Why is treating tendinopathy so tricky?


Tendinopathy is an exceedingly common musculoskeletal condition among active individuals.  Tendinopathy has been an increasingly studied topic of sports medicine and rehab with research actually creating more divergence in the pathophysiological mechanisms with the term “tendinopathy” itself leading insight into this history of equivocation.  Painful tendon conditions were termed “tendonitis” pre-1990s then shifting to “tendinopathy” and even “tendinosis” in light of histological studies demonstrating lack of inflammatory cells in chronic, pathological tendons.  However, advances in histological techniques have recently shown that inflammation likely does play some role in the early stages of tendinopathy while it remains generally accepted that later stage, chronic, degenerative tendinopathies are devoid of these inflammatory markers, but this is a growing topic of debate.  In light of the pathology explanation fluctuations, it is without wonder that rehabbing tendinopathy remains difficult.  Treatment options for those treating painful tendons exist with varying degrees of evidence.

Many models and theories of tendon pathophysiology exist.  The most prevalent and accepted theories are those of mechanical overload resulting in a condition of eventual disrepair and disorganization of the tendon.  These could entail possible minor fibril rupture which leads to acute fibroblast proliferation and release of factors surrounding an initial attempt of healing.  This is proposed to lead to neovascularization, the in-growth of blood vessels and nerves, when this healing process does not, for some reason, complete.  We can see these individual steps, such as the common observation of neovascular in-growth, however the actual initial step of partial rupture has not been observed with no evidence demonstrating they actually occur.  Furthermore, in most cases tendinopathies arise symptomatically in a sort of gradual manner without a clear injurious incident, which would be expected with partial rupture.  Biochemical and histological studies have also shown major differences between complete rupture and healing tendons compared to those with tendinopathy with ruptured tendons lacking the presence of common tendinopathic findings suggesting that tendon rupture/failure may not be linked to pre-existing tendinopathy.

There does appear to an acute stimulus triggering tendinopathy with new research now accumulating suggesting inflammation does, in fact, play a role in the early stages of tendinopathy and possibly in the continual progression of the condition.  Some researchers, such as Jill Cook’s group at La Trobe University, assert that this is likely more of a cellular activation than an actually inflammatory response.  This cell activation idea has lead to attempts at staging tendinopathy with the acute and painful tendon being described as the reactive stage whereby mechanical overload triggers cellular activation leading to increases in proteoglycan production.  Increased hydration of these proteoglycans are then said to increase tendon swelling prompting the disruption of collagen alignment and creating areas corresponding to hypoechoic areas prone to neovacularization.  Tendinopathy is proposed by Cook to occur in stages of reactive tendinopathy, tendon dysrepair, and finally tendon degeneration.

Another hypothesis is a sort of pain-first mechanism with the onset of tendon pain representing a change in nociception via primary ingrowth of nerves and vessels.  We do know that eventual nerve and vessel in-growth is present in late stage tendinopathy but it is difficult to determine when this occurs and the directional relationship towards tendinopathy-does tendinopathy result from this neovascular ingrowth or because of it.  It’s plausible that increases in tendon nociception could lead to mechanical offloading both with movement offloading and offloading at the tissue level.  Offloading at the level of tissue itself is an idea termed tendon stress-shielding which is another hypothesis of tendinopathy supported by evidence that chronically unloaded tendons undergo degenerative processes.

Another plausible hypothesis is that mechanical overload could exceed a sort of tendon homeostasis whereby cells responsible for tissue support and regeneration to continual tissue turnover become stressed beyond their capacity to heal the tendon.  This then may even lead to cellular apoptosis at the tendon which has been observed in large increases of load. It has also been suggested that perhaps there is an oxidative stress component in areas of the tendon which become hypoxic under inadequate oxygen supply and have help explain the mechanism of neovascularization observed in chronic tendinopathy.   Clearly other variables could be involved such as genetics and individual factors with such things as high cholesterol and adiposity being correlated with incidence of tendinopathy.

Compression of the tendon at areas of contact with bone also likely play a role especially with insertional tendinopathies whereby muscle contraction causes increased tendon compression into bone perpendicular to the length of the tendon.  A clear example is of the rotator cuff tendons which must bend or wrap around the head of the humerus at their distal attachments.  Muscle activation would cause the tendon to be firmly pressed into the bone as a sort of bow-stringing effect.  In fact, most tendinopathies are likely insertional with the exception being mid-substance achilles tendinopathy.

Adding to the nearly enigmatic pathophysiology  there also is not clear consensus regarding clinical diagnostic criteria for tendinopathy.  Typically,.tendinopathy is generally diagnosed clinically via local pain related to isometric load and tenderness to palpation.  These criteria are said by Mascia to be anecdotal and lacking specificity Furthermore, imagining modalities are typically unavailable to the rehab specialist with imaging results not consistently correlating to clinical presentation (Masci, 2016.)  Pain does not appear to correlate well to the degree of neovacularization and it is known that asymptomatic athletes can undergo pathological degeneration in the absence of pain.  As such it can be difficult to determine the degree of progression of the condition when a patient presents with tendon pain – is this apparent reactive tendon occurring in a recently otherwise healthy tendon, or was there significant degeneration that has now become symptomatic?   So while it is difficult to diagnose and define tendinopathies it does appear that tendons can undergo normalization over a extended periods of time to improvements in tissue structure as observed with ultrasonography.  So how do we, as clinicians, go about treating and rehabbing painful tendon conditions?

There are several proposed therapies for tendinopathy including plasma-rich platelet injection, high volume injection, extra-corporeal shockwave therapy, stem cell therapy, and of course loading therapies.  The best current evidence in treating tendinopathy is that of tendon loading through exercise.  This is an interesting paradox as it is typically accepted that tendon overload and lack of adaptation to load demands to be a primary driver of tendinopathy.  However, research in the area of loading initiated by Hakan Alfredson and others have shown clear benefit to progressive loading.  An unloaded tendon will regress in it’s load capacity and become prone to increased pathology.  This unloading as noted by possible tissue shielding and/or changes in movement patterns are ways a person may instinctively avoid pain by unloading, but could contribute to continued tendinopathic processes as a result.  Tendon loading provides benefits through the mechanisms of mechanotransduction whereby cells respond to physical load with biophysical and biochemical adaptation.  These adaptations occur as results of tenocyte response with changing cellular structure and composition via alteration in gene expression and protein synthesis.  It also appears that load by muscle contraction is better than stretching for maintaining and promoting load capacity in tendons, although some research exists suggesting static stretching may promote improved tendon efficiency/energy preservation as noted with decreased hysteresis (energy loss) when tendons release their stored energy from load after a stretching program (Kubo, 2002.)  In terms of muscle contraction there is more evidence, at present, for eccentric contraction providing benefit, however, evidence of benefit from concentric contraction exist as well just not in as robust of number as those supporting eccentrics.

The paradox of treating a tendinopathic tendon caused by overload with load makes clinical decisions challenging and there does not appear to be any clear consensus advice on the topic.  I tend to favor Jill Cook’s perspective of the acute pain of tendinopathy as a sort of reactive state which should be allowed to subside before controlled loading is initiated.  My general method for treating tendinopathy (which is ever-evolving) is to reverse titrate any clear offending stimulus or activity with some preservation of of tendon loading with pain-free exercise such as isometrics in positions favoring as little tendon compression as possible.  As an example, isometrics for insertional achilles tendonopathy would be avoided initially  in dorsiflexed positioning as it has been proposed this position could promote insertional compression.  When the pain has shown evidence of regression, typically after about a week, I introduce a gradual loading program.  Research at this point indicates that pain is likely to occur but should not be debilitating, such as to the point of making ambulation difficult; pain is expected, but must be endured to an extent during exercise.

Medical intervention show only tenuous benfefit with anti-inflammatory strategies, such as glucocorticoids and NSAIDs, showing inconsistent benefits but mostly in the short, initial time-frame.  Furthermore, longer duration use, or use after the initial reactive stage, may be harmful as we know that longer durations of glucocorticoids decrease tendon quality and NSAIDs impede healing of muscle and bone injury with both carrying other health risks.  PRP injections so far have not shown much benefit in larger, high quality studies, however, some argue that this has come from variance in the quality of PRP used.  Time will tell the extent of benefit of PRP injection though it does seem that more evidence is emerging dissuading their use.

The British Journal of Sports Medicine released a good guide to treating tendinopathy on their blog that you can access HERE.


1.  Kubo, K., Kanehisa, H. and Fukunaga, T. 2002. Effects of transient muscle contractions and stretching on the tendon structures in vivo. Acta Physiological Scandinavica, 175: 157-164.

2.  Masci, Lorenzo. “Is Tendinopathy Research At A Crossroads?”. British Journal of Sports Medicine 49.16 (2015): 1030-1031. Web. 2 July 2016.

3.  Rees, Jonathan D, Matthew Stride, and Alex Scott. “Tendons – Time To Revisit Inflammation”. British Journal of Sports Medicine 48.21 (2013): 1553-1557. Web. 2 July 2016.

4.  Scott, Alex, Ludvig J. Backman, and Cathy Speed. “Tendinopathy: Update On Pathophysiology”. J Orthop Sports Phys Ther 45.11 (2015): 833-841. Web. 2 July 2016.

5.  Tilley, Benjamin J et al. “Is Higher Serum Cholesterol Associated With Altered Tendon Structure Or Tendon Pain? A Systematic Review”. British Journal of Sports Medicine 49.23 (2015): 1504-1509. Web. 2 July 2016.

6.  Wang QW,Chen ZL,Piao YJ Mesenchymal stem cells differentiate into tenocytes by bone morphogenetic protein (BMP) 12 gene transfer. J Biosci Bioeng2005;100:41822.


Conservative Treatment Ideas for Acetabular Labral Tears

There are important considerations for treating acetabular labral tears which can help guide patient care.

There is no doubt that acetabular labral tears are becoming increasingly common in sports medicine and rehab.  It is unknown whether the incidence is on the rise from increased or changing patterns of activity or if we are simply better at finding these lesions with improvements in diagnostic imaging.  It is likely a combination of each.  Regardless, rehab professionals should be prepared with a solid rationale for intervention strategies when treating individuals with labral tears.

Acetabular labral tears are typically caused by trauma or developmental etiologies.  The developmental causes often occur as linked to morphologic variance such as femoroacetabular impingment (FAI) and hip dysplasia.  Frequent aggravating movements of the hip can also cause and accelerate labral degeneration. 

cam pincer fai

The forms of FAI are seen above.


The vast majority of labral tears in western society will occur in the anterior-superior margin with anterior translation of the head of the femur contributing to labral overload.  The increased anterior translation of the femoral head occurs with excessive hip extension with standing or moving with hip hyperextension or in posterior pelvic tilt. Also remember that with external rotation we also get accessory anterior gliding. In individuals with excessive anteversion if they are to center the femoral head in the acetabulum, without compensatory tibial external rotation, they will walk with a degree of in-toeing. If they correct the in-toeing at the hip, the femur will be in a relatively externally rotated position with a propensity for increased anterior glide of the femoral head.  On the other hand retroversion has been linked to labral tears as the retroverted femur will more likely impinge the anterosuperior labrum with flexion especially when combined with adduction.  It is pertinent to assess femoral version.  Craig’s test has been shown both valid and reliable for detecting femoral version (studystudy.)

So with these considerations, here are some items to keep in mind when treating a patient with an anterosuperior acetabular labral tear.

  1.  Do not stretch into hip extension!  This should be pretty clear considering the location of injury and the mechanics associated with hip extension as mentioned above.  Stretching into extension will only further irritate the anterior hip as the femoral head will slide anteriorly in this position.
  2. Strengthen (and pattern) the glute max without driving the hip into hyperextension.  The glute max can help direct a posterior translation force on the proximal femur.  The glute max should be trained with attention to end range position avoiding driving into hip (hyper)extension.
  3. Address any posterior pelvic tilt.  As mentioned above posterior pelvic tilt can increase load to the anterior labrum.  Examine for possible causes of posterior tilt especially tight/stiff hamstrings and/or abdominals and weak lumbar erectors and/or iliopsoas.  The iliopsoas has been implicated by Lewis and Sahrman as a contributor to stabilization of the anterior hip during straight leg raise activity.  Weakness/inactivity in this muscle as compared to the rectus femoris may be noted in those with anterior labral injury as the rectus femoris will tend to translate the femur forward while the iliopsoas was modeled to stabilize the anterior hip.
  4. Perform gait analysis.  If an individual who has been determined to have increased anteversion walks with compensatory external rotation of the hip to walk with toes forward the femur will glide anteriorly.  I would not recommend teaching gait in a toe-in position even with anteverted hips, however, any out-toeing beyond neutral should be corrected in these instances.  Also assess for knee and hip hyperextension as marked by prolonged foot flat position late in stance phase.
  5. Limit isolated training of quadriceps and hamstrings, both of which can cause anterior translation of the femur.
  6. And finally good guiding principles of rehab are to simply avoid aggravating positions, strengthen joints and surrounding areas outside of the painful positions, and gradually reintroduce required and acceptable movements as tolerated by the patient.

For a good read on the topic see Shirley Sahrmann and Cara Lewis’s paper on the topic of labral tears. 



Mulligan Tape for Patellofemoral Pain

I have always attempted  patellofemoral pain (PFP) symptom modification with taping using only the McConnell method.  However, a recent study in the May 2016 issue of American Journal of Sports Medicine (Study) found that mulligan taping significantly decreased PFP and improved kinematics with decreased femoral internal rotation.  I think this new method of taping can potentially be quite useful for those individuals who do not respond to McConnell taping and whose comparable sign can be elicited with manual tibial external rotation or relieved with manual internal rotation during movement.

The Mulligan taping method involves applying rigid tape with an internal rotation force applied to the tibia.  The tape is wrapped from lateral to the tibial tubercle medially and superiorly above the knee ending on the posterolateral portion of the distal thigh.  Try it out with your patients and let me now if you find any benefit!


Time to Let Motion Palpation Die?

Unreliable, invalid, and creating a sense of fragility in patients. Does motion palpation deserve a place in clinical practice?

Having recently graduated from physical therapy school I can say that motion palpation is still being taught, but in a fettered or restrained manner consistent with the known unreliability of these methods.  It was approached as if we had to learn it because we would experience it in the real world from other clinicians, which we most certainly do, and as such we must understand the rationalization of their methods.  But somewhere along our clinical career paths many lose the skeptical mindset cautioning us of the unreliable, invalid premise of motion palpation and instead use the dated rationale unscrupulously ignoring that the practice of evidence based practice would preclude motion palpation.

I admit my bias against motion palpation originated immediately upon its presentation of physical therapy school with the known validity and reliability issues.  I recognize evidence based practice is not only comprised of scientific literature, but also clinical experience, and patient values.  I would argue, however, that each of these tenets of evidence based practice are compromised in this area.  Motion palpation is not just unwarranted because it is based on unvalidated concepts and unreliable techniques, but because it is inherently not in our patients’ best interest.  This comes not solely from the act of motion palpation itself or subsequent treatment, but in our attempt to explain why we are palpating and what we are correcting.

To explain this, I will use the common motion palpation surrounding the sacroiliac joint, an area of minuscule movement which clinicians have been attempting to feel for altered position and dysfunction for decades.  Let’s say a patient comes in complaining of pain around the sacroiliac joint.  A thorough lumbar, pelvic, and hip examination with use of the test item cluster for SI joint pain leaves you confident that the SI joint is the offending location.  At this point many will take to palpating the various landmarks of the sacrum and pelvis in vain attempt to detect any malpositioning of the sacrum or either innominate.  With this, validity has already flown out the door.  Landmarks on the pelvis and sacrum are known to normally vary based on normal morphology (See Study), which is observed both between sides in the same individual and between individuals.  Secondly, we know our hands are not sensitive enough to feel with any reliability the tiny (See Study) amounts of rotation or translation that would occur at the SI joint(See Study)(See Study)(See Study)(See Study)(See Study)(See Study)(See Study)(See Study), especially when we are palpating through the soft tissues around these landmarks.  Radiostereometric radiography with metal ball implantation into the pelvis is the only reliable method of assessing pelvic motion.  So despite the evidence we come to the conclusion that a specific malpositioning exists at the SI joint and a very specific intervention is required.  But this isn’t the truly bad part.  The bad part is that we then TELL the patient, in any number of concerning terms, that they were “out of place”-but not to worry because we can fix them.  So not only have we come to an invalid conclusion, but we use this conclusion to create a sense of fragility and dependency within the patient.  They now know to associate this pain they have with being “misaligned”, “subluxed”, “rotated”, etc. and that this issue can only be addressed with expert hands putting it back into place.  And just like that dependent, fragile patient created.  Does this sound like any model of healthcare you have heard of?  Hmm…

Let me clarify that I am NOT arguing against the notion of sacroiliac dysfunction nor am I arguing that the traditional treatment of SI joint pain do not get clinical results.  There is no doubt that clinicians using the motion palpation method and specific treatments of manipulation/mobilization and muscle energy techniques of SI “correction” can still have good clinical outcomes. In fact, there are some aspects in the methodology that resembles how I still treat some SI joint patients.  But this effectiveness can be explained a large number of ways that are not related to correcting positional faults.  We know manual therapy helps with pain despite highly tenuous biomechanical explanations (more likely neurophysiological in nature.)  We know that the muscle energy techniques are basically just isometrics; isometrics help with pain.  We often combine these strategies with other treatments including exercises (creating mindfulness and self-efficacy) and passive, pain-relieving modalities.  Therapeutic alliance, sense of expectancy, and placebo effects are also gained just by having the patient seen by a clinician who acts with empathy and care towards their concerns.  Not to mention that most musculoskeletal disorders simply get better naturally as a mechanism of regression towards the mean.  So while I still do manual therapy, muscle energy techniques, and other exercises for SI pain; My argument is that we must change what we are telling the patients.  We must stop telling them they are fragile, dependent creatures incapable of resolving pain without being put back into place.  It’s a load of BS and creates an unnecessary psychological burden on our patients and financial burden on the healthcare field.  We must recognize the pareidolia creating biased clinical reasoning and jeopardizing our patient’s physical and psychological well-being; it may be time to move past motion palpation.

Argument Against Biomechanical Explanation of Manual Therapy

Manual therapy is a mainstay in physical therapy and rehab but there’s a lot we we don’t truly understand about its mechanism of action.  We know it works; many studies show manual therapy has a positive influence on pain outcomes.  But how manual therapy works has not been clearly elucidated.  For those who have not critically investigated the details of manual therapy mechanisms will surely be quick to argue on behalf of biomechanical explanations.  But these mechanical effects really have not been clearly demonstrated in literature.  For example, did you know that it is really only possible to mobilize a joint in a direction completely perpendicular to the surface of the contact area on the skin.  This is because the skin-fascia interface is frictionless as found in a 2002 study in the Journal of Clinical Biomechanics.  This throws a wrench into the rationale of many thrust techniques that attempt to mobilize segments using variation in hand placement and force vectors.

I am not arguing that biomechanics absolutely do not matter in manual therapy.  However, I do believe that a more promising mechanism is that the forces applied in manual therapy initiate a sequence of peripheral and central nervous system neurophysiologic changes which positively modulate the pain experience.  Into this also plays the placebo effect, the effects of patient expectancy, and therapeutic alliance, all of which would contribute to the pain-relieving effects of manual therapy regardless of any mechanical explanation.  I think as clinicians we need skepticism to mechanistic explanation of our interventions, especially when the rationale for these interventions contradict basic scientific evidence.  We need to start considering how we educate patients and understand that if we use strict biomechanical explanations for our interventions we may perpetuate the patients’ perceptions of their bodies as fragile entities dependent on a clinician’s hands to “correct” their “misalignments.”  While this is good for business, and some businesses depend on creating a sense of fragility in the minds of patients,this is not good for our patients.  We should acknowledge that humans are innately resilient, adaptable, and capable of pain relief without being dependent on continual “correction” and “adjustments.”

Assessing Squat Form. Part 3

If you have not read the previous two posts on this squat assessment series read them (Here and Here.)

In this third and final blog on this topic I will discuss how we will take the considerations of body proportions and variation in mobility and motor control to individualize squat form.  As stated in part 1 our goal of this squat pattern is to achieve good depth while limiting lumbopelvic flexion to promote the ability to efficiently and safely move under loaded situations.

The first thing I do in a squat assessment is simply have the patient squat in their preferred position without cuing and note the quality of movement.  The qualitative judgement part does require some experience but you should have a general sense of when the squat looks off .  If it doesn’t look quite right, try following the steps below and you should arrive be able to determine what is limiting correct squat technique.  If the squat is nearly correct but some lumobpelvic reversal takes place in the bottom of the squat you may consider widening the stance a bit to see if this addresses the issue.  If it completely resolves the issue, then great, but I would still advise going through the steps below to rule out any concomitant limitations.

The next thing I do is to elevate the person’s heels and have them reattempt the squat.  This: 1)  Eliminates insufficient dorsiflexion from affecting the squat and 2) Shifts the person slightly forward to compensate for inability to “sit back” sufficiently during a squat.  “Sitting back” is a strength and conditioning term for moving the hip posteriorly and into flexion with an increase in corresponding forward trunk lean.  An inability to sit back can come from hip flexion limitations, hip extensor tissue extensibility issues, or a motor control issue.  Often if a patient exhibits this inability to sit back with hip flexion while maintaining good lumbopelvic position, it is a situation where the posterior chain muscles are actually stiff (artificially tight) in an attempt to impart stabilization to the lumbopelvic area in situations of reduce trunk stability.  So here it is important to recognize that “stiffness” is not the same as “tightness.”  Stiffness comes as a result of increased tone to stabilize a joint whereas true tightness comes from a shortening of muscles and their associated connective tissues often from maintaining positions of decreased tissue length.  This mechanism of stabilization is a primitive adaptation strategy because while it does improve the body’s ability to overcome the body’s overall external flexion moment it also predisposes the lumbar spine to excessive mobility requirements.  The topic of tightness vs stiffness is not a true dichotomy, however, as the two can exist in varying amounts at the same time.   Also to note,there is not a ton of abdominal strength required during a squat rather it is likely more a goal of stability and control.  A study by Stuart McGill showed surprisingly modest levels of abdominal musculature activity during functional exercises such as squats (Study.)

Now if the squat has improved with heels elevated you can assume that the problem exists with corrective explanations given in points 1 and 2 in the above paragraph.  To further the assessment I find it most useful (and simple) to begin with the ankle.  We must determine whether dorsiflexion insufficiency is hindering the squat technique.  To do this have the individual assume a half kneeling position in front of a wall with the forward toes about 4 inches from the wall.  Next have them lean the front knee forward towards the wall while keeping the heel down.  The amount of dorsiflexion achieved in this position is sufficient for any squat form.  If significantly lacking then dorsiflexion mobilizations and soleus stretching should be implemented before squat training.

If the ankle dorsiflexion test is negative, showing sufficient dorsiflexion, then we will assess the second point from above- the ability to sit back.  To check this have the patient perform a squat with the arms extended in front of them.  As mentioned in a part 2 this shifts the center of mass slightly forward which allows the squatter to remain slightly more forward and can decrease the amount of hip flexion and forward lean.  Next I compare this arms forward form with the squat form with a relatively light weight held against the chest.  This also shifts the weight forward but also acts to impart a flexion load to the lumbar spine which should engage the lumbar extensors and abdominals prior to movement.  If the form improves further with this strategy is likely that their exists a motor control issue involving the dissociation of hip and lumbar flexion.  If the form does not improve or only partially improves, I then look further into what is happening at the hip and lumbar spine.

I have the client supine on a table and perform an assessment of core stabilization using a comparison of the active straight leg raise and passive straight leg raise test.  During the active straight leg raise the client should begin with both legs extended straight.  The client then lifts one leg keeping both knees straight and the down leg in contact with the table.  Observe the active range of each leg and note whether the contralateral leg moved out of full extension.  Next perform a standard straight leg raise on each leg while palpating the anterior superior iliac spine to check for posterior rotation of the pelvis.  Stop the motion when pelvic rotation begins.  If the active straight leg raise flexion range of motion to the furthest point without contralateral hip flexion is significantly less (> 10 degrees) as compared to the passive straight leg raise to the point of pelvic rotation then there likely is a lumbopelvic stability issue.  This is because with poor stabilization of the lumbar spine during active straight leg raise the building tension in the hip extensors will cause an unchecked posterior rotation of the pelvis which will lift the contralateral thigh slightly off the table.

I then perform a gentle scour test on both hips to get a general sense of the hip shape and depth.  Typically you will notice that the hip achieves hip flexion much easier in a slightly abducting and externally rotated femoral position.  Check to be sure that sufficient hip flexion can be achieved, usually requiring 120 degrees for a parallel squat.  If passive hip flexion is limited in this position it is likely that limitations in the tissue extensibility of hip extensors is contributing to lumbopelvic reversal or lumbar flexion deeper in a squat.  Incorporating tissue extensibility and hip flexion mobilization should precede squat training if this is the case.

Next I have the patient quadruped on the floor or table and have them perform quadruped rocking observing the angle of hip flexion at which lumbar flexion occurs.  I then have the patient assume the same hip position as was determined to be the most mobile into flexion via the scour test above.  Greater hip flexion should occur and this gives you a good idea of where the person’s feet should be positioned during the squat.  If the patient has difficulty differentiating hip flexion and lumbar flexion in this position then you should coach them in this position until they achieve a feel for allowing the hip to flex while stabilizing the spine.

From here, I will use what I have observed to appropriately position the individual’s stance and then have them sit down onto a low box to get the individual in a near parallel squat position.  From the low box I use tactile cues to get the patient to achieve appropriate neutrality in their lumbar spine with some paraspinal muscle contraction if they have some amount of flexion.  I will have the patient cross their arms across the chest and lean forward, cuing them to keep thoracic extension, just until they are about to un-weight themselves from the box.  Here is where those strange proportions I talked about in part 2 may come into play.  If the patient happens to have very long femurs you will notice that they may maintain good lumbar position, exhibit satisfactory dorsiflexion, but they require a lot of forward lean to balance and require a ton of hip flexion due to having to sit way back.  These individuals may even look like their torso is nearly parallel to the floor.  In these cases you will need to adjust the width of the stance wider and continue to assess.  It comes down to clinical judgement on what you deem acceptable for squat form.  This individuals with disadvantaged proportions will do better with anterior loading, significant attention to maximizing dorsiflexion, and possibly even using elevated heel shoes to properly achieve parallel in the squat.

This is simply my method of assessing squat form and this manner is usually only done for those with grossly aberrant movements.  In those clients with form that shows only slight limitations they may benefit from immediate cuing or coaching to correct their form.  This should be done only if it is clear that mobility and stability impairments are not limiting the squat and that it is simply motor control.  Mobility and stability components are not directly influenced with cueing, only motor control is.  Furthermore, I also believe it is important to have the patient achieve a full squat pattern as outlined in Gray Cook’s FMS/SFMA systems.  This system would advocate training the full pattern before the squat pattern laid out in this blog series.  I do not necessarily disagree with the rationale of teaching the full squat before the “loaded” squat form, but I believe many clinicians will prefer to teach the mechanically efficient pattern I have described which allows for safe loading.

Feature Image from: Starting Strength 2nd ed. by Mark Rippetoe

Assessing Squat Form. Part 2

In part 2 I will dissect the squat pattern itself and explain how anthropometric, or body dimension, differences affect squat form and performance.  Not everybody is built to squat the same way and trying to fit a person into a preconceived form can have poor results if their body is not built for that pattern and style.

For those who are have skipped part 1 you can read it Here.

Part 2: Key Points

  • The goal of a squat is not to maintain a vertical torso, although a vertical torso can be achieved with special loading and movement strategies
  • Variation in body proportions alter an individual’s optimal squat pattern
  • Short femurs and long tibias are good squatting proportions, long femurs and short tibias are disadvantaged proportions
  • Disadvantaged proportions can often be overcome with specific changes in form


It’s pertinent to acknowledge the general physics and kinematics of the squat to better understand how body proportions change the way load is handled by the body.  To start we will consider how movements relate to the line of gravity.  The line of gravity extends through the center of mass to the ground.  Let’s approximate this line by using the center of pressure of the foot, just anterior to the malleoli.  Also keep in mind that the center of mass is the point at which an objects entire mass is equally distributed around.  For an unloaded human standing in anatomical position the center of mass is said to be just anterior to the body of the S2 vertabra.  With increased load held on the shoulders the center of mass progressively moves towards that load.

So during a squat, external and internal “moments” will occur.  A moment is the turning effect of a force about an axis.  The magnitude of the moment depends on the magnitude of force and distance from the axis.  Think of a wrench.  The longer the handle and the more force you apply to the handle the greater the turning force exerted and the easier it is to turn the bolt.  Same concept in the body.  An external moment is the result of the force of gravity and the internal moment is the body’s reaction by using muscular force.

So as you descend into a squat the hip moves backwards and the knee travels forwards relative to the line of gravity.  The line of gravity is the force in the moment equation and the center of each joint is the axis.  Remember we are going to assume that the line of gravity stays around the standing center pressure of the foot, although this certainly changes a bit while squatting.  So the further back the hip moves the more gravity will exert a flexion force about the hips.  The further forward the knee moves forward the greater the flexion force exerted about the knee.  As such, the further backward the hip the greater the demand on the hip extensors and the further forward the knee the greater the demand on the knee extensors as both are fighting against the overall external flexion moment.  Pretty straightforward.

We also must realize that the forward/backward position of the hip and knee is intimately linked because both are connected via the femur.  The same overall external flexion moment has to be combated regardless of the hip/knee position, the relative contributions from hip extensors and knee extensors are what change with variation in form.  Another thing to note is, all other things the same, when the hip move further backward an increase in forward lean of the trunk must occur to maintain balance.  This forward lean also increases the external lumbar flexion moment.  It may seem like it would make for the primary goal to be to keep the torso as upright as possible,  but this is not the case.  Torso inclination comes as a consequence of load acceptance and patterning in the ankle, knee, and hip rather than the torso dictating the entire lower extremity’s kinematics.

In order to keep the spine vertical it is necessary to have a much more anterior knee position as this helps balance a load which is located more posteriorly with an upright spine.  Try this yourself.  Focus on keeping your spine as vertical as possible, feet straight ahead (for now), and squat.  Most will notice tension builds in their calves as the necessary amount of anterior rotation of the tibia requires is restricted by limitation in the range of dorsiflexion.  If you take dorsiflexion our of the picture and squat on your toes, or with something under your heels, it is much easier to achieve an upright spine as you can now more easily achieve the forward knee position.

There are really two negative things that can happen when a squatter’s goal is to keep the torso upright.  If the ankle lacks the necessary dorsiflexion then pressure will go onto the toes (not ideal.) If the trunk compensates for preservation of even foot contact then the hip and knee will shift backward necessitating a forward trunk lean to quickly increase at the bottom of a squat.  We do not want to be accelerating into peak anterior trunk lean in the bottom of a squat, because in the bottom of a squat we have to suddenly stop this motion and reverse back upwards.  With increasing anterior trunk lean we increase the lumbar flexion external moment and increase the stabilization requirements of the lumbar spine.  It is best to not be accelerating into forward trunk lean in the bottom of the position, but rather have this amount of lean already set and controlled once we reach the bottom so that we may stop and reverse back upwards more safely.  So for these reasons, it is most appropriate to determine the stability and mobility of the ankle, knee, and hip before consideration of the vertical nature of the torso.  The degree of torso incline is a byproduct not the primary goal.

Body proportion considerations in the squat:

As I’ve discussed, the further the hip and the knee are away from the line of gravity (approximated by the center of pressure through the foot) the greater the external moment on these joints and thus the more force is required from the corresponding hip extensors and knee extensors.  Well what happens if BOTH the hip and the knee are far away from the line of gravity, which happens when an individual has a very long femur.  Well this is a double whammy.  Because not only does a long femur increase the required force from hip and knee extensors, but it also drastically increases the forward trunk lean and dorsiflexion required.  Let me draw you a picture…

Long femur paint

This illustrates that because the left stick figure’s femur is so long that it necessitates both the hip to be further backward and knee further forward.  All other things the same, the more forward the knee, the more dorsiflexion is required.  The further backward the hip the more forward inclination required.  Furthermore, you will find many individuals have difficulty stabilizing their spine at greater degrees of hip flexion, so as the stick figure on the left (above) descends he is more likely to have resulting lumbar flexion.  A long femur is not good for squatting.

A long tibia, on the other hand, is great for squatting.  With a long tibia, for every degree of dorsiflexion the knee is allowed to move forward more anteriorly.  Another way to phrase it, is that for any given knee position a person with a long tibia will require less dorsiflexion.

Long tibia

The notion of a long tibia has important and relevant implications especially when we consider the use of weightlifting shoes with elevated heels.  What the elevation of the heel does, either with a special shoe or by placing the heel on a plate, is to effectively lengthen the tibia and to decrease decrease dorsiflexion requirements by placing the foot into a more plantar flexed starting position.  As we discussed above this situation can allow for a more vertical torso.

Another reason that elevated-heel squatting allows for a more vertical torso is that it slightly shifts our center of mass forward.  Here is another thing to try.  Take whatever squat stance is comfortable and extend your arms straight out in front of you as far as you can.  Now trying to keep the back vertical squat down.  Notice how it feels.  Now switch and do the squat with the arms either right at the side or just behind your pockets.  You’ll notice it is likely more difficult to maintain the upright torso with the arms at the side.  This is because when you have your arms in front of you, you have shifted your center of mass slightly forward.  This helps to offset the posterior displacement in the center of mass as the hip flexes.  When you have your arms at your side and you go to squat the center of mass again moves posteriorly with hip flexion but because you lack the counterbalance of the arms you must lean your torso forward to maintain your balance.  The same counterbalance situation exists when you load a squat from the front as opposed to the back.

These conditions are PART of how an olympic weightlifter is able to achieve incredible depth while maintaining an upright back (see the photo below.)  And to note, the torso position in these olympic weightlifters is achieved out of necessity mostly because it would not be possible, or safe, to catch a weight on the front of the shoulder, as done in a clean, without being upright–this is a topic for another blog so I’ll keep that point short.


One last proportional consideration of the squat is that of torso length.  A short torso will require a greater forward lean to keep the center of mass balanced over the line of gravity down through the foot.  This only implies consideration of the load placement during a squat, but this typically comes down to personal preference.

I will now bring to your attention that all of these kinematics have been described within the sagittal plane exclusively.  However, we can incorporate the frontal plane into the squat which can effectively shorten a long femur’s sagittal plane length.  If you are to picture one of my stick figure squatters above and take the femur section and envision externally rotating/ abduction the femur bringing the knee section towards you, you will notice that with the sagittal plane dimension of the femur is now shorter.  This is how we can circumvent a disadvantaged squatting proportion.  With a the femur now shorter in the sagittal plane a long femur will not require as forward of a knee position nor as backward of a hip position, which decreases not only the external flexion moments but also decreases the requirements of dorsiflexion and forward trunk lean, respectively.

So now you are wondering what are these measurements/ ratios of femur to tibia length that are ideal for squatting.  I do not have those, and I do not believe the exist.  The reason I have brought up the discussion is to point out that we should not be mashing our clients/ patients into what we think a good squat should look like if we haven’t considered that their dimensions may not fit this mold.  But there are ways of determining if an individual’s body dimensions should guide us to changing their squat form or if we are dealing with a mobility or stability impairment we can treat instead.

How you ask?  See Part 3