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

Have you seen this?

Patterns. That’s what it’s about a lot of times. Dr Allen and I are always looking for patterns or combinations of muscles which work together and seem to cause what appear to be predictable patterns; like a weak anterior compartment and a weak gluteus maximus, or a weak gluteus medius and contralateral quadratus lumborum.

Here is an interesting story and a new combination that at least I have never seen before

I had a 11-year-old right footed soccer player from my son’s soccer team coming to see me with bilateral posterior knee pain which began during a soccer game while he was “playing up” on his older brothers team. He did need to do a lot of jumping as well as cutting. He is generally a midfielder/Forward. Well experienced player and “soccer is his life“.

My initial thoughts were something like a gastroc dysfunction or a Baker’s cyst. On examination, no masses or definitive swelling noted behind either knee. He did have tenderness to moderate degree over the right plantaris and tenderness as well as 4/5 weakness of the left popliteus. There was a loss of long axis extension of the talo crural articulations bilaterally with the loss of lateral bending to the right and left at L2-L3.

If you think about the mechanics of the right footed kicker (and try this while kicking a soccer ball yourself) it would be approximately as follows: left foot would be planted near the ball and the tibia/femur complex would be internally rotating well the foot is pronating and the popliteus would be eccentrically contracting to slow the rotation of the femur and the tibia. The right foot will be coming through and plantarflexion after a push off from the ball of the foot firing the triceps surae and plantaris complexes. He would be “launching“ off of the right foot and landing on his left just prior to the kick, causing a sudden demand on the plantar flexors; with the plantaris being the weak link. As the kicking leg follows through, the femur of the stance phase leg needs to externally rotate (along with the tibia) at a faster rate than the tibia (otherwise you could injure the meniscus) the popliteus would be contracting concentrically. A cleat, because it increases the coefficient of friction with the ground would keep the foot on the ground solidly planted and The burden of stress would go to the muscles which would be extremely routine leg and close chain which would include the semimembranosus/tendinosis  complex as well as the vastus medialis and possibly gracilis and short adductor, along with the popliteus.

I have to say and all of my years of practice I’ve never seen this combination type of injury before involving these two muscles specifically and am wondering if anyone else has seen this?

Dr Ivo Waerlop, one of The Gait Guys

#footproblem #gait #thegaitguys #soccerinjury #bilateralkneepain #popliteus #plantaris

image credit: https://commons.wikimedia.org/wiki/File:Slide2ACCA.JPG

image credit: https://commons.wikimedia.org/wiki/File:Slide2ACCA.JPG

Muscle activation and gait: EMG studies that differentiate!

image credit:  Cappellini G ,  Ivanenko YP ,  Poppele RE ,  Lacquaniti F . Motor patterns in human walking and running.  J Neurophysiol.  2006 Jun;95(6):3426-37. Epub 2006 Mar 22.

image credit: Cappellini G, Ivanenko YP, Poppele RE, Lacquaniti F. Motor patterns in human walking and running. J Neurophysiol. 2006 Jun;95(6):3426-37. Epub 2006 Mar 22.

Got Muscle activation? Looking for some EMG data on what fires when in walking vs running gait? The conclusion and point of the study are good, but the EMG data and diagrams are awesome for those of you seeking a greater understanding of what goes on when

“The major difference between walking and running was that one temporal component, occurring during stance, was shifted to an earlier phase in the step cycle during running. These muscle activation differences between gaits did not simply depend on locomotion speed as shown by recordings during each gait over the same range of speeds (5–9 km/h). The results are consistent with an organization of locomotion motor programs having two parts, one that organizes muscle activation during swing and another during stance and the transition to swing. The timing shift between walking and running reflects therefore the difference in the relative duration of the stance phase in the two gaits.”

A great read and FREE FULL TEXT

Dr Ivo, one of The Gait Guys

Cappellini G, Ivanenko YP, Poppele RE, Lacquaniti F. Motor patterns in human walking and running. J Neurophysiol. 2006 Jun;95(6):3426-37. Epub 2006 Mar 22. link to free full text: http://jn.physiology.org/content/95/6/3426

#gait, #gaitanalysis, #thegaitguys, #gaitabnormality, #EMGgait, #muscleactivation, #musclerecruitmentpattern

On the subject of manual muscle work…

image credit: https://commons.wikimedia.org/wiki/File:Muscle_spindle_model.jpg

image credit: https://commons.wikimedia.org/wiki/File:Muscle_spindle_model.jpg

Here is an older article that may seem verbose, but has interesting implications for practitioners who do manual muscle work with their clients. We would invite you to work your way through the entire article, a little at a time, to fully grasp it’s implications.

Plowing through the neurophysiology, here is a synopsis for you:

Tactile and muscle afferent (or sensory) information travels into the dorsal (or posterior) part of the spinal cord called the “dorsal horn”. This “dorsal horn” is divided into 4 layers; 2 superficial and 2 deep. The superficial layers get their info from the A delta and C fibers (cold, warm, light touch and pain) and the deeper layers get their info from the A alpha and A beta fibers (ie: joint, skin and muscle mechanoreceptors).

So what you may say

The superficial layers are involved with pain and tissue damage modulation, both at the spinal cord level and from descending inhibition from the brain. The deeper layers are involved with apprising the central nervous system about information relating directly to movement (of the skin, joints and muscles).

Information in this deeper layer is much more specific that that entering the more superficial layers. This happens because of 3 reasons:

  1. there are more one to one connections of neurons (30% as opposed to 10%) with the information distributed to many pathways in the CNS, instead of just a dedicated few in the more superficial layers

  2. the connections in the deeper layers are largely unidirectional and 69% are inhibitory connections (ie they modulate output, rather than input)

  3. the connections in the deeper layers use both GABA and Glycine as neurotransmitters (Glycine is a more specific neurotransmitter).

Ok, this is getting long and complex, tell me something useful...

This supports that much of what we do when we do manual therapy on a patient or client is we stimulate inhibitory neurons or interneurons which can either (directly or indirectly)

  • inhibit a muscle

  • excite a muscle because we inhibited the inhibitory neuron or interneuron acting on it (you see, 2 negatives can be positive)

So, much of what we do is inhibit muscle function, even though the muscle may be testing stronger. Are we inhibiting the antagonist and thus strengthening the agonist? Are we removing the inhibition of the agonist by inhibiting the inhibitory action on it? Whichever it may be, keep in mind we are probably modulating inhibition, rather than creating excitation.


Semantics? Maybe…But we constantly talk about being specific for a fix, not just cover up the compensation. Is it easier to keep filling up the tire (facilitating) or patching the hole (inhibiting). It’s your call


Yan Lu Synaptic Wiring in the Deep Dorsal Horn. Focus on Local Circuit Connections Between Hamster Laminae III and IV Dorsal Horn Neurons J Neurophys Volume 99 Issue 3

March 2008 Pages 1051-1052 link: http://jn.physiology.org/content/99/3/1051

Muscle Spindles and Proprioception

image source: https://en.wikipedia.org/wiki/File:Fusimotor_action.jpg

image source: https://en.wikipedia.org/wiki/File:Fusimotor_action.jpg

And what have we been saying for the last 6 years? 

Connected to the nervous system by large diameter afferent (sensory) fibers, they are classically thought of as appraising the nervous system of vital information like length and rate of change of length of muscle fibers, so we can be coordinated. They act like volume controls for muscle sensitivity. Turn them up and the muscle becomes more sensitive to ANY input, especially stretch (so they become touchy…maybe like you get if you are hungry and tired and someone asks you to do something); turn them down and they become less or unresponsive.

Their excitability is governed by the sum total (excitatory and inhibitory) of all neurons (like interneuron’s) acting on them (their cell bodies reside in the anterior horn of the spinal cord).

Along with with Golgi tendon organs and joint mechanoreceptors, they also act as proprioceptive sentinels, telling us where our body parts are in space. We have been teaching this for years. Here is a paper that exemplifies that, identifying several proteins responsible for neurotransduction including the Piezo2 channel as a candidate for the principal mechanotransduction channel. Many neuromuscular diseases are accompanied by impaired  muscle spindle function, causing a decline of motor performance and coordination. This is yet another key finding in the kinesthetic system and its workings. 

Remember to include proprioceptive exercises and drills (on flat planar surfaces, like we talked about here) in your muscle rehab programs

 

 

 

 

Kröger S Proprioception 2.0: novel functions for muscle spindles. Curr Opin Neurol. 2018 Oct;31(5):592-598. 

Woo SH, Lukacs V, de Nooij JC, Zaytseva D, Criddle CR, Francisco A, Jessell TM, Wilkinson KA, Patapoutian A. Piezo2 is the principal mechanotransduction channel for proprioception.Nat Neurosci. 2015 Dec; 18(12):1756-62. Epub 2015 Nov 9.

Fusimotor control of proprioceptive feedback during locomotion and balancing: can simple lessons be learned for artificial control of gait?

Hulliger M. Fusimotor control of proprioceptive feedback during locomotion and balancing: can simple lessons be learned for artificial control of gait? Prog Brain Res. 1993; 97:173-80.

Dry Needling and Muscle Activation Patterns

A nice study looking at how sequential muscle activation patterns can change with dry needling. Think about the applications for gait?

"Removing LTrPs changes the order of muscle recruitment to a more sequential, stable pattern that is not significantly different to that displayed by the control group prior to fatiguing exercise. This suggests that removing LTrPs may allow subjects to better cope with the effects of fatigue, as evidenced by the reduced variability in activation times and the reduced co-activation of the muscles investigated. "

FREE FULL TEXT here: https://isbweb.org/images/conf/2003/longAbstracts/LUCAS_198-208_SB_LONGE.pdf

Hmmmm…  The question is: “is the earlier activation a good thing”?  What do you say?  “A study of patients with chronic ankle instability (CAI) suggests the onset of knee and ankle muscle activity occurs significantly earlier when shoes and orthoses are worn than when the patients are barefoot.”   http://lermagazine.com/issues/october/shoes-orthoses-improve-muscle-activation-onset-in-unstable-ankles

Hmmmm…

The question is: “is the earlier activation a good thing”?

What do you say?

“A study of patients with chronic ankle instability (CAI) suggests the onset of knee and ankle muscle activity occurs significantly earlier when shoes and orthoses are worn than when the patients are barefoot.”

http://lermagazine.com/issues/october/shoes-orthoses-improve-muscle-activation-onset-in-unstable-ankles

tumblr_nv42pyzoQp1qhko2so1_1280.jpg
tumblr_nv42pyzoQp1qhko2so2_1280.jpg

Notice the differences in running (top) vs sprinting (bottom) activation patterns?

This picture (along with the MIchaud muscular firing pattern ones) are becoming some of my favorite ones to talk about. I just stare at them and look for differences and similarities. 

Check out that the abs do not seem to fire in running (in this study at least), but do in sprinting. Note also that most muscles fire longer (and we wil assume harder) during sprinting. Also check out the peroneals, which fire just as the foot touches down in sprinting, probably to make up for the instrinsics not firing, and assist in creating a rigid lever for push off. 



from: Mann et al 1986

What creates muscle tone, anyway?   Not for the timid, here is an excellent ,  free , full text article on spasticity. More importantly, it is an excellent review on what creates muscle tone and how it is maintained, starting and the spindle and moving centrally.  Think about this the next time you have a patient with mm spasm and you can se things in a whole new light   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009478/

What creates muscle tone, anyway?

Not for the timid, here is an excellent , free, full text article on spasticity. More importantly, it is an excellent review on what creates muscle tone and how it is maintained, starting and the spindle and moving centrally.  Think about this the next time you have a patient with mm spasm and you can se things in a whole new light

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009478/

Patello femoral pain? Thinking weak VMO? Think again…   “Atrophy of all portions of the quadriceps muscles is present in the affected limb of people with unilateral PFP. There wasn’t any atrophy of the quadriceps in individuals with PFP compared to those without pathology. Selective atrophy of the VMO relative to the vastus lateralis wasn’t identified in persons with PFP.”    http://www.physiospot.com/research/atrophy-of-the-quadriceps-is-not-isolated-to-the-vastus-medialis-oblique-in-individuals-with-patellofemoral-pain/

Patello femoral pain? Thinking weak VMO? Think again…

“Atrophy of all portions of the quadriceps muscles is present in the affected limb of people with unilateral PFP. There wasn’t any atrophy of the quadriceps in individuals with PFP compared to those without pathology. Selective atrophy of the VMO relative to the vastus lateralis wasn’t identified in persons with PFP.”

http://www.physiospot.com/research/atrophy-of-the-quadriceps-is-not-isolated-to-the-vastus-medialis-oblique-in-individuals-with-patellofemoral-pain/

The mighty Gluteus Medius, in all its glory!   Perhaps the delayed action of the gluteus medius allows an adductory moment of the pelvis, moving the center of gravity medially. This could conceivably place additional stress on the achilles tendon  (via the lateral gastroc) to create more eversion of the foot from midstance on   “The results of the study demonstrate altered neuromuscular control of the GMED and GMED in runners with Achilles Tendonitis. During running, GMED typically activates before heel strike so as to stabilize the hip and the pelvis. In runners with Achilles Tendonitis, GMED is activated with a delay, which consequently might affect the kinematics of knee and ankle resulting in rear foot inversion. Similarly, GMAX is activated with a delay and for a shorter duration in runners with Achilles Tendonitis. GMAX is the primary hip extensor and via a kinetic chain, a decreased hip extension moment might be compensated by an increased ankle plantarflexion moment which could potentially increase the load on the Achilles tendon.”   Franettovich Smith MM1, Honeywill C, Wyndow N, Crossley KM, Creaby MW. : Neuromotor control of gluteal muscles in runners with achilles tendinopathy. Med Sci Sports Exerc. 2014 Mar;46(3):594-9.

The mighty Gluteus Medius, in all its glory!

Perhaps the delayed action of the gluteus medius allows an adductory moment of the pelvis, moving the center of gravity medially. This could conceivably place additional stress on the achilles tendon  (via the lateral gastroc) to create more eversion of the foot from midstance on

“The results of the study demonstrate altered neuromuscular control of the GMED and GMED in runners with Achilles Tendonitis. During running, GMED typically activates before heel strike so as to stabilize the hip and the pelvis. In runners with Achilles Tendonitis, GMED is activated with a delay, which consequently might affect the kinematics of knee and ankle resulting in rear foot inversion. Similarly, GMAX is activated with a delay and for a shorter duration in runners with Achilles Tendonitis. GMAX is the primary hip extensor and via a kinetic chain, a decreased hip extension moment might be compensated by an increased ankle plantarflexion moment which could potentially increase the load on the Achilles tendon.”

Franettovich Smith MM1, Honeywill C, Wyndow N, Crossley KM, Creaby MW. : Neuromotor control of gluteal muscles in runners with achilles tendinopathy.
Med Sci Sports Exerc. 2014 Mar;46(3):594-9.

Foot “core” anyone?   And a good time was had by all. Day 1 of the event in Vancouver. Lots of info and a bonus exercise session. Thanks to all who attended and looking forward to another great day tomorrow!  We spent a great deal of time talking about muscular firing sequences and the reasoning as to why things fire when.   Take a look at the picture and focus on the tib posterior, flexor digitorum longus, and flexor hallucis longus. They fire from loading response and fire through terminal stance. Up to midstance, they act eccentrically to slow pronation and after midstance, they fire concentrically to assist in supination. Note the sequence starts with the tib posterior (more proximal attachments in the foot) and ends with the flexor hallucis longus, more distal attachements (because in “ideal” gait, the hallux is the last to leave the party (or the ground, in this case)). Stability is a priority, so the central or “core” of the foot needs to fire before adding on peripheral (appendicular) muscles. Remember the foot intrinsics fire from midstance to pre swing, further stabilizing the foot “core”  The Gait Guys

Foot “core” anyone?

And a good time was had by all. Day 1 of the event in Vancouver. Lots of info and a bonus exercise session. Thanks to all who attended and looking forward to another great day tomorrow!

We spent a great deal of time talking about muscular firing sequences and the reasoning as to why things fire when.

Take a look at the picture and focus on the tib posterior, flexor digitorum longus, and flexor hallucis longus. They fire from loading response and fire through terminal stance. Up to midstance, they act eccentrically to slow pronation and after midstance, they fire concentrically to assist in supination. Note the sequence starts with the tib posterior (more proximal attachments in the foot) and ends with the flexor hallucis longus, more distal attachements (because in “ideal” gait, the hallux is the last to leave the party (or the ground, in this case)). Stability is a priority, so the central or “core” of the foot needs to fire before adding on peripheral (appendicular) muscles. Remember the foot intrinsics fire from midstance to pre swing, further stabilizing the foot “core”

The Gait Guys

Can the VMO be selectively activated?

They have a common nerve innervation, so many studies say no. Perhaps altering internal/external orientation of the lower extremity (1) or joint angles (2) may play a role. Of course, it also depends on how you are measuring (3). Intramuscular seems to be most accurate!

In the Link Below, section 4, is a nice, brief review of the literature. Thanks to Daithi Grey for the inspiration to put this up!

1. J Strength Cond Res. 2014 Sep;28(9):2536-45. doi: 10.1519/JSC.0000000000000582.
Range of motion and leg rotation affect electromyography activation levels of the superficial quadriceps muscles during leg extension.Signorile JF1, Lew KM, Stoutenberg M, Pluchino A, Lewis JE, Gao J.

2. Phys Ther Sport. 2013 Feb;14(1):44-9. doi: 10.1016/j.ptsp.2012.02.006. Epub 2012 Jun 26.
Muscle activation of vastus medialis obliquus and vastus lateralis during a dynamic leg press exercise with and without isometric hip adduction. Peng HT1, Kernozek TW, Song CY.

3. J Electromyogr Kinesiol. 2013 Apr;23(2):443-7. doi: 10.1016/j.jelekin.2012.10.003. Epub 2012 Nov 8.
The VMO:VL activation ratio while squatting with hip adduction is influenced by the choice of recording electrode. Wong YM1, Straub RK, Powers CM.


http://www.mikereinold.com/2009/05/10-principles-of-patellofemoral.html

10 Principles of Patellofemoral Rehabilitation - Mike Reinold

“Emphasize the QuadricepsThe next principle of patellofemoral rehabilitation is to strengthen the knee extensor musculature. Some authors have recommended emphasis on enhancing the activation of the VMO in patellofemoral patients based on reports of isolated VMO insufficiency and asynchronous neuromuscular timing between the VMO and VL.While the literature offers conflicted reports on selective recruitment and neuromuscular timing of the vasti musculature, the VMO may have a greater biomechanical effect on medial stabilization of the patella than knee extension due to the angle of pull of the muscle fibers at approximately 50-55 degrees.  Wilk et al(JOSPT 1998) suggest that the VMO should only be emphasized if the angle of insertion of the VMO on the patella is in a position in which it may offer a certain degree of dynamic or active lateral stabilization.  As you can see by the figure, if the fibers are not aligned in a position to assist with patellar stabilization, VMO training will likely not be effective.  This orientation of the muscle fibers will differ from patient to patient and can be visualized.Several interventions and exercise modifications have been advocated to effectively increase the VMO:VL ratio, based mostly on anecdotal observations. These include hip adduction, internal tibial rotation, and patellar taping and bracing. Powers(JOSPT 1998) reports that isolation of VMO activation may not be possible during exercise, stating that several studies have shown that selective VMO function was not found during quadriceps strengthening exercises, exercises incorporating hip adduction, or exercises incorporating internal tibial rotation. Powers also states that although the literature offers varying support for VMO strengthening, successful clinical results have been found while utilizing this treatment approach.My belief is that quadriceps strengthening exercises should be incorporated into patellofemoral rehabilitation programs. Strength deficits of the quadriceps may lead to altered biomechanical properties of the patellofemoral and tibiofemoral joints. Any change in quadriceps force on the patella may modify the resultant force vector produced by the synergistic pull of the quadriceps and patellar tendons, thus altering contact location and pressure distribution of joint forces. Furthermore, the quadriceps musculature serves as a shock absorber during weightbearing and joint compression, any abnormal deviations in quadriceps strength may result in further strain on the patellofemoral and/or tibiofemoral joint.In reality, I believe that quadriceps strengthening is very important for patellofemoral rehabilitation, but many exercises designed to “enhance VMO” strength or activation may actually be disadvantageous to the joint.  Take for example the classic squeezing of the ball during closed kinetic chain exercises such as squatting and leg press.  This creates an IR and adduction moment at the hip that is now known to be detrimental to patellofemoral patients.  I would actually propose that we work on quadriceps strengthening without an adduction component and rather emphasize hip adbuction and external rotation.  This can be performed with the use of a piece of exercise band around the patient’s knees during these exercises. “

tumblr_nndwhh7w481qhko2so1_1280.jpg
tumblr_nndwhh7w481qhko2so2_1280.jpg
tumblr_nndwhh7w481qhko2so3_1280.jpg

More on weak muscles. Just WHY are they weak? Know before you activate!

Dr Allen’s post last week on chronic ankle instability (click here for post) served as an inspiration for many of us. It brings to mind the many reasons muscles can become “weak”.

So why does a muscle become weak? We like to categorize the causes as follows:

  • local
  • segmental
  • long loop/cortical

Local causes include muscle injury and muscle pathologies, like muscular dystrophy and neuromuscular endplate disorders like myasthenia gravis. Segmental causes are largely due to reflexes which occur at the spinal cord level. Long loop and cortical causes ae due to an increased inhibition or lack of drive from higher centers, such as the motor cortex and cerebellum.

Lets examine local causes in more detail. To understand causes we must understand what makes a muscle contract.

Muscles are composed of many proteins, 2 of which are actin and myosin (see above). Actin has 2 forms, F (filamental) and G (globular) actin. Imagine 2 grapefruits side by side (G actin) held together in the middle by small filaments (F actin). Now imagine these another set immediately below, in a repeating pattern. These groups of 2 are held together at the sides by an additional protein called tropomyosin. This whole complex looks a little like train tracks. Along the strands of tropomyosin, at regular intervals is yet another protein called troponin. We like to think of troponin as a triangular shaped protein and each part of the triangle has a particular binding site: one for tropomyosin, one for actin and another for calcium ions.

Myosin is another component of muscle, that looks similar to a bunch of golf clubs. The head of the club will, under the right circumstances, interact with actin, the body (tail) of the club interacts with other myosin bodies.

Globular actin and myosin heads are like 2 teenagers and like to interact with one another. Normally, in a resting state, troponin protein covers the active site of myosin binding on G actin. In the presence of calcium, there is a change in shape of the troponin molecule, moving it off of the active site of actin, allowing myosin to bind there. When this happens, the head ratchets and muscle contraction occurs. In the presence of adequate fuel (ie ATP) the myosin head detaches from actin and “recocks”, ready for another contraction cycle (see 2nd picture above).

So where does the calcium come from? It is stored in areas of the muscle called the terminal cisterns. It is released when an action potential fires the peripheral nerve to the neuromuscular endplate of a muscle.

Can calcium be released any other way? Sure it can. How about if the terminal cisterns are damaged, from an injury to the muscle? How about if they are damaged from a disease process?

So, when calcium is released, no matter how it is released, muscles contract. If calcium is not released, then muscles do not contract.

From a local cause, If a muscle is weak, one of the following are usually causing the weakness:

  • there is physical damage to the muscle causing fewer of the working units of the muscle (called sarcomeres) contract

this is by far the most common, due to overuse or trauma

  • there is a problem with the connection of the nerve to the muscle

Disruption of nerve to muscle connections can be also be due to trauma or disease. Weakness that is becoming progressive and worsening, needs to be evaluated further and may be the signal for a progressive muscular or neurological disorder (muscular dystrophy, myasthenia gravis, Gullian Barre, etc)

  • there is insufficient neurotransmitter at the neuromuscular end plate to fire the muscle

this is usually due to a disease process

  • Insufficient calcium could theoretically hamper a muscles contraction, but since calcium is involved with nerve transmission as well, tetany (ie sustained contraction and spasm) would most likely occur due to other reasons that we will not explore at this juncture.

OK, so that sums up local causes. Look for a follow up post about segmental causes next…

We are: The Gait Guys

tumblr_ne2sg64OZ11qhko2so1_400.gif
tumblr_ne2sg64OZ11qhko2so3_500.jpg
tumblr_ne2sg64OZ11qhko2so2_1280.jpg

More thoughts on stretching

   We get a lot of interest in our posts on stretching. Seems like this is a pretty hot subject and there is a lot of debate as to whether it is injury preventative or not. Are you trying to physically lengthen the muscle or are you trying to merely bring it to its physiological limit?  There’s a big difference in what you need to do to accomplish each of these goals. Lets take a look at each, but 1st we need to understand a little about muscles and muscle physiology.

 Muscles are composed of small individual units called sarcomeres. Inside of these “sarcomeres” there are interdigitating fibers of actin and myosin (proteins) which interact with one another like a ratchet when a muscle contracts.  Sarcomeres can be of various lengths, depending on the muscle, and are linked and together from one end of the muscle to the other. When a muscle contracts concentrically (the muscle shortening while contracting) the ends of the sarcomere (called Z lines or Z discs) are drawn together, shortening the muscle fiber over all (see the picture above).
 
 Signals are sent from the brain (actually the precentral gyrus of the cerebral cortex areas 4, 4s and 6) down the corticospinal tract to the spinal cord to synapse on motor neurons there.  These motor neurons (alpha motor neurons) then travel through peripheral nerves to the muscles to cause them to contract (see picture above).

   The resting length of the muscle is dependent upon two factors:
The physical length of the muscle
2. The “tone” of the muscle in question.

The physical length of the muscle is determined by the length of the sarcomeres and the number of them in the muscle.   The “tone” of the muscle determined by an interplay of neurological factors and the feedback loops between the sensory (afferent) receptors in the muscle (Ia afferents, muscle spindles, Golgi tendon organs etc.), relays in the cerebellum and basal ganglia as well as input from the cerebral cortex.

 If you’re trying to “physically lengthen” a muscle, then you will need to actually add sarcomeres to the muscle. Research shows that in order to do this with static stretching it must be done 20 to 30 minutes per day per muscle.

 If you were trying to “bring a muscle to its physiological limit” there are many stretching methods to accomplish this.  Pick your favorite whether it be a static stretch, contract/ relax, post isometric relaxation etc. and you’ll probably be able to find a paper to support your position.

  Remember with both not to ignore neurological reflexes (see above). Muscle spindle loops are designed to provide feedback to the central nervous system about muscle length and tension. Generally speaking, slow stretch activates the Ia afferent loop which causes causes physiological contraction of the muscle (this is one of the reasons you do not want to do slow, steady stretch on a muscle in spasm). This “contraction” can be fatigued overtime, causing the muscle to be lengthened to it’s physiological limit.  Do this for an extended period of time (20-30 mins per day) and you will physically add sarcomeres to the muscle.

 Next time you are stretching, or you were having a client/patient stretch, think about what it is that you’re actually trying to accomplish  because there is a difference.

We are and remain The Gait Guys.  Bald, good-looking, and above-average intelligence. Spreading gait literacy with each post we publish.

thanks to scienceblogs.com for the corticospinal tract image

Ankle muscle spindles play a significant role in the control of posture and balance during the swing phase of locomotion

 
                                                                                                              
“The results provide strong evidence that the primary endings of ankle muscle spindles play a significant role in the control of posture and balance during the swing phase of locomotion by providing information describing the movement of the body’s COM with respect to the support foot. Our results also provide supporting evidence for the proposal that there are context-dependent changes in muscle spindle sensitivity during human locomotion."                                                                                    

  • This study tells us what we already know: The muscles surrounding the ankle, especially of the leg you are standing on (the "stance” phase leg) provide important information to the central nervous system about both that leg AND the leg not on the ground (The “swing” phase leg).  Remember the central integration of things like the Crossed Extensor Response we have talked about in prior podcasts ?
  • The implications are that if you have an ankle injury, this mechanism can be altered, resulting in loss of balance (or proprioception) as well as opening you up to greater (or additional) injury.
  • The other implication is that the whole ball of wax is “situationally dependent”; meaning plastic and adaptable. Pretty cool !
The Gait Guys. Bringing you the latest and greatest, each and every post.
                                                                                       
                                                                                                                
 SOURCE:
Exp Brain Res. 2002 Mar;143(1):24-34. Epub 2001 Dec 18.

The effects of human ankle muscle vibration on posture and balance during adaptive locomotion.

Source

Gait and Posture Laboratory, Department of Kinesiology, University of Waterloo, Ontario N2L 3G1, Canada.

Abstract

This study investigated the contribution of ankle muscle proprioception to the control of dynamic stability and lower limb kinematics during adaptive locomotion, by using mechanical vibration to alter the muscle spindle output of individuals’ stance limbs. It was hypothesised that muscle length information from the ankle of the stance limb provides information describing location as well as acceleration of the centre of mass (COM) with respect to the support foot during the swing phase of locomotion. Our prediction, based on this hypothesis was that ankle muscle vibration would cause changes to the position and acceleration of the COM and/or compensatory postural responses. Vibrators were attached to both the stance limb ankle plantarflexors (at the Achilles tendon) and the opposing dorsiflexor muscle group (over tibialis anterior). Participants were required to walk along a 9-m travel path and step over any obstacles placed in their way. There were three task conditions: (1) an obstacle (15 cm in height) was positioned at the midpoint of the walkway prior to the start of the trial, (2) the same obstacle was triggered to appear unexpectedly one step in front of the participant at the walkway midpoint and (3) the subjects’ walking path remained clear. The participants’ starting position was manipulated so that the first step over the obstacle (when present) was always performed with their right leg. For each obstacle condition participants experienced the following vibration conditions: no vibration, vibration of the left leg calf muscles or vibration of the anterior compartment muscles of the lower left leg. Vibration began one step before the obstacle at left leg heel contact and continued for 1 s. Vibrating the ankle muscles of the stance limb during the step over an obstacle resulted in significant changes to COM behaviour [measured as displacement, acceleration and position with respect to the centre of pressure (COP)] in both the medial/lateral (M/L) and anterior/posterior planes. There were also significant task-specific changes in stepping behaviour associated with COM control (measured as peak M/L acceleration, M/L foot displacement and COP position under the stance foot during the step over the obstacle). The results provide strong evidence that the primary endings of ankle muscle spindles play a significant role in the control of posture and balance during the swing phase of locomotion by providing information describing the movement of the body’s COM with respect to the support foot. Our results also provide supporting evidence for the proposal that there are context-dependent changes in muscle spindle sensitivity during human locomotion.