still are….The Gait Guys…..