Traditional vs Minimalist Shoes: When Science Meets the Road

January 26, 2012

Hotel Vancouver

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Panel Members:

• Jack Taunton, MD
• Blaise Dubois, BSc, PT, RCAMPT
• Adam Janke, BSc (Kin), C Ped (C)
• Curb Ivanic, MSc, CSCS
• Jim Bovard, MD (moderator)

For more information, click here.

Also, as of today (Monday, December 19, 2011) there are only 2 spots available for the “New Trends in the Prevention of Running Injuries” workshop with Blaise Dubois and Daniel Crumback. If you’re even remotely interested, I’d suggest you register real quick. Here’s the link.

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Related posts:

1. TEDx Vancouver – Ideas Worth Spreading Vancouver, British Columbia - November 12, 2011...

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Authors: T. Noakes

Journal: British Journal of Sports Medicine

Date: November 2011

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Summary:

• Here’s a recent article published in BJSM and shared to me by my graduate co-supervisor, Joe Baker. Rather than being a randomized control trial, this is a highly opinionated and perhaps controversial paper expressing his feelings towards the American College of Sports Medicine outlining the significance of the omission of his previous findings on exercise-associated hyponatremia (EAH) during prolonged exercise. Specifically, based on research that does not include his previous studies in 1985 and 1991, it was promoted by the ACSM that athletes should consume, during exercise, as much fluid as tolerable. On the contrary, it was proposed by Noakes and colleagues that exercise-associated hyponatremia “appears to be (related to) voluntary hyperhydration with hypotonic solutions combined with moderate sweat sodium chloride losses“. As an aside, it is not uncommon to witness typical EAH symptoms of vomiting, nausea, dizziness, altered mental status in less skilled (aka “slower”) endurance athletes. While the principle argument for this paper was to suggest that very low levels of postexercisue serum sodium concentrations in athletes suffereing from EAH result from body weight gain secondary to fluid retention irrespective of volitional electrolyte (i.e. sodium) consumption, the main “takeaway” from this paper was that his research may be largely ignored due to commercial influence. What Noakes does suggest however, is that increasing sodium ingestion with increasing duration of exercise may not provide any biologically significant effect to countering EAH. So should we really still be drinking our Gatosauce or should we be paying more specific attention to our water consumption levels if we’re less gifted and toward the “back of the pack”.

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Noakes, T. (2011) Changes in body mass alone explain almost all of the variance in the serum sodium concentrations during prolonged exercise. Has commercial influence impeded scientific endeavour? British Journal of Sports Medicine.

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For those of you interested in another summary of this paper, please take a look at Alex Hutchinson’s blog.

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You walk into a specialty store dedicated to running. For the Canadians, you know which one I’m talking about. You’re a relatively fit individual looking to run your first half marathon or are someone new to the fitness industry and would like to run to get into shape. A store employee asks how he or she can help you and you inform them of your intentions. “Great” he or she says and proceeds to ask you to remove your shoes and socks so that he or she can take a look at your feet.

“Since we all have different types of feet and walk/run uniquely, then it’s important that you wear sneakers best suited to your running style,” he or she says.

You’re excited.

You quickly remove your footwear and the employee then checks your shoe wear-pattern, looks at your arches, and watches you walk.

“Great. You need a stability shoe!”

Does this sound familiar? Good. Because for some reason, everyone and their mother seems to require a “stability” shoe.

It really amazes me that some retailers go through all the trouble of looking at your arch and asking you to walk when all they will do is recommend the exact same sneaker to 95% of individuals every time.

Selling tactic? Maybe.

Time waster? Probably.

Something important? You be the judge. Have a look at this paper, published in the American Journal of Sports Medicine last year and ask yourself that question again.

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Now if they suggest a motion control shoe, run away. Far far away. Even if you’re running barefoot, just keep running. You’ll likely suffer from less pain running barefoot than you will with a “motion control” shoe. In reality, you’ll probably be fine with a neutral or stability shoe but this randomized controlled trial by Ryan et al, demonstrated that motion control shoes are NOT the way to go!

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Now what about my arches?

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The Solution

Below you will find several links to posts throughout this site to help facilitate “stability” and “motion control“. There are certainly no shortage of options so rather than giving you a generic solution, I have decided to provide you with a list of links that may assist in adding to the strategies that you may already employ.

• The Short Foot
• Ankle Dorsiflexion
• Frontal Plane Instability
• The Glutes
• Low Level Stretch Shortening
• The Glutes…again
• The Hip
• and finally, the core
• And the core some more!

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The following is a review of several of Craig Purdam’s presentations on tendinopathy at the recent 2011 Pan Pacific Conference for Medicine and Science in Sport, held in Honolulu.

Craig is the head of physical therapies for the Australian Institute of Sport and had a wealth of information to share during the weekend. I was very grateful to be in attendance.

Craig proposed that the pathology and the response to treatment are different in the various tendinopathy presentations and therefore interventions should be dictated by the specific pathology. More specifically, that there exists a continuum of tendon pathology. Namely:

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• Reactive tendinopathy
• Tendon Dysrepair (failed healing)
• Degenerative Tendinopathy

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Craig stressed that rather than looking at the above as three distinct phases, that a continuum should be kept in mind.

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Source: http://bjsm.bmj.com/content/43/6/409/F1.large.jpg

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Classification of Stages must be identified via:

• Clinical picture, and
• Diagnostic imaging

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Stage characteristics:

Reactive Tendinopathy

• Pathology: Non-inflammatory proliferative response secondary to acute tensile or compressive overload (i.e. too much too soon). Note that tensile forces cause also compression (think of an elastic band narrowing in width (compression) as it is being stretched (tension). Tendon thickening results, presumably as a protective mechanism. Upregulation of large proteoglycans, resulting in increased binding with water, accounts for the observed swelling
• Diagnostic Ultrasound: Cleaving of collagen (longitudinal separation) as exhibited by diffuse hypoechogenicity
• Demographic: Common in younger athletes (i.e. a lengthy basketball tournament) or in the young deconditioned athlete who is now exposed to moderate load exposure.

Tendon Dysrepair

• Pathology: Failed attempt at healing (greater tissue matrix breakdown) results in matrix disorganization and further collagen separation. Changes are more focal and increased thickening is certainly present
• Diagnostic Ultrasound & Doppler: collagen fascicle discontinuity and focal hyoechogenicity, as well as increased vascularity
• MRI: swelling and increased signal intensity
• Demographic: May be secondary, but not limited, to chronic overload in young athletes. In older athletes with less adaptive, stiffer tendons, this stage may develop with lower loading exposure

Degenerative Tendinopathy

• Pathology: Perhaps the most clearly described stage in the literature. Cell death is apparent, as well as matrix disorganization, vascularity, and little collagen. Reversibility of pathology is minimal
• Diagnostic Ultrasound & Doppler: Hypoechogenicity and vascularity
• MRI: Increased tendon size and intratendinous signal intensity
• Demographic: Primarily in older athletes but may present in chronically overloaded tendons of young elite athletes. Focal nodularity with or without general thickening. Typical history of repeat bouts of tendon pain with short-term relief. Injury often returns with changes in tendon load. Rupture may occur.

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For ease of interpretation, the above continuum is divided into:

• Reactive/Early Tendon Dysrepair, and
• Late Tendon Dysrepair/Degenerative

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Cornerstones of Rehabilitation:

• Confirmation of actual tendon involvement
• Stage identification
• Symptom and function quantification via outcome measures
• Load modification via training alteration and biomechanical efficiency
• Load progression
• Pharmacological and Modality interventions

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Considerations:

• Mono-therapy is rarely successful
• Tendon unloading must only be reserved for significantly “hot tendons” and must be performed for only short periods of time. Otherwise may result in decreased tissue strength

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Rehabilitation Principles:

• Unloading interventions – i.e. biomechanical efficiency
• Priority given to muscle wasting – need hypertrophy
• Early rehab – static and slow
• Speed progression
• Volume progression of functional activities
• Late rehab – elasticity
• Load management

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Treatment Strategy:

Reactive Tendinopathy:

• Load management
• Slow tempo
• Moderately heavy loads with full recovery between sessions
• Inner range then outer range
• Isometric
• Downregulate sensitization – you do not want to push this stage and aggravate further

Tendon Dysrepair:

• Gradually increase length (outer range)
• Introduce Speed and Contractility
• Undulate loading in 3 day (High, Low, Moderate) cycles

Degenerative Tendinopathy:

• Introduce Contractility and Elasticity
• Load undulation
• Eccentric progression
• *Note that this is the only stage where eccentric exercise was suggested. Perhaps this may shed some light as to why eccentric exercise has demonstrated mixed-results in tendinopathy rehab. Are some of you utilizing rehabilitation modality at the wrong stage?

*Note modalities such as cross-friction, therapeutic ultrasound, and shockwave are only appropriate in the Late Tendon Dysrepair and Degenerative Tendinopathy Stages

*For (hopefully) obvious reasons, I have intentionally omitted recommendations pertaining to pharmacological treatment..

Purdam has authored and co-authored numerous articles on tendinopathy but perhaps three of the most significant ones you may be interested in are:

• Cook JL & Purdam CR. (2009). Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine, 43; 409-416
• Allison GT & Purdam C. (2009). Eccentric loading for achilles tendinopathy – strengthening or stretching? British Journal of Sports Medicine, 43; 276-279
• Malliaras P, Purdam C, Maffuli N & Cook J. (2010). Temporal sequence of greyscale ultrasound changes and their relationship with neovascularity and pain in the patellar tendon. British Journal of Sports Medicine, 44; 944-947

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The boat...there it goes again.

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A little while back I posted a little shortie entitled “Injured? Take a Break!” The message behind this post was simply for endurance athletes to step out of their “comfort zone” and make wise…ahem, *common sense…choices when suffering from an injury.

Please consider this current post its sequel.

Often we, as clinicians, frown upon the volume of training some coaches espouse upon their athletes, criticizing the high mileage their athletes spend on the road and in the pool.

Our argument? “They are fatigued, they need to rest and recover.” The coaches’ argument? “I’ve sent many athletes to world championships and this is how we’ve always done it.”

Both may perhaps be valid points. Perhaps. So where is the disconnect?

Is high volume training really that bad?

Without question, high volume training may increase the severity of musculoskeletal injuries sustained (Brooks et al, 2008), especially in contact sports where the variables that influence the risk factors of injury are greater than that of non-contact sports. And absolutely, ultra and extreme endurance training regimens may result in acquired training intolerances of which high volume training may lead to unwanted skeletal muscle pathologies in those with such intolerances (Grobler et al., 2004). But in an appropriately individualized and periodized program for a given athlete, I really cannot place 100% blame on high volume training as the cause of injury for non-contact sports.

So let’s shift our focus just a little bit here. Where could we place some of the blame?

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The blame game.

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I recently listened to a podcast interview between Mike Robertson and Tim Vagen where they discussed this very topic. You are more than welcome to listen to this podcast here. I think Tim and I share similar sentiments in that perhaps some of this blame should be placed on the complementary training, or more specifically the lack thereof, that such athletes perform. Specifically when it pertains to addressing muscle imbalances.

You see, in 2010 we are working with athletes who live in a different generation. A generation that includes facebook, drive-thrus and escalators. And a generation where perhaps not everyone in western society are fit to wear vibrams, let alone run a marathon in them.

But let’s get back to muscle imbalances. Very often I use the analogy of a car with a slight alignment issue (I’m sure many of you do as well). Driving from home to work on any given day will not likely result in a malfunction or breakdown. But driving across the country?

I hope you get my point.

The problem I see quite often is in the lack of complementary training non-contact athletes perform. Swimmers and runners alike, these athletes (and often their coaches) seem to be pre-occupied with getting their mileage in.

“My knee hurts but I need to run 12 miles tomorrow“, or

“My elbow hurts halfway through training and I know I need to come see you but coach won’t let me miss practice”

Do you see what I’m getting at?

I am all for adhering to one’s training regimen and by no means do I have the right to question the amount of volume a specific coach programs into their…well…program. In fact, this IS their program and who am I to question it. But, the point I am trying to convey is that we must complement this training with the addition of exercise means that address those imbalances that may present themselves as a result of the lifestyle that we live. Especially in novice, intermediate, recreational, and student athletes. We simply cannot apply programs meant for professionals in such populations. This just opens up the possibility for “repetitive strain” injuries.

So if you consider yourself a non-contact athlete, be it a runner, a swimmer or the like, and are either self coached or coached by a professional, then I encourage you to take the time to start employing complementary strategies to your program. Even if it does mean cutting your training short.

And if you are a coach, trainer or rehab professional looking for a program for your athlete that encourages and devotes time to such strategies, then may I kindly suggest that you look into those programs put forth by ironguides and core performance. Your athlete will thank you for it!

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In a systematic review by van Gent et al, it was reported that the incidence of lower extremity running injuries can reach as high as 79.3%! This is not good news considering the increased interest in running as a means of improving one’s health.

Many factors may cause one to sustain an injury. Systemic factors such as (older) age, sex (females are at higher risk), and height (males > 1.70 meters) can increase one’s risk. Running and training related factors may also increase this risk such as year-round running (without a break), weekly volume (> 64 km/wk), and longer race distances. Health and lifestyle factors are also contributors to the risk of lower extremity injury via a history of previous injury and participation in other sports.

While there are many controllable ways to decrease one’s risk, what many runners fail to understand is the importance of rest and recovery once an injury is sustained. Far too often runners are more concerned with “getting in their miles” and in my opinion, this is perhaps one of the biggest reasons why injuries become chronic. They become addicted to the numbers and as a result, common sense gets thrown by the wayside. And I’m not even talking about the fact that running efficiency may be a better way to train in the first place! If you ask a professional runner or elite level running coach what you should do if you sustain an injury, I guarantee they’ll tell you  that your first and foremost priority will be to fully recover from that injury!

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Get the proper care and rehabilitate that injury. Even if you have a race coming up, you’ll be better off with full recovery. Logging in those painful garbage miles really won’t make you any faster!

So if you’re a runner suffering from an injury…take some time off. Grab a Kit Kat, find the weak link, and gradually get yourself back out there!

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For those of you who are unaware, there has been quite a stir recently regarding the role various types of sneakers play in injury prevention. Alex Hutchinson of Sweat Science wrote an excellent post on this topic last week so if you have yet to read it, click here.

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But Is It Faster? by Matt Fitzgerald: An excellent read providing an enlightening viewpoint in regards to the barefoot running craze.

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DO YOU RUN?

If you answered “yes” to the above, please proceed to the next question. If not, thanks for visiting!

Question # 2:

DO YOU PREPARE YOURSELF TO RUN?

If you answered “no” to the above, please view the following videos to help you prepare for your next run using the GRID by Trigger Point Performance Therapy.

Calves – 45 seconds each leg (Total = 1.5 min)

Quadriceps – 60 seconds each leg (Total = 2 min)

Tensor Fascia Lata – 30 seconds each hip (Total = 1 min)

Thoracic Spine Rotation – 45 seconds each side (Total = 1.5 min)

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• Transition of 2 m/s (running is more energy efficient)
• Increased Ground Reaction Forces with running
• Flight & Float phases only occur in running
• Double support & stance phases only occur in running
• Decreased stance phase and increased swing phase in running
• Overlap of swing phase (vs stance phase)
• Running requires greater eccentric contractility

In General…

• Sprinters – are more often midfoot strikers
• Endurance runners – are more often heel strikers

Running incorporates a double float phase (vs the double stance phase in walking)

• Immediately after toe off and immediately before initial contact
• At the beginning and end of the swing phase

Running Kinematics

• Stride Length – distance between initial contact to next initial contact of same foot
• Step Length – distance between initial contact to initial contact of opposite foot

Each stride consists of…

• A Support Phase
• A Recovery phase (Follow through, Forward acceleration, Foot descent)

Running Gait Cycle

• Stance Phase
  • Initial Contact
    • Heel strikers absorb increased vertical Ground Reaction Forces (close to 2.2x BW)
    • These forces should normally be absorbed by the hip, knee, and ankle complexes
• Heel-off
  • Ankle plantar flexion initiates propulsion, lengthens stance phases, and increases stride length of opposite foot
  • Supination of foot begins!
    • Transverse tarsal joint converges for rigidity
    • Due to external rotation of the tibia, gastroc contraction (attachment point), and the metatarsal break phenomenon
    • Metatarsal Break Phenomenon: Contributes due to extension of the Metatarsophalangeal joint
  • Windlass Effect due to extension of Metatarsophalangeal joint
    • Leads to tension in the Plantar Fascia
    • This also increases stability of transverse tarsal joint
  • Contraction of intrinsic muscles of the feet
  • Max Ground Reaction Forces occur when the foot pushes off the ground
    • 2.8x BW
• Toe off
  • Posterior lower leg muscles shut off and anterior musculature kick in for foot clearance
  • Hamstring group changes from knee stabilizer to hip extensor
  • Knee extensor mechanisms begin to contract concentrically to maximize knee extension (for propulsion)
• Swing Phase
  • 1^st part – knee flexes
    • Resisted by eccentric contraction of knee extensor mechanism
    • However, Rectus Femoris complex also acts to flex hip
    • Therefore knee extensors become prone to injury! (as do other muscles that cross 2 joints)
• After 1st Float Phase, opposite foot touches down
  • Hip ABDuctors contract to stabilize pelvis
• As the leg swings through, pelvis rotates putting hip into ABDuction
  • External rotation of the hip helps prepare for supination
  • This is controlled by eccentric ADDuction/ADDuctors (which are active throughout the entire swing phase)
• Anterior lower leg compartment again kicks in to dorsiflex the ankle
• Terminal swing (2^nd Double Float)
  • Hip flexion stops and posterior chain (glute/ham complex) initiates hip extension
  • Knee extension results due to rapid knee extensor mechanism contraction
• Force couple of the anterior and posterior lower leg musculature dampen the foot initial contact

Upper Extremities

• Angular momentum of the arms balance the rest of body
• Therefore, relatively low total body angular momentum

GRF

• Highest stress (GRF) occurs just at toe-off (2.8x BW)
• 2 rearfoot spikes
  • 2^nd peak is influenced by muscle activity during support
  • Midfoot strikers have a single peak
    • Decreased GRF!
    • Posterior lower leg, knee, and hip musculature act as shock absorbers – for Proximal Stability
    • They act as shocks AND springs

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I said RANDOM, didn’t I?

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Recently, I had the pleasure today of attending Movement U and subjecting myself under the watchful eye of Jessi Stensland.

This was a valuable experience for myself, not only as a professional, but also as an athlete who, like everyone else, spends countless pushing my own physical limits. And while I always strive for ideal form and proper mechanics, I may not always be doing what I think I am doing. As such, it was nice to have the eyes of another professional picking apart my leaky valves…aka, my flaws. Take a look above, my right knee is in slight valgus and my tibia is externally rotated…something I have not noticed since I don’t like training in front of a mirror.

Last year I raced Ironman Canada hiding all sorts of injuries. It pays as a sports doc and strength coach to know what to do to be able to make it to the start line. I never felt pain, but deep down I knew I had the potential to blow up. This year, on the other hand, the goal is to think like a doctor, train like a coach, and perform like an athlete!

So whether or not you are an expert or intern, independent of “talking shop” with another colleague or taking notes at a national conference, every now and then I suggest everyone “working” in the industry to take part in an interactive learning session and physically fall back into the “student” role.

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Professional triathlete, Jessi Stensland recently tweeted the following:

“Injury free running is not about the right shoe it’s about the right U!”

This immediately reminded me of Ironman, Mirinda Carfrae, who last August the Ironman Calgary 70.3 triathlon. I was there spectating that race (as my wife participated) and was fortunate enough to catch a glimpse of Mirinda’s beautiful running form. Here’s a shot I took of her after she swam 1.2 miles, biked 56 miles, and ran 11 miles.  Notice her form with  2 miles left to go!

Posture… check!

Now for those of you who want to see her running form in real time, then here’s an excellent breakdown I stumbled upon on youtube.

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