Knee hyperextension and delayed heel rise in an interesting sport, Racewalking.

If you have been in practice long enough, you should know by now that in order to truly help an athlete you have to know their sport, the subtleties and the specifics.  You have heard us talk about premature heel rise off an on for years. Today, you must consider the opposite, delayed heel rise and the bizarre loading responses that come into the kinetic chains from such a behavior.

Racewalking is a long-distance event requiring one foot to be in contact with the ground at all times. Stride length is thus reduced and so to achieve competitive speeds racewalkers must attain cadence rates comparable to those achieved by Olympic 800-meter runners for hours at a time. Most people cannot truly appreciate how fast these folks are going.

There are really only two rules that govern racewalking:

1-The first rules states that the athlete’s trailing foot’s toe cannot leave the ground until the heel of the leading foot has created contact. 

2-The second rule specifies that the supporting leg must straighten, essentially meaning knee extension (and for some, terminal extension, ie. negative 5-10 degrees !) from the point of contact with the ground and remain straightened until the body passes directly over it. Again, essentially meaning full range knee extension for the entire stance phase of gait (early, mid and late midstance phases). 

Delated heel rise ?

Clearly some folks are going to take knee extension a little more literally. Look at the fella in the red and yellow. Can you say knee HYPER extension ? This is right knee anteriormeniscofemoral impingement looming on the horizon, this is an anterior compression overload phenomenon via the quadriceps. This is often met in this sport with the delayed heel rise that the sport seems to often drive. Prolonging the foot ground contact phase, attempting to abide by Rule#2, “the support  leg must straighten”, can lead to knee hyperextension if one is not careful. This will put a longer stretch load into the achilles and posterior compartment mechanism and this prolonged stretch-contract load can eventually lead to local pathology let alone in combination with the anterior knee compression we just eluded to. These folks will also be at risk for more anterior pelvic tilt, distraction of the anterior hip capsule-labral interval, unique hip extension and gluteal integration, and even possibly altered hip extension motor patterning driving abnormal loads into the hamstrings and low back.  Just imagine the changes in the hip flexor strategies in this scenario. 

To help your athletes, know their sport, know your normal biomechanics and know the pathologies when the rules of clean biomechanics are broken.

Today, on Rewind Friday, we will repost a more in-depth, with video, piece we did a few years ago on Race Walking. You may learn more about normal and abnormal gait than you think, today we translate some of the rules of the sport of race walking into deeper thoughts on gait mechanics.

Here is the link to our more in-depth video assessment and dialogue on the fascinating sport of race walking. If you have never truly looked at this sport before, you should enjoy this Rewind Post. (link).

– Dr. Shawn Allen

Dragging your tongue ? When the tongue of your shoe keeps getting pulled to the side. Do you know what it means ? It means plenty, if you are sharp.

By: Dr. Shawn Allen

This one pisses off most people it happens to. Why does it typically happen only on one side, on one shoe ? Look at the photo case above. Look closely to the left foot, the tongue of the shoe is pulled laterally compared to the right, or shall I say, dragged.

This is a fairly common phenomenon, and there is a reason for it, several actually. So, no, you do not need to staple the tongue to the shoe upper, or tighten your shoe laces, or stitch the tongue to the medial shoe upper. You need to stop externally spinning your foot in your darn shoe.  What ?!

Yes, you very well may be avoiding normal internal rotation progression of the pelvis over the fixated limb. Loss of internal hip rotation is often a common finding clinically. As one passes the swing leg forward, the forward progressing pelvis eventually meets this loss of internal rotation over the fixated leg and femoral head. The swing leg none the less progresses further forward to get to its’ heel strike and the stance phase leg has to externally spin over the ground (I like to give the analogy of putting out a cigarette butt on the ground or squishing a bug (PETA don’t come after me)). This is called an Abductory or Adductory twist (good video demo here) depending on whether your reference point is the forefoot or rear foot. Regardless, the heel is spinning inward, the forefoot is relatively spinning outward. This spin of the foot inside the shoe (this happens minutely just before the shoe spins on the ground) and pulls the tongue laterally with it.  

This problem can also come from, and often does, a premature heel rise from things like a:

  •  loss of ankle rocker
  • short calf
  • lack of hip extension
  • hallux rigidus / limitus or even a painful big toe
  • etc

There are even several other causes I will not list here today, I could have you waste your whole day on the list and the mental gymnastics of things to consider. Basically, anything that impairs the stance phase mechanics creating a premature heel rise or failure of completing internal hip rotation can cause an Abd/Adductor twist of the foot/heel and drag the tongue laterally. Sure, there are others, but the purpose of my blog post here today was to explain a neat little biomechanical phenomenon that  has huge clinical insight if you know what it means.  You cannot fix this problem if you do not do a physical exam, understand clean and faulty gait biomechanics, and maybe can even find small objects in a dark room.  What I mean is it takes some educated exploration and a curiosity to want to fix things.  

There are clues often right in front of you, all you have to do is pay attention and sometimes ask a simple question. 

“Mr. Jones, when you stick out your tongue, does it drag laterally ?”  

Ok, maybe not that exact question. But, when I see a loss of internal rotation or terminal hip extension in a runner, and when I have time to explain things deeply with a openly receiving client, I might start the conversation with that fun question and then explain what I really meant was the tongue of the shoe on that affected side. 

You can’t swallow bandaids to fix things, as much as you wish it was that easy. Sure, you can avoid all of this fun by buying a shoe that has the tongue of the shoe sewn to the medial upper of the shoe, but then you wouldn’t have to fix anything.  Where would you “get your fun on” then ?  Be brave, go all in, fix the problem dammit.  

These are the things that keep me up at night. Welcome to my nightmares.

Dr. Shawn Allen, one of the gait guys

Photo courtesy of this link:

The Bouncy Gait: Premature heel rise gait. Taking another look.

This is a great video example of a premature heel rise during gait. You should be able to clearly see it on the left foot (and this was toned down after we brought it to his awareness!).  The heel rise occurs early in the stance phase of gait, instead of the late stance phase.

We have talked about this bouncy type vertically oriented gait many times in blog posts and in our podcasts.  This is a pretty prevalent problem in the world, mostly because so many people have impaired ankle rocker/dorsiflexion from weak anterior compartments and short/tight posterior compartments.  None the less, for the majority, this is a pathologic gait pattern and it will impart undue stress into the posterior mechanism (calf-achilles complex). Just think about it, this person is going vertical at or prior to the tibia achieving 90degrees (perpendicular to the ground) instead of continuing to progress the tibia to 110+ degrees to enable normal timely pronation and foot biomechanical events.  This is not a normal gait. Period. This will change the function of the entire posterior chain upward. 

If you want to see another great example  from the frontal plane, check out this cute video representation of a vertial/premature heel rise bouncy gait. 

This gait style is caused by a premature heel rise from joint range limitation and/or from premature engagement of the gastrosoleus (and sometimes even the long toe flexors, you will see them hammering and curled in many folks). It can be a learned habitual pattern and nothing more, we have even seen it even in child-parental gait modeling in our offices. These people will never get to NORMAL full late-midstance of gait (without biomechanical compromise) and thus never achieve full hip extension nor adequate ankle dorsiflexion / ankle rocker. The gait cycle is an orchestrated symphony of timely events and when one or several timely events are omitted or impaired the mechanics are passed into other areas for compensation. This vertical gait style is very inefficient in that the gluteals cannot adequately power into hip extension into a forward progression drive, because the calf is prematurely generating vertical movement through ankle plantarflexion.  This strategy is sometimes deployed because the person actually is significantly ankle dorsiflexion (ankle rocker) deficient.  Meaning, they hit the limitations of dorisflexion and in order to progress forward they first have to go vertical.  This vertical motion, because they are moving into ankle plantarflexion, re-buys more ankle dorsiflexion range which then can be used if they so choose. Obviously, the remedy is to find the functional deficit, remove it and retrain the pattern.  There are a whole host of other problems that go with this compensation pattern but we wanted our mission to stay focused today.  Remember, this is usually a subconscious motor pattern compensation. Is it like the toe walking issue we talked about last week (post link here) ? It is similar in some ways and can have primitive and postural motor pattern implications. We will follow up the “Idiopathy Toe Walking Gait: Part 2” shortly but we wanted to strategically put this blog post ahead of it, because there are similar characteristics and implications. Trust us, there is a method to our madness 🙂

Shawn and Ivo

The Gait Guys

More Foot Rocker pathology Clues.

Is ankle rocker normal and adequate or is it limited ?  Is it limited in early midstance or late midstance ? How about at Toe off?  Is it even possible to distinguish this ? Well, we are splitting hairs now but we do think that it is possible. It is important to understand the pathologies on either end of the foot that can impact premature ankle rocker. 

Look at the photo above. You can see the clinical hint in the toe wear that this runner may have a premature heel rise. However, this is not solid evidence that every time you see this you must assume pathologic ankle rocker. The question is obviously, what is the cause.


1- weak anterior compartment, which is quite often paired with the evil neuroprotective tight calf-achilles posterior complex to offer the necessary sagittal protection at the ankle mortise.  This will cause premature heel rise from a posterior foot aspect.

2- rigid acquired blocked ankle rocker from something like “Footballer’s ankle”. This will also cause premature heel rise from a relatively posterior foot aspect.

3- there are multiple reasons for late midstance ankle rocker pathology. The client could completely avoid the normal pronation/supination phase of gait because of pain anywhere in the foot. For example, they could have plantar fascial pain, sesamoiditis, a weak first ray complex from hallux vaglus, they could have a painful bunion, they could be avoiding the collapse of a forefoot varus. There are many reasons but any of them can impair the timely pronation-supination phase in attempting to gain a rigid lever foot to toe off the big toe-medial column in “high gear” fashion. And when this happens the preparatory late midstance phase of gait can be delayed or rushed causing them to move into premature heel rise for any one of several reasons.  Rolling off to the outside and off of the lesser toes creates premature heel rise.  

4- And now for one anterior aspect cause of premature heel rise. This is obviously past the midstance phase but it can also cause premature heel rise. Turf toe, Hallux rigidus/limitus or even the dreaded fake out, the often mysterious Functional Hallux limitus (FnHL) can cause the heel to come up just a little early if the client cannot get to the full big toe dorsiflexion range.  

We could go on and on and include other issues such as altered Hip Extension Patterning, loss of hip extension range of motion, weak glutes, or even loss of terminal knee extension (from things like an incompleted ACL rehab, Osteoarthritis etc) but these are things for another time. Lets stay in the foot today.

All of these causes, with their premature heel rise component, will rush the foot to the forefoot and likely create Metatarsal head plantar loading and could cause forces appropriate enough to create stress responses to the bone. This abrupt forefoot loading thrust will often cause a reactive hammer toe effect.  Quite often just looking at the resting nature of a clients toes while they are lying down will show the underlying increase in neuro-protective hammering pattern (increased long toe flexor and short toe extensor activity paired with shortness of the opposing pairs which we review here in this short video link).  The astute observer will also note the EVA foam compressing of the shoe’s foot bed, and will also note the distal displacement of the MET head fat pad rendering the MET head pressures even greater osseously. 

Premature ankle rocker and heel rise can occur for many reasons. It can occur from problems with the shoe, posterior foot, anterior foot, toe off, ankle mortise, knee, hip or even arm swing pathomechanics.  

When premature heel rise and impaired ankle rocker rushes us to the front of the foot we drive the front half of the shoe into the ground as the foot plantarflexion is imparted into the shoe.  The timing of the normal biomechanical events is off and the pressures are altered.  instead of rolling over the forefoot and front half of the shoe after our body has moved past the foot these forces are occurring more so as our body mass is still over the foot. And the shoe can show us clues as to the torture it has sustained, just like in this photo case.

You must know the normal biomechanical gait events if you are going to put together the clues of each runner’s clinical mystery.  If you do not know normal how will you know abnormal when you see it ? If all you know is what you know, how will you know when you see something you don’t know ?

Shawn and Ivo, The Gait Guys … .  stomping out the world’s pathologic gait mechanics one person at a time. 

During a recent trip to the zoo with the family, I noticed this young lady walking in front of me (yes, We ALWAYS have a camera with us and YES, We ALWAYS look at everyone’s gait and YES, we really are that geeky).

Watch the clip a few times and note these points about the gal on the left; keep in mind, she could have hip or muscle pathology as well

  • notice the subtle toeing in (decreased progression angle) of the feet, most likely due to internal tibial torsion
  • notice how she doesn’t have her shoes tied; this would necessitate her clenching or clawing her toes to keep her shoes from falling off. This inhibits the activity of the glutes and causes her to have to extend from the hams and lumbar spine; as a result, note how straight she keeps her legs when ambulating
  • there is little to no ankle rocker; she goes from heel rocker to forefoot rocker
  • premature heel rise
  • due to the lack of hip extension and decreased activity of glute max, note how she “rotates” around each leg
  • how about that cross over gait?


For starters:

  • tie your shoes
  • 1 legged standing exercises, being careful to keep hips level and not have a pelvic shift
  • walk with toes up or slightly extended during all phases except for that brief moment during midstance where you need the toes for balance and ground purchase
  • shuffle exercises to engage glute max
  • never wear pants that are sooooo tight that you cannot generate normal fluid gait

Ivo and Shawn…The Gait Geeks…We leave no gait unanalzed…even at the zoo. Watch it; we may have YOU on film!

Yesterday’s Video Case: The Gaits of Hell

We have received many emails on this case already. Overwhelmingly people are saying……. “Hey, this isn’t easy….. It’s easy when you guys tell us right away because we can see it.”  
Yes, when we are all alone to solve these gait problems our heads can start to swim with all the variables. Gait analysis is not easy.  Even the video assessment computer programs do not give you the answers and diagnosis, they just give you variables and data.  The thinking still has to be  done at the end of the day.

I remember how much I struggled with this case back during my orthopedics residency. I remember even pulling out my undergrad notes from Univ. of Waterloo as a student of the famous Dr Stewart McGill and mapping out FBD’s (Force-Body Diagrams) on this case. Oh, the horror !!!  I still have occasional FBD nightmares, being asked to solve an equation in front of the whole class. Pure anxiety ! Holy night terrors ! But, it is amazing what a few decades of study will do for you, we can now look at this case and see things for what they are, see them quickly and know what is going on almost immediately.  It takes some time, so if you are new to this stuff, be patient…… it will come.


in this video we see the following:

  1. large step length off of the left foot abruptly onto the right, this step is sudden and he crashes down on to the right foot sooner than he normally would to catch his forward moving body mass. ( this will make more sense after reading #5).
  2. there is a delayed left heel rise and delayed left calf recruitment , actually, it’s not delayed, it’s absent. )
  3. the left foot remains supinated through the entire gait cycle. 
  4. the left foot shows extraordinary long toe flexor recruitment (seen on the end of the video during the foot close up)…….this point is important
  5. pelvic unleveling is apparent but a mirage for the most part. We really do not see a true Trendelenberg style gait (although it sort of looks like the left hip drops) rather, what you see is the result of the manufactured delayed left limb departure and subsequent impact at right limb load … but this is not a Trendelenberg gait, he had no Gluteus medius weakness.  Explained another way, he is having troubles departing off of the left foot (this diagnosis is the reason, he has compensated from a neurologic lesion affecting the strength of the calf) and so he extends ( behind him) the left leg longer and further than normal because he cannot push off, plus he hyperextends the left knee because of these factors. Normally, the calf fires after passive heel lift occurs. But with a lesion affecting the calf it has arrested the push off. So, in his case, the heel stays on the ground until it is dragged off from enough  forward body carriage. So, when you see this from a sagittal view the left hip will look like it is dipping as it does here, but it is not truly, he is just taking a long lurching step off of the left and onto the right, the longer left hip extension behind him sets up the illusion of a left hip drop.  Try this at home to feel this gait, walk down your hallway and try to delay the left heel rise for as long as you can.  You will find that you get into your left gluteals more, take a longer step on the left, and take a sudden lurching load onto the right limb to catch your forward progressing body mass. This is exactly what this chap is doing.  But why ? The left calf lesion. 
  6. continuing on #5, there is abrupt right frontal plane loading (because of the sudden transition from left foot to right the frontal plane is engaged longer than normal) and thus the pelvis is carried further to the right in the frontal plane.  He makes a  noble attempt to protect this range by turning out the right foot into the frontal plane (aka. increased right foot progression angle) to allow the quadricep muscles to assist the gluteus medius, abdominal obliques and lateral limb stabiliers in decelerating this frontal plane challenge.

Diagnosis:This doctor came to see me while I was completing my orthopedics residency and mid way through my course work in the neurology post doctoral program. He had been treated for mechanical low back pain with failed results ( well, to be accurate. his low back pain had resolved but pain had peripheralized into the left leg. To review, peripheralizing pain is rarely a good neurologic sign.)  After an examination showing an absent left S1 Achilles reflex it was highly suspicious we were dealing with a radiculopathy. An MRI confirmed a substantial left foraminal disc herniation obliterating the left S1 nerve root foraminally. The S1 nerve root expands into branches feeding input into the lower limb muscles.  In this case, the unfortunate group affected was the gastrocnemius almost exclusively. So in this case this makes sense to what is presented clinically and on gait evaluation. He is overutilizing his long toe flexors (fortunately untouched) as seen in the video because they are basically all that is available to him to plantarflex the foot ( create heel rise and push off).  They are certainly not well suited for this task but subconsciously the brain will use what is available to it, worthy or not. In this case they are a feeble attempt at best. There is no way the long toe flexors can lift his body mass into heel rise and propulse it forward, they are synergists of this task and not agonists / prime movers.
Sequencing Summary:So, this is a case of an aberrant or pathological gait pattern that will be permanent because the nerve damage was fixed by the time i had seen him.  Muscular wasting of the gastroc complex had already occurred.  The culprit was the space occupying lesion (disc in this case) in the left spinal vertebral foramina effacing and deforming the nerve root sufficient enough to create dennervation.  A surgical consult and EMG/NCV (as best as i can recall) confirmed this case was non-surgical at that time (no one wanted to touch the case).  The nerve damage disabled the calf so that push off was impaired.  He thus delays his ability to create adequate heel rise and propulsion so the long toe flexors are called to attempt the feat.  The foot supinates to maintain its rigidity ( it is also hard to pronate through the foot when the toe flexors are in an all out contraction). And because the heel does not rise on its own from muscular strategies, the foot waits to be lifted off of the ground by simple forward progression of the body.  This creates an increased left hip extension range and gives the appearance of a left hip drop which is a false appearance pseudo-Trendelenberg sign.  Due to the fact that he is on the left limb longer, he will be on the right limb for a shorter period.  This right stance phase is initiated abruptly as he falls from the delayed left stance phase. The abruptness of the load on the right challenges the right frontal plane as evidenced by the right foot turn out and right pelvis sway (subtle).  He then departs off the right to  begin the cycle once again.
PS: It is coming a little late, but thank you Dr McGill. Your teachings to a young undergrad set my biomechanical thinking on the right path very early in my studies of human kinetics. Thank you, Sincerely. 
Dr Shawn Allen…… The other half of The Gait Guys