Core stability and low back pain: How stability exercises might help. Part Two


In part one of this post I very simple reviewed some of the ideas behind core stability and how I questioned their relevance to a patient's pain presentation.  In this follow up post I will briefly review how people with pain have different function than those without pain and give an opinion on how core 'stability" exercises may help with patients in pain in a manner that has nothing to do with stabilizing the spine.

What do we know and what can we do with patients with low back pain

- some patients with low back pain show delays in Tranny firing

- this delay can be correlated with the presence of low back pain

- changes in muscle timing occur with perturbations to the spine

-improvements in pain and function can occur and have nothing to do with changes in firing onset (see here )

-changes in firing onset can occur and have nothing to do with a motor control retraining plan (see Gary Alison's recent work here which he has been trumpeting this idea for more than a decade, here and here)

- some clinical prediction rules help identify who best responds to a "spine stability program"

- I published two literature reviews years ago that outline how peoples spines function differently with pain (Here and here). The research shows those with pain have differently behaving muscles, changes in proprioception, differences spine kinematics and differences in how they move

But so what if there are changes in function?  Do we need to know this to make improvements in pain?

None of the research suggests that these differences occurred before the pain nor does any research suggest that changing these dysfunctional parameters is necessary for pain resolution.  We probably don't need to specifically address these changes in function with our treatment and most of us aren't.  From the above list there are at least 8 means that the spine is "dysfunctional" as measured with some advanced biomechanical testing.  All of us do not do these testing on our patients yet we are often able to make them feel better.  What does this tell you about advanced testing? It probably isn't necessary.  Or is the test that is most important just the one that your clinic happens to have access to (I'm talking to you you people with Rehabilitative Ultrasound Imaging - I guess you have to justify the cost somehow :) )  We may just need to address the patient's pain, their beliefs, their attitudes, their activity levels and their habits and we will get changes in these functional outcome measures or we won't get changes in those outcome measures and we don't even need to.

These changes in how muscles work can definitely occur in the presence pain.  Where we are confused is correlation and causation. When did these changes begin in relation to onset of pain?  We have some suggestion that changing these motor control variables does not relate to improvements in symptoms (Mannion 2012).  So are these changes just a defense of the body rather than some defect?  They are assumed to be surrogates for stability but are they?

Maybe we should see them as secondary casualties in how our brain works.  The brain changes with pain.  Pain is an output of the brain.  So is motor control.  We can also see changes in swelling, heat, blood flow.  No one thinks that we have to address these secondary adaptations to help with back pain but we think we have to address the motor control or stability issues.  All of which can be secondary byproducts of the persistent pain experience rather than some original criminal mastermind of the patients pain.


What do I think my exercise prescription is doing

Breaking habits of motion, changing fear and building self efficacy

Directional preference, flexion intolerant, extension intolerant, activating neurotags etc. Patients have movements that hurt.  Sometimes they continually perform these movements and they keep hurting.  Maybe they were told that they were supposed to sit up straight, brace their spine, suck in their belly and always activate their lazy glutes.  And guess what, sometimes you have these patients relax, move their spine, sometimes slouch, sometimes put their feet up, stop worrying about their glutes and keep active and voila their pain feels better. Instead of "correcting" some stability problem we just gave the patient permission to move with a lot of variety.   We just broke a pain habit.

Sometimes, patients get pain with flexion and for some reason they keep doing activities that flex their spines and they keep having pain.  Sometimes, we suggest that they move the opposite direction, try to find a position of relief and every hour they arch backwards for a few weeks.  Then we slowly have them start flexing their back again (because we don't want them to be afraid of flexion, its what we are meant to do) and now they can flex their spine without pain.  Are these patient's spines any more or less stable? Did their tranny start firing earlier? Who knows, they have less pain.  They began to move differently than what they were previously doing and this helped.  We broke a habit, found positions of relief, built confidence that they could move without pain and transferred that confidence over to other activities.

In some patients you can give them a full spine stability program aimed at buttressing their entire spine. The exercises feel good when doing them.  The patient gets more confident.  They feel stronger and even their pain decreases.  Did their spine's stability become more robust? Maybe.  Is this what caused less pain?  Probably not.  You got this patient moving, maybe you caused exercise induced analgesia.  You put them in control and they felt better.  It probably helped if you didn't tell them there spine was unstable before you gave the exercises.


What is my point?

Keep it simple. Adam Meakins (A sport physiotherapists at  wrote a simple tweet


"In physio you cant go wrong if u do the simple things exceptionally well & save the fancy crap for show offs & bullshitters #ROM #power etc "

This might encapsulate my treatment philosophy in all its foul mouthed glory.  While the body is extremely complex and the pain experience difficult to fully understand our interventions can be quite simple.  We are not car mechanics where we are tightening something or loosening something.  We just provide some input into the body.  The body and brain then decide what to do with it.

I still advise bird dogs, side planks, front planks, curl ups, squats and all the exercises that are in the traditional North American stability paradigm.  Sometimes, I even check to see if you someone can suck in their belly button without other muscles turning on and if doing that decreases the pain in their back when they move their leg.  Do I think that any stability changes occur and this is causing their pain to decrease?  NO. There are other reasons that these movements help.

Do I think that all those planks are creating rigidity in the spine.  Of course not, this is much too simplistic.  So what the hell do I do and what do I think I am doing.

My approach and my rationale

All of the following assumes I have ruled out the nasty stuff.

1. Educate about pain.  Don't catastrophize.  Explain the difference between tissue injury and pain.  Explain that we are meant to move and that pain is normal and is not some indication that they are falling apart.  Explain that their scary x-rays and MRIs are poorly correlated with their pain.   Explain that pain is so much more than just the tissues in their back and reassure them that they can do something about it.

2. Touch them with your hands:  Move them, push, pull, rub, crack, traction, distraction, compression. Whatever.  Manual therapy has some neurophysiological pain modulator effect.  Skip the bullshit explanation about the complexity of the SI joint having an upslip, downslip, a shear or flare or whatever.  You can't feel this and you can't correct it.  But using your hands can modulate the perception of pain and can change muscle and joint performance.  This gets your patients confident that change is possible.

3. Move meaningfully.  What is important to your patients?  Find some movement related goal that is important.  Figure out a way to do this.  Set small goals related to this movement and achieve them.  They might have pain during this task but they know that pain does not mean damage and that they can do it.  Don't hammer them into fighting through pain so that they feel "Wind Up" the next day.  But keeping pushing that pain threshold up.  Keep empowering them.

4. Stress the body.  This is where I use exercise.  I find a movement that is painful.  I figure out someway to modify that movement so that it is not painful (think Mulligan).  Train that movement.  Start to break the habit of pain.  Pain is a habit.  If we activate a pain neurosignature with certain movements we can sometime modify that movement so that that neurosignature is not activated.  Do this.  This is where "spine stability" exercises can come in.  Get them working their achey back in ways that don't cause pain.  This is awesome they train a painful area without experiencing pain.  This decreases the threat associated with movement, decreases kinesiophobia and changes how they think about pain.

5. Train harder: pick a movement that is kind of related to their painful site but does not hurt at all.  Train the hell out of this.  This can be build confidence in their body.  For example, they might have shoulder pain but they can deadlift.  What a great shoulder exercise.  You work your entire body, train the shoulder but experience no nociception.  Hammer this.

6. Address beliefs: we need to understand what our patients think about their condition and how that impacts their psychosocial profile.  If they have some serious catastrophizing, fear avoidance, depression, perceptions of injustice etc this shit needs to be addressed.

An opinion on motor patterns

I have seen "faulty" motor patterns and I have also seen them "corrected" by doing exercises that have nothing to do with retraining the supposedly faulty muscles.  If a motor pattern is corrupted this pattern is most likely corrupted at the level of the brain.  If I train some movement, modulate pain with some education or mobilization we often see changes in these motor patterns.  But I didn't change these as a mechanic.  There was no tweaking at a local level of "muscle imbalances".  We aren't bloody puppeteers The imbalances get "corrected" via other means.  Or they don't get corrected and my patient is pain free and I know that "muscle imbalances" can certainly be normal variations of your complex system.

So just remember this mnemonic: KISDAS.  Keep it simple Dumb AsS.


Future posts and questions for research

Corrective Exercise: this approach, besides being an unethical cash grab for CE dollars by some questionable organizations by making good intentioned personal trainers and physios feel insecure, has a number of assumptions about human function that we all need to question.  I also want to investigate it because it is an approach that I kind of use daily (see my defense here of the lowly clamshell) although I try to simplify it and pain neuroscience it up a bit.  And besides, isn't "corrective exercise" what every good coach or therapist does automatically? Find a deficit and improve it?  Anyways,  corrective exercise has a number of interesting things that we can look at and I don't think it is worth completely discounting.  Here are some areas I hope to address:

1. It assumes that there is an ideal way that the body functions.  I think this is everything most physios, trainers and coaches do yet our research is so piss poor.  I would love a catalogue of articles that attempt to categorize the best way to move.  We need to settle this debate once and for all.  The catalogue might just show exceptions and the huge variety that is acceptable.  It might show that their instances when it is best to move on way over another.  I know it is more complicated than just avoiding knee valgus, keeping a neutral spine, not letting 'global movers" shut down "local movers" and assuming that all asymmetry is evil.

2. It assumes that isolated testing (e.g single leg squat, prone leg extension, single leg glut bridge) gives us some insight into altered functioning.  It then assumes that the altered functioning in some isolated test actually correlates with assumed altered functioning during some more meaningful performance task (e.g running, deadlifting, squatting).  I wrote a PhD proposal on this area and you would be surprised how poor our tests are at actually testing anything we think they are testing and also correlating with functional activities. Guess what? Did you know that the quadruped rock back test coupled with spine rotation actually does not "lock out" the lumbar spine and only result in thoracic rotation?  Crazy.  Or that the thoracic spine has just about the same amount of rotation capacity as the lumbar spine.

3. Muscle activation?  Such a neat, simple and prevalent idea.  Training some small movement (e.g squeezing your glutes during a bridge) while "turn on" some muscle during another activity.  I would love to see this idea put through a simple experiment.  Flippantly, it again views the body as something that is so stupid.  Certainly worthy of some good research.

4.   I would love to see a series of blog posts look at altered joint kinematics (what a corrective post assumes it is correcting) and how these alterations correlate with changes in pain or improvements in function. My big hesitation with the corrective exercise approach is that it complicates things and does not seem to recognize the uncertainty that exists in human function. Further, corrective exercise assumes that there is a limited way to "correct" the dysfunction.  aka. you need the "correct" corrective exercises.  I would suggest that there are a multitude of exercises or approaches that can influence pain perceived to becoming from a joint and the resultant aberrant kinematics.  Anyone want to look at this topic?

5. Of course we could also talk about foam rolling.   It is interesting that there does seem to be a shift in the rolling world to get away from the idea of digging out knots and adhesions and focusing on the possible neural aspect for the treatment mechanism.  But fascia is still king in some circles and I can't fathom why.

I would guess that if we look at the biomechanics and motor control literature we would find that our treatments can be much simpler, we would have lots of variety and many approaches would be successful.  We would not have to have incredible complicated solutions to simple problems (avoid the Rube Goldberg trap of exercise prescription).


Happy new year!  Anyone interested in collaborating on blog posts please email.


Structure is not Destiny - please don't rush to freaking out about your x-ray, MRI or ultrasound

Audience: Patients Purpose: To highlight the poor link between the bogeymen found on imaging with pain or dysfunction.

Our current technology is amazing when it comes to viewing the insides of our body.  The problem with this fantastic technology is that we can see something (e.g. a tear in a muscle or a joint with some osteoarthritis) and assume that there is something wrong or that this is the source of our pain.  However, the link between tissue "abnormalities" on MRI, x-ray or Ultrasound is often quite poor.  Many, if not most, people have "bad stuff" on their MRIs or x-rays yet have no pain.

A quick anecdote...I was with a patient that had horrible left shoulder pain. Poor movement and worse strength.  His doctor ordered an MRI and my patient reported to me that sure enough the shoulder was a mess.  Torn rotator cuff, bursal thickening, arthritis in many joints, some fluid collecting - an absolute disaster.  BUT, there was a problem.  He wanted to know if the MRI picture could have been "flipped" or "mirrored" because these results were for his Right, painfree shoulder.  The results weren't flipped or mirrored, we got the results for the left later.  They were just as "bad".  Point being, structure is not destiny.  Damage or scary stuff on any imaging report does not equal pain.  This patient ended up pain free in a couple months.  His MRI report would not have changed despite the changes in his strength, mobility and pain.

This is not new

I am not breaking any news here.  We have known this for at least 15 years.  Joint degeneration, disc bulges (even herniations), rotator cuff tears, calcifications in ligaments or joints are all normal variations that can exist without pain.  At certain ages this changes, assumed to be abnormal, are actually normal and more common than a lack of these changes.

Below is a sampling of research highlighting the limitations of structural anomalies and pain.  I was going to provide some insight but instead I will use this post as a catalogue of the research that looks at the relationship between tissue damage/abnormalities and pain.


Bottom Line:  Pain is poorly correlated with damage.

One caveat: I hesitate to say this but sometimes these structural changes can be related to pain... it is just not a guarantee or some harbinger of pain doom. What I want to emphasize is that it is just not as cut and dry as many make it seem.  There are many factors that lead to pain but we tend to blame the simplest one (e.g. joint damage) when we actually know better but persist in this fallacy.

Some other links on this topic:

Diane Jacobs:

Bboy Science (Tony Ingram):

Spine Imaging Abnormalities are really just normalities

Maurer M, Soder RB, Baldisserotto M Spine abnormalities depicted by magnetic resonance imaging in adolescent rowers.Am J Sports Med. 2011 Feb;39(2):392-7. Epub 2010 Oct 2.

Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS N Engl J Med.Magnetic resonance imaging of the lumbar spine in people without back pain. 1994 Jul 14;331(2):69-73. (abstract  here)

Weinreb JC, Wolbarsht LB, Cohen JM, Brown CE, Maravilla KR. Prevalence of lumbosacral intervertebral disk abnormalities on MR images in pregnant and asymptomatic nonpregnant women. Radiology. 1989 Jan;170(1 Pt 1):125-8.  Link here

Takada E, Takahashi M, Shimada K.Natural history of lumbar disc hernia with radicular leg pain: Spontaneous MRI changes of the herniated mass and correlation with clinical outcome.J Orthop Surg (Hong Kong). 2001 Jun;9(1):1-7. Abstract here.

Stadnik TW, Lee RR, Coen HL, Neirynck EC, Buisseret TS, Osteaux MJ.Annular tears and disk herniation: prevalence and contrast enhancement on MR images in the absence of low back pain or sciatica. Radiology. 1998 Jan;206(1):49-55.

Matsumoto MFujimuraY, Suzuki N, Nishi Y, Nakamura M, Yabe Y, Shiga H.MRI of cervical intervertebral discs in asymptomatic subjects.J Bone Joint Surg Br. 1998 Jan;80(1):19-24. Abstract here.

Shoulder abnormalities not related to pain

Connor PM, Banks DM, Tyson AB, Coumas JS, D'Alessandro DF. Magnetic resonance imaging of the asymptomatic shoulder of overhead athletes: a 5-year follow-up study.Am J Sports Med. 2003 Sep-Oct;31(5):724-7. Abstract here.

Miniaci A, Mascia AT, Salonen DC, Becker EJ Magnetic resonance imaging of the shoulder in asymptomatic professional baseball pitchers. .Am J Sports Med. 2002 Jan-Feb;30(1):66-73. Abstract here

Jost B, Zumstein M, Pfirrmann CW, Zanetti M, Gerber C.MRI findings in throwing shoulders: abnormalities in professional handball players.Clin Orthop Relat Res. 2005 May;(434):130-7. Abstract here


Shellock FG, Hiller WD, Ainge GR, Brown DW, Dierenfield L.Knees of Ironman triathletes: magnetic resonance imaging assessment of older (>35 years old) competitors. J Magn Reson Imaging. 2003 Jan;17(1):122-30. Abstract here

Beattie KA, Boulos P, Pui M, O'Neill J, Inglis D, Webber CE, Adachi JD. Abnormalities identified in the knees of asymptomatic volunteers using peripheral magnetic resonance imaging.Osteoarthritis Cartilage. 2005 Mar;13(3):181-6. Abstract here

Shellock FG, Deutsch AL, Mink JH, Kerr R Do asymptomatic marathon runners have an increased prevalence of meniscal abnormalities? An MR study of the knee in 23 volunteers.

Zanetti M, Pfirrmann CW, Schmid MR, Romero J, Seifert B, Hodler J.  Clinical course of knees with asymptomatic meniscal abnormalities: findings at 2-year follow-up after MR imaging-based diagnosis. Radiology. 2005 Dec;237(3):993-7. Epub 2005 Oct 26.



More to come.

Are you sure your hip flexors are tight? If so, why and who cares?

Update: I am not the first to write about this area.  I found a great post by Todd Hargrove tackling the same topic and saying much the same (he does it more succintly and I address a few other areas as well).  His post is here: Tight Hip Flexor Bogeyman

We too often tell patients that their pain, dysfunction or poor performance on any movement is due to the great bogeyman of hip function - TIGHT HIP FLEXORS.  It is quite a go-to explanation for all things bad.  Where this idea started I don't know but it is certainly propagated by the Lower Crossed Syndrome Theory.  This theory contends that dysfunction occurs when your pelvis is tilted forward as a result of tight hip flexors, weak glutes, tight low back muscles and weak abs.  At its heart, this theory assumes the body works like a puppet where we can tension and loosen our strings (aka muscles) and watch our pelvis dance into some assumed nasty or happy position.

What is the theory behind tight hip flexors

A common explanation (and from people I respect very much) for the assumed tight hip flexors is our 20th century sedentary lifestyle.  This explanation contends that if we sit for eight hours a day at our desks our hips will be flexed, the hip flexors will be constantly short and we will then cause those hip flexors to stay short.  While this is an attractive theory I just can't buy it.  I have a 15 year gripe with this theory and with the other unsupported functional beliefs that then arise from this theory.  So here goes.

Can sitting all day tighten your hip flexors?  I say no way. Here's why.

1.  Even if you did sit for a straight, uninterrupted 8 hours a day this isn't enough to create shortening in muscle tissue.  Shortening occurs when you are in a cast, immobilized in someway in a shortened position for prolonged periods.  I mean days and weeks.  8 hours ain't jack.  Even with an hour day you aren't really stuck in that position. You get up throughout the day and stand up, thus interrupting the shortening possibilities.

2. If this 8 hours is so horrible you would negate this when you sleep for 8 hours with your legs straight or during all of your other upright activities.  On the opposite side of that wouldn't we be more likely to shorten our hip flexors if we sleep in the fetal position for 8 hours a night?  Is no one telling their patients to stop sleeping on their sides with their knees up?  Speaking of Fetuses aren't they scrunched up in ball for 9 months? Shouldn't they have decreased hip extension?

3.  The argument against our sedentary culture is often contrasted with other cultures that choose to sit differently than us.  With these cultures we celebrate their deep squat.  Should we be worried about them sitting in a deep squat for prolonged periods?  Won't their hip flexors shorten? I will send a telegram immediately with these warnings.

Possible contentious extensions of the Tight Hip Flexor Theory

If you support the tight hip flexor theory than logically there are many ways that this will shape how you view muscle function and movement.

1. An inappropriate use of reciprocal inhibition.

By my interpretation I think that this occurs with us therapists inappropriately applying Sherrington's law of reciprocal innervation (aka reciprocal inhibition). It is often concluded that a tight hip flexor will cause an inhibition of one its antagonists, the Gluteus Maximus. However, we can argue against this use in two ways.

1. reciprocal innervation requires that a motor command to an agonist is associated with some inhbition of its antagonist.  The proposed tight hip flexor secondary to  prolonged sitting is not due to some tonic muscle contraction of the hip flexors but rather changes in the passive length of the hip flexor.  There is no neural drive that creates the shortening therefore no means for the reciprocal innervation to occur.

2. Even if there is neural drive to an agonist it may not be sufficient to create any significant inhibition of its antagonist.   This is not how reciprocal innervation works.  A great review and full text paper can be seen here.    Reciprocal inhibition typically occurs greatest at a reflexive level during gait rather than during volitional movements. I am not even sure if it has been documented when we try to test the strength of the "inhibited" muscle because once we do this that antagonist that was supposedly being inhibited is now the agonist.  Further, muscular co-contraction is pretty much the norm during many activities.  We contract (think hamstrings and quadriceps at the knee) to provide stability and controlled movement.  If reciprocal inhibition worked in the manner suggested by the tight or overactive hip flexors than it would be difficult to obtain the stability required in joints via co-contraction.  To conclude, I don't think that any evidence that reciprocal innervation leads to weakness as is postulated exists.  However, I am open to  hearing some research that I don't know about.  I wonder if this paper here pokes holes in my ideas (my guess is no, I actually think it strengthens it) but I think that this paper here looking at neuromuscular adaptations to stretching definitely strengthens it.

2. Tight Hip Flexors need to be released

I have had my hip flexors "released" by several ART instructors and never thought they actually touched my psoas.  At least the deep component of that muscle.  They definitely squeezed my guts and beat the shit out of three layers of abdominal muscles and maybe some intestine or omentum but they didn't "release" my psoas by poking it.  And how could 3 minutes of a psoas release influence years of 8 hours a day of sitting posture via mechanical means?  Neural mechanism? Absolutely but no one is touting this theory. We might also consider what attempting to stretch the psoas can actually result in if we consider the limits of stretching on changing long term muscle stiffness and therefore resting length.  See a brief post here on stretching and muscle.

3. Believing in tight hip flexors can lead to the danger of hip (over)extension.

I am subject to confirmation bias.  I have a view of the body that changes constantly but also informs what I see in my patients and what I do.  if you believe in the lower cross syndrome than you go looking for it.  You then want to increase extension because that is the natural follow up of diagnosing this clinical entity.  But I would contend that stretching or treating into hip extension may be detrimental to your patients or athletes. Please see my post on the dangers of hip extension.  It is akin to cranking a shoulder into abduction and external rotation...what are you doing to the anterior capsule?  Is this an adaptation or a stress that you want to place on everyone?

4. Why do you want hip extension?  How much do you need?

You need 10-15 degrees during walking and you need about the same amount during running.  Hip extension is over rated.  Related to this, you don't even use your glut max during walking to extend your hip and during running you don't use your Glut max to extend your hip past zero degrees.  By the time your leg swings back, is on the ground and starts to extend past neutral the glutes have shut off.  That's the extensor paradox dude.

5. A caveat of possible clinical relevance: Hip Extension during running is related to anterior pelvic tilt.

There is a neat paper from JR Franz and one by Schache et al (2000) showing that limited hip extension during running is coupled with increased lumbar lordosis.  The authors suggest that this is related to injury.  I have three points on that:

1. Whether this is related to injury or performance decrement has not been tested and is purely conjecture.

2. Your tests for measuring hip extension (e.g. Thomas test) do not correlate with the amount of hip extension that occurs during running ( full text here Schache et al 2000).  Meaning, while running you might not extend your hip and this will be related to an increased anterior pelvic BUT this is not due to you having tight hip flexors.  Less hip extension availability was not correlated with anterior pelvic tilt. This is a great example of how the kinematics of quasi-static tests of function (e.g. Thomas test, one leg squat) don't often correlate with the kinematics that occur with dynamic function during tasks of interest (e.g. running).  Our motor planning may choose to limit your extension rather than a physical limitation tested during the Thomas Test.  You are going to have eyeball your video of them running to see if your athlete lacks hip extension.  Good luck doing that accurately.

3.  The increased anterior tilt is not a function of a tight muscle pulling the pelvis into a new position.  Rather the tilt may occur because the thigh must extend and it can do this in two ways.  Hip extension or pelvic tilt.  Some individuals seem to involuntarily choose to do this with more pelvic tilt and they therefore don't need to extend their hip.

Final Thoughts

1. I think that tight hip flexors are overdiagnosed.  The thomas test may even test something besides hip flexors and produce false positives (no reference et al 2012).  I often test patients in prone and just pull their leg into extension.  I rarely see a loss of movement.

2. I certainly don't think that even eight hours of sitting can shorten your hip flexors.

3. The perception of hip flexor "tightness" may be just that, a perception.  Tight does not have to mean short it can just be a way for your brain to tell that something feels off.

4. Tightness or lack of range may exist but does not have to be something so mechanical.  We have a nervous system and range deficits may be related to guarding or threat behaviour.

5.  All of the techniques used to address the lower cross syndrome can still be wonderful for treating your patient's pain or dysfunction.  We don't need to throw the treatment baby out with the dirty psoas bathwater.



Two neat papers that I don't have but want on reciprocal inhibition and stretching.

1. Hayes et al   Neuromuscular Origins of Adaptation do not Exist Following a Long-term Stretching Program. J Sport Rehabil. 2012 Mar 2. [Epub ahead of print]

2. Blazevich AJ, Kay AD, Waugh C, Fath F, Miller S, Cannavan D. Plantarflexor stretch training increases reciprocal inhibition measured during voluntary dorsiflexion.J Neurophysiol. 2012 Jan;107(1):250-6. Epub 2011 Oct 5.

Side Bridge Variation Exercise Sheet - training inside and out.

Purpose: Exercise Sheet handout Attached is a handout for four variations on the sidebridge.  If you do not know what you are doing please speak with a professional before incorporating these into  your strength and conditioning program.

HERE IS THE FULL SHEET IN PDF: side bridge variations sheet

Stu McGill's Big Three Exercises for Spine Stability

Audience: Patients, Trainers & health professionals

Utility: Exercise sheet handout for basic spine "stability" training

What exercises: Bird dog, side bridge, curl up

Stability is in quotes because you can certainly debate whether these exercises actually increase "stability".  Or more accurately make the stable system more Robust.  What these simple but great exercises definitely do is work the entire trunk and hip musculature without imposing a large compressive or shear load on the spine.  The initial research justification for those exercises (almost 16  years ago but they have only been catching on for the past 5 or so) is that they train the spine musculature but do so in a manner that may not increase the injury risk.  Many exercises can train the spine musculature (e.g. double leg raises, back hyperextensions) but do so in a manner that might increase your risk of injury.  These exercises avoid this which may be ideal in a low back injured population.  Athletes are a separate kettle of fish.

Attached is a pdf of the basic Big Three.  Future posts will show variations.

Click here for Stu McGill's Big Three right here: thebodymechanic mcgill big three

All the best,

Greg Lehman, Physiotherapist/Chiropractor