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Article Reviews

A Regional Interdependence Model of Musculoskeletal Dysfunction

June 5, 2020 by gordon browne

Premise

This article is a statement of clinical reasoning related to regional interdependence, rather than a true ‘study’.  It is perhaps the flagship article for a rehab idea or principle. Bodies are integrated, connected and dependent upon each other—manifesting not just locally, but regionally and globally as well. The authors do a nice job of defining regional interdependence (RI) and relating it to clinical musculoskeletal practice:

 

    • ‘The underlying premise is that seemingly unrelated impairments in remote anatomical regions may contribute to and be associated with a patient’s primary report of symptoms’.
    • ‘The clinical implication of this premise is that interventions directed at one region of the body will often have effects at remote and seeming unrelated areas’.

 

Paraphrasing then—‘this is connected to that and limitations or dysfunction distally can contribute to negative effects locally’. And—‘assessing and treating areas other than just at the site of pain are an important part of the rehab process’. Though RI primarily relates to inter-actions and effects of one somatic region to another, the authors were thorough by including references to ‘neurophysiological, somatovisceral, and biopsychosocial’ inter-relationships with and effects on the health of the musculoskeletal system.

 

Mechanisms

How does it happen that mobilization of the thoracic spine reduces neck pain? How does strengthening the gluteus medius reduce anterior knee pain? How does improving hip internal rotation help reduce low back pain in a golfer? How does an ankle sprain turn off the gluteal muscles? These examples are taken directly from regional interdependence-related research.

 

Kinetic Mechanical Engineering Model is the first proposed mechanism by which RI works. This Kinetic Chain model ‘describes the body as a series of interconnected joints where the movement of one joint directly effects the movement of other joints above and below’. We already know this intuitively—if we lack ankle dorsi-flexion we get more foot pronation. If we lack hip flexion we get more lumbar flexion. If we lack thoracic extension we get more cervical extension.

 

If you can’t move in one place you end up moving more somewhere else, which is a recipe for joint hypermobilities. This phenomenon of movement imbalance or inefficiency has been aptly described by Shirley Sahrmann with language of ‘path of least resistance’ and ‘relative flexibility’. We can extrapolate, or can enlarge upon this concept, to include muscle imbalances. If you don’t work appropriately in one muscle, some other muscle will have to pick up the slack. This leads to muscle hypertonicities.

 

Neurophysiological Mechanisms is the second proposed mechanism for RI. The authors decline to define exactly what this means, other than to say it’s ‘related to temporal summation and pain perception related to manual therapy interventions’.  While the kinetic engineering model is more nuts and bolts and Newtonian physics, the neurophysiological model is more micro chips, fiber optic cable and Jungian psychology. How does the brain react to stimuli? Which chemicals are created? What affect does being touched have? When are neurotransmitters nullified? Where are hormones are housed? How are signals relayed through the nervous system and what inexplicable detours do they take into the endocrine and limbic systems? Why is pain reduced in the neck or shoulder immediately upon receiving thoracic mobilization or manipulation?

 

Mystery Solved?

Nobody really knows yet and, with continuously new discoveries about how wonderfully complex the mind is, perhaps we never will know. It’s not magic, but only because we have an impressive scientific name for it. We know the generalities (nervous system phenomenon creating somatic effects) but not the specifics (exact pathways, reliable and reproducible intervention strategies).

 

Dry needling of trigger points and cranio-sacral therapy are examples of rehab interventions that rely more on neurophysiological mechanisms. Joint mob/manipulation has a nuts and bolts aspect (more joint mobility or centering of the joint) and a neurophysiological aspect and there is a fair amount of research from manual therapy enthusiasts on the benefits of joint mob/manipulation.

 

Many more articles are cited looking at somatic relationships—hip to knee, hamstring to plantar fascia, hip rotation and low back pain. These types of studies are more supportive of the kinetic chain aspect of RI. Where do the authors fall? Right in the middle—there is probably a combination of biomechanical and neurophysiological factors (as well as biopsychosocial factors) and, as always, further study is warranted. Take home?

 

    • Musculoskeletal interdependence exists between regions of the body. Interconnected kinetic chains and synergistic muscle groups are the reality—isolate and localized is illusory.
    • Changes in the musculoskeletal system must also be accompanied by changes in neurophysiology because these and other systems work in concert to perform tasks.

 

Choices

There are actually 125 citations at the end of this article. Many are manual therapy focused, with some perhaps indicating more of a ‘neurophysiological model’ benefit—mobilizing the thorax helps the neck, mobilizing the neck helps the elbow, etc. But, many also fit into the ‘kinetic mechanical engineering model’—strengthening the hip helps the knee, loosening the hip helps the low back, etc.

 

You will likely be drawn to the kinetic model if you tend to think in terms of exercise and the mechanics of joint movement, muscle activation or muscle inhibition. Or, you might be more drawn to the neurophysiological model if you like the manual therapy paradigms—or if you consider yourself a healer. However, it’s not really an either/or choice. Both mechanisms are in play, with varying degrees of impact, with either type of intervention we propose:

 

    • Joint mobilization gets a person touched, lubricates joints, stimulates blood flow, creates a slew of proprioceptive and neurological information, provides pressure against joint surfaces and ligamentous articular structures, improves joint play and range of motion, or helps center the joint.
    • Dynamic movement training, in the form of motor control exercise—does all that too, except for the touch part. But movement has the following advantages:

 

      • Nervous system involvement in muscle control. Activating and inhibiting their own muscles. Coordinating synergists. Coordinating and cooperating antagonists. Training the Motor—wiring and firing muscle activation patterns.
      • Nervous system involvement in ‘control tower’ activities. ‘What can I sense’ and ‘what do I want to do’? Training the Sensor and the Decider—attention to feedback and intension to target.
      • They can practice at home.

 

So, can we piggyback regional interdependence research based on manual therapy paradigms, or on localize and isolate exercise techniques, to dynamic integrated movement training? Can we expect the same kinetic and neurophysiological benefits with motor control exercise that we have seen in these studies? In our view, yes—and probably even better.

 

We don’t normally provide a bibliography, but wanted to in this instance. This is just a short list of regional interdependence material out there, and just taken from the bibliography of this one article—glance through the titles to get a flavor:

 

    • Thorax to neck and shoulder.
    • Hip to lumbar.
    • Hip to knee.
    • Ribs to shoulder.
    • Low back to foot.
    • Lower extremity strength to shoulder.
    • Think that this is an all-inclusive list of body inter-connections?

 

A regional interdependence model of musculoskeletal dysfunction: research, mechanisms, and clinical implications. Sueki DG1, Cleland JA2, Wainner RS3 J Man Manip Ther. 2013 May;21(2):90-102.

 

      1. Wainner RS, Whitman JM, Cleland JA, Flynn TW. Regional interdependence: a musculoskeletal examination model whose time has come. J Orthop Sports Phys Ther. 2007;37(11):658–60 [PubMed] [Google Scholar]
      2. Boyles RE, Ritland BM, Miracle BM, Barclay DM, Faul MS, Moore JH, et al. The short-term effects of thoracic spine thrust manipulation on patients with shoulder impingement syndrome. Man Ther.2009;14(4):375–80 [PubMed] [Google Scholar]
      3. Cleland JA, Childs JD, McRae M, Palmer JA, Stowell T. Immediate effects of thoracic manipulation in patients with neck pain: a randomized clinical trial. Man Ther. 2005;10(2):127–35 [PubMed] [Google Scholar]
      4. Mintken PE, Cleland JA, Carpenter KJ, Bieniek ML, Keirns M, Whitman JM. Some factors predict successful short-term outcomes in individuals with shoulder pain receiving cervicothoracic manipulation: a single-arm trial. Phys Ther. 2010;90(1):26–42 [PubMed] [Google Scholar]
      5. Souza RB, Powers CM. Differences in hip kinematics, muscle strength, and muscle activation between subjects with and without patellofemoral pain. J Orthop Sports Phys Ther. 2009;39(1):12–9 [PubMed] [Google Scholar]
      6. Strunce JB, Walker MJ, Boyles RE, Young BA. The immediate effects of thoracic spine and rib manipulation on subjects with primary complaints of shoulder pain. J Man Manip Ther. 2009;17(4):230–6 [PMC free article] [PubMed] [Google Scholar]
      7. Bialosky JE, Bishop MD, George SZ. Regional interdependence: a musculoskeletal examination model whose time has come. J Orthop Sports Phys Ther. 2008;38(3):159–60; author reply 160 [PubMed] [Google Scholar]
      8. Cibulka MT. Low back pain and its relation to the hip and foot. J Orthop Sports Phys Ther.1999;29(10):595–601 [PubMed] [Google Scholar]
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      2. Gonzalez-Iglesias J, Fernandez-de-las-Penas C, Cleland JA, Gutierrez-Vega Mdel R. Thoracic spine manipulation for the management of patients with neck pain: a randomized clinical trial. J Orthop Sports Phys Ther. 2009;39(1):20–7 [PubMed] [Google Scholar]
      3. Stupar M, Cote P, French MR, Hawker GA. The association between low back pain and osteoarthritis of the hip and knee: a population-based cohort study. J Manipulative Physiol Ther. 2010;33(5):349–54 [PubMed] [Google Scholar]
      4. Arab AM, Nourbakhsh MR. The relationship between hip abductor muscle strength and iliotibial band tightness in individuals with low back pain. Chiropr
      5. Johnson EN, Thomas JS. Effect of hamstring flexibility on hip and lumbar spine joint excursions during forward-reaching tasks in participants with and without low back pain. Arch Phys Med Rehabil.2010;91(7):1140–2 [PMC free article] [PubMed] [Google Scholar]
      6. Mellin G. Correlations of hip mobility with degree of back pain and lumbar spinal mobility in chronic low-back pain patients. Spine. 1988;13(6):668–70 [PubMed] [Google Scholar]
      7. Rothbart BA, Estabrook L. Excessive pronation: a major biomechanical determinant in the development of chondromalacia and pelvic lists. J Manipulative Physiol Ther. 1988;11(5):373–9 [PubMed] [Google Scholar]
      8. Brantingham JW, Lee Gilbert J, Shaik J, Globe G. Sagittal plane blockage of the foot, ankle and hallux and foot alignment-prevalence and association with low back pain. J Chiropr Med. 2006;5(4):123–7 [PMC free article] [PubMed] [Google Scholar]
      9. Powers CM. The influence of abnormal hip mechanics on knee injury: a biomechanical perspective. J Orthop Sports Phys Ther. 2010;40(2):42–51 [PubMed] [Google Scholar]
      10. Bolgla LA, Malone TR, Umberger BR, Uhl TL. Comparison of hip and knee strength and neuromuscular activity in subjects with and without patellofemoral pain syndrome. Int J Sports Phys Ther.2011;6(4):285–96 [PMC free article] [PubMed] [Google Scholar]
      11. Finnoff JT, Hall MM, Kyle K, Krause DA, Lai J, Smith J. Hip strength and knee pain in high school runners: a prospective study. J Inj Funct Rehabil. 2011;3(9):792–801 [PubMed] [Google Scholar]
      12. Rowe J, Shafer L, Kelley K, West N, Dunning T, Smith R, et al. Hip strength and knee pain in females.N Am J Sports Phys Ther. 2007;2(3):164–9 [PMC free article] [PubMed] [Google Scholar]
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      1. Lucado AM, Kolber MJ, Cheng MS, Ecternach JL. Subacromial impingement syndrome and lateral epicondylalgia in tennis players. Phys Ther Rev. 2010;15(2):55–61 [Google Scholar]
      2. Ben Kibler W, Sciascia A. Kinetic chain contributions to elbow function and dysfunction in sports. Clin Sports Med. 2004;23(4):545–52, viii [PubMed] [Google Scholar]

Filed Under: Article Reviews

Prone Leg Extension Test Viability

March 27, 2020 by Gordon Browne

Muscle recruitment patterns during the prone leg extension. Gregory J Lehman,1 Duane Lennon,2 Brian Tresidder,2 Ben Rayfield,2 and  Michael Poschar2. BMC Musculoskelet Disord. 2004; 5: 3.

Setting the Table

This 2004 article is a good example of a traditionally held rehab thought process that conflates muscle recruitment patterns in one position with muscle recruitment patterns in an entirely different position and related to an entirely different functional context. Here is the basic set up of the article (italics mine):

“The prone leg extension test is commonly used in the evaluation of lumbopelvic function. It has been theorized that the activation of muscles during a prone leg extension (PLE) simulates the muscle recruitment pattern of hip extension during gait. The theory suggests that the temporal activation of the posterior muscle groups should occur in the following order (right PLE exercise): right gluteus maximus, right hamstring, left lumbar erector spinae, right lumbar erector spinae, left thoracolumbar erector spinae and lastly right thoracolumbar erector spinae.” Muscle spasm – a proposed procedure for differential diagnosis. Janda V. Journal of Manual Medicine. 1991;6:136–139).

Let’s look at these assertions one at a time.

Is PLE a clinically valid test?

One—'the prone leg extension test is used to evaluate lumbopelvic function’. This test embodies a typical Static Integration view of movement—that the leg should move relative to the pelvis, which is then stabilized by the muscles of the waist. ‘Proximal stability facilitates distal mobility’ is a static integration motto or underlying theme. But in the case of application to gait, this test, along with the underlying thought process, is faulty. Let’s take a closer look at what is actually happening here.

In addition to proposing the theory that this article is based on, the same author (Vladimir Janda, when articulating the concept of Regional Interdependence) also famously stated: “It is principally a wrong approach to try and understand impairments of different parts of the motor system separately without understanding the function of the motor system as a whole”. Stated bluntly, static integration concepts, principles and techniques are illustrative of a mistaken, or more accurately an incomplete understanding of the function of the motor system as a whole. There is actually another way, a better way, of understanding the motor system—Dynamic Integration.

Taking a dynamic integration approach to movement, we should be asking a crucial question: what would happen to the pelvis if the only thing to work was the gluteus maximus or the hamstrings (either or both hip extensors).

This ability to differentiate the hip extensors from trunk musculature (turn off back extensors while engaging hip extensors) is actually humanly possible, though few people have the motor control to do so. If, while prone, a person lifted their leg just using some combination of hip extensors, the pelvis would be pulled into posterior tilt—the pubic bone would press into the floor, the lower back would lengthen or flex, and the pelvis would rotate away from that lifting leg (left rotation of the pelvis if the right hip extensors engaged). We could say that the pelvis is unstable in this scenario (however, this is not what actually happens with most people).

See if you can visualize this. The weight of the lifting leg would pull the pelvis toward that leg, unless the pelvis is stabilized or prevented from moving. And this is what the vast majority of people will do, for reasons discussed later in this review. What stabilizes the pelvis against being pulled into posterior tilt by the hip extensors? Some combination of back extensors or posterior shoulder girdle muscles—the timing or sequence of which seems to be of great interest to the authors of this article.

Again, this is classic static integration understanding of ‘how the motor system functions as a whole’. The limb moves relative to a stabilized pelvis, which is prevented from moving (stabilized) by the muscles of the waist or trunk. The pelvis is controlled ‘top down’. A dynamic integration view of how the motor system functions is different—it advocates for a more realistic ‘ground up’ control of the pelvis. In a dynamic integration view, it is functionally much more common for the pelvis to move relative to the legs—and for the hip muscles to control the movement, balance and stability of the pelvis. This is a reversal of our ‘origin & insertion’ derived understanding of lumbopelvic function or organization. In dynamic integration assessment and exercise prescription, we keep in mind that the hip muscles are responsible for (the vast majority of the time and for the vast majority of people):

  • The movement of the pelvis into anterior or posterior tilt.
  • The prevention of the movement of the pelvis (stability) into anterior or posterior tilt.
  • The balance of the pelvis between anterior/posterior tilt.
  • Constraining the pelvis (limitation short of physiological end-range) into anterior/posterior tilt (which translates into hip flexion and hip extension respectively), along with ligaments/fascia/capsule.
  • The movement, stability, balance and limitation of the pelvis in rotational and diagonal directions.

Here are just a few examples. In unsupported sitting, the hip flexors control or constrain posterior tilt and drive anterior tilt, while the hip extensors constrain anterior tilt and drive posterior tilt. The hip muscles clearly are responsible for sitting postural balance and, in fact, unsupported sitting is impossible without hip muscle control of the pelvis. In standing, the hip extensors drive posterior tilt or control anterior tilt and lumbar lordosis.

In both sitting and standing, the pelvis is rotated (or is stabilized against being rotated) by the muscle of the hips (reach across or behind, open a sliding glass door, saw wood, mop a floor, play golf, throw a ball, cutting/pivoting). In bending, the hip extensors work eccentrically to reach hands toward the floor and concentrically to come back up again—anterior and posterior tilt control again. And, crucially for our discussion, the hip muscles control the movement and stability of the pelvis in gait.

Even during the prone leg extension, this dynamic is present. Obviously, the hip extensors can and do move the pelvis in this position—otherwise the pelvis would not ‘need’ to be stabilized. So, bottom line, this test does not evaluate ‘lumbopelvic function’ for anything except…lying prone and lifting a leg within a static integration framework.

Does PLE muscle recruitment simulate gait?

Two—'prone leg extension simulates muscle recruitment patterns during gait’. No, sorry. Prone leg lift hip extension and gait-related hip extension are completely different. Functionally, prone leg lift is first seen in early childhood development. The inquisitive youngster (all of us), once we found ourselves lying on our bellies, quickly found the view limited and uninteresting. We all had to figure out how to lift our heads to (ideally) vertical in order to be able to orient better to our environment (see what’s going on).

We didn’t stabilize (immobilize) our trunk as we lifted our head (static integration thinking). We used all the posterior trunk muscles and moved into extension all the way through our spines to assist the smaller neck muscles. We moved our head as an extension of a dynamically moving torso. This is also a feature of dynamic integration thinking, and it illustrates two of the four principles of optimal movement—appropriate distribution of movement and proportional use of synergists. We engaged our thoracic and lumbar extensors, along with our scapular ‘retraction’ muscles—the arms lifted or extended as the upper extremity and scapular muscles were ‘slaved’ globally to the extending trunk muscles—to assist us in lifting our heads.

What would happen to the pelvis in this scenario? It would be pulled into anterior tilt—the bottom end (pelvis) of this larval-like structure would lift at the same time the top end (head) lifts, because of the engagement of the back extensors. But, the head would be able to lift higher (better orientation to our environment) if the pelvis wasn’t pulled into full anterior tilt. To this end, the hip extensors kicked in to add the weight of the legs to the pelvis—they anchored the pelvis or stabilized the pelvis to minimize anterior tilt and to maximize head verticality.

If you have access to one, watch a baby when they lift their head while prone (before they figure out how to push up with their arms—arms need to be off the floor for this to happen) or go online and type ‘prone baby image’ in your search engine. You will see that the legs lift when the head and arms lift—all the extensors are engaged in the service of optimal orientation. So, we could say that the nervous system has associated prone leg lift with trunk extensor use—the hip extensors and trunk extensors were, and for most people still are, wired and fired together within this position-specific context.

Conversely, in my understanding, and without having ultrasound imaging or EMG to confirm, this how the hip extensors function in gait:

  • The hip extensors are not (primarily) engaging to prevent the back extensors from pulling the pelvis into anterior tilt, as they are when dynamically lifting the head.
  • Instead, the hip extensors act to prevent anterior pelvic tilt created by gravity or by bumping into end range hip extension (the pelvis will anteriorly tilt as you run out of hip extension ROM of the push-off leg).
  • And, the more hip extension mobility or ROM you have, the less the hip extensors have to work.
  • The hip extensors also act to convey the pelvis forward in space (propulsion or acceleration function).
  • The hip extensors and abductors also act to prevent the pelvis from collapsing or ‘side bending’ to the opposite side (Trendelenburg) during single leg stance phase.
  • In other words, the hip muscles work dynamically during gait to control the pelvis in a closed kinetic chain organization. This is not at all the same as the back muscles controlling the pelvis statically during prone leg lift in an open kinetic chain organization. This is not just apples and oranges (which are at least both fruits)—it’s apples and asteroids.

In my understanding, and without having ultrasound imaging or EMG to confirm, this how the back  extensors function in gait:

  • The back extensors are not utilized to prevent the hip extensors from pulling the pelvis into posterior tilt, as they are in a prone leg lift ‘test’.
  • The back extensors act to prevent the spine from collapsing into flexion—they maintain uprightness in an AP direction.
  • And, the more you can position the pelvis vertically or limit anterior pelvic tilt (from the hip muscles), the less these back extensors muscles have to work.
  • The opposite back extensors also work with the opposite hip extensors during the single leg stance phase to prevent spinal side bending (right back extensors kick in with left single leg stance).
  • And, the more you can control pelvic Trendelenburg effect (from the hip muscles), the less these trunk muscles have to work to control spinal side-bending.
  • In other words, the posterior trunk muscles are not working during gait to control the movement or stability of the pelvis, they are working to control the relationship between the pelvis and chest. They are not pelvic stabilizers, but trunk stabilizers. And this is also a dynamic integration principle.

The concepts that inform this way of thinking are pattern specificity (or the specificity principle) and the transfer principle. For example, let’s say we have a function (gait, sitting posture, standing posture, pelvic rotation while swinging a golf club, etc.) that we want to: a. assess or evaluate for efficiency or optimization, and then b. prescribe motor control exercise to effect a positive change toward optimization.

The specificity and transfer principles state that we should be both assessing and prescribing corrective exercise in a way that: a. closely approximates the components of the motor skill (the same bony relationships and muscle synergy recruitment patterns), b. closely simulates the functional context that is being evaluated or optimized (gait and prone orientation are not similar contextually), and c. mimics the cognitive processing involved in the targeted activity (we don’t train a baseball pitcher by having him throw darts). In light of this, the prone leg extension ‘test’ violates both of these principles, for the reasons stated above—it does not, as claimed, ‘simulate the muscle recruitment patterns during gait’.

In what order should these muscles synergists fire?

Three—'the temporal activation of the posterior muscle groups should occur in the following order’. This is another common rehab belief—that we can determine ‘what should be’, and that ‘what should be’ is the same for everyone. While part of our job needs to be assessment and clinical judgment, informed by principles of optimal movement, of ‘what should be’ for that person in front of us with particular movement and postural patterns and with a particular presenting complaint, this does not mean that everyone should be expected to move or recruit in the same way (trying to define what is ‘normal’).

We are not stamped out of a uniform template. We are not tuned to factory specifications. There is no normal and there is no natural. There is not uniformity regarding ‘what should be’, though many rehab-related studies conflate ‘common’ or ‘what most people do’ with ‘what should be’ or ‘what is optimal’. There are only a vast array of choices. The Bernstein Problem states that we have ‘too many choices’ in joint degrees of freedom and muscle activation patterns, but that we self-limit those choices by creation of individual motor habits. People can have similar motor habits (common), but this doesn’t mean they are optimal.

Apropos to this article, there are actually many ways of organizing this movement of prone leg lift. One basic choice has already been described. You can lift a leg and engage your back extensors to stabilize your pelvis, or you can lift a leg and allow your pelvis to be moved by your hip extensors This second choice was not articulated in this article because it is not what the vast majority of people actually do, and I doubt the authors even considered the possibility. But I can do it, and I have taught others to do it as well (though it’s more of a party trick than a functionally relevant motor skill).

This study featured 14 people, asymptomatic for low back pain, with 10 males and 4 females. The choices provided in this article primarily have to do with proportion of effort and timing or sequencing of the same basic muscles. Gluteal/hamstring proportionality and timing is one theme—the theory being that weak gluts provide less pelvic stability. One of the findings of this study, as well as previous studies with contradictory findings that this study had hoped to resolve or clarify, is that the gluteus maximus was uniformly the last muscle to be recruited (by a whopping average of 370 milliseconds). (The influence of ankle sprain injury on muscle activation during hip extension. Bullock-Saxton JE, Janda V, Bullock MI. Int J Sports Med. 1994;15:330–4. Dynamic testing of the motor stereotype in prone hip extension from neutral position. Vogt L, Banzer W. Clin Biomech. 1997;12:122–127).

All the authors seem to bemoan this gluteal delay, but it makes more sense when you have an understanding of how people behave and ‘what happens if’. One study found a nearly simultaneous activation of hamstrings and back extensors, with gluteal delay. The other found back extensor activation preceded hamstring activation, again with gluteal delay. In terms of the hamstrings kicking in before the gluts, I’m not at all surprised—this is what I feel proprioceptively as well when I try it.

Probably, this timing is due to the tendency to lift the foot first, then the knee. Lifting the knee before the foot would be counter-productive—this would likely be quadraceps activation. Therefore, we would expect the hamstrings to come in before the gluts and, in this position, the discrepancy cannot be attributed to or be interpreted to mean gluteal weakness (especially in the presence of extension-related low back pain—where lumbar extensor activation will trigger lumbar pain, which inhibits the action of the hip extensors and gives a false positive result of gluteal weakness).

In terms of back extensor/hip extensor timing, this makes sense as well. Some part of the nervous system knows ‘what happens if’—it knows that it needs to stabilize the pelvis (or had been programmed in early childhood to believe the pelvis needs to be stabilized in order to orient to the horizon). Some people anticipate the need and proactively engage their back extensors, while others engage simultaneously—this is simply a matter of choice and it matters not if the end result is the same (pelvic stability).

The foot lifts before the knee—hamstrings before gluts. The back extensors either ‘anticipate’ the effect on the pelvis (posterior tilt would result from either hamstring or gluteal activation) and pre-engage, or they would act to stabilize simultaneously—back extensors before gluts. Once the foot lifts and the pelvis is stable, then the knee/thigh lifts—the gluts bring up the rear.

From the abstract: “It has been theorized that a normal and consistent pattern of muscle activation exists”.

  • We have a belief that this is what ‘should happen’ with ‘normal’ people—because it sure would be nice to have everything all nice and tidy.

From the conclusion—"A consistent pattern of activation was not found. Variability was seen across subjects. These findings suggest the PLE is not sufficient for a diagnostic test due to the notable physiological variation. This study found no consistent order of activation for the biceps femoris, contralateral erector spinae and ipsilateral erector spinae during prone leg extension.

  • Whoops! Our belief is mistaken—back to the drawing board.
  • The ‘test’ is not valid in the way we thought it was—how can we test lumbopelvic function more accurately?

From the discussion—"The analysis of EMG data in this study shows a large variability in muscle activation order between subjects, with no consistent firing pattern in asymptomatic individuals. Different muscles came on first and on average 3 muscles fired within 33 ms of each other, a statistically non-significant difference.”

  • There is no ‘normal’ order or sequence—there are only choices (some of which might be more optimal than others for each individual).
  • The amount of timing difference between muscle activation is about a third of a second—can we actually detect this clinically (manual palpation) without resorting to EMG?

From the conclusion—"Consistently, the gluteus maximus is the last to become active with onset timing ranging from 70 ms to 676 ms.”

  • How does that happen? We thought the gluteals are supposed to be stronger—shouldn’t they fire first?

What have we learned?

One—does the prone leg extension test evaluate ‘lumbopelvic function’? No, not in the way the study and cited theories imply. This static integration test is functionally related to orientation from prone, not gait. There are choices in muscle activation while prone (one of which was not even considered)—without understanding ‘what happens if’, and without having a target or an understanding of ‘what I would like to see’, the test is confusing or meaningless.

Two—does the engagement of the hip extensors during prone leg lift simulate hip extensor and back extensor engagement during gait? No. The specificity and transfer principles are not taken into account—the muscle synergy specificity, muscle function (which muscles stabilize/control the pelvis and which muscles stabilize/control the trunk), functional context (orientation vs locomotion) and cognitive processing features are wildly different.

Three—what can we conclude from the timing issue? That the amount of timing variance or gluteal delay is well less than a second. Clinically, we can’t train up or ‘improve’ a change in sequence or timing given the millisecond differences seen. So, really, what does this information actually tell us? Especially given that the subjects were all asymptomatic. Perhaps if there were some symptomatic folks thrown in (people who are currently experiencing low back pain, especially of the extension type), there would be larger differences? But again, are the likely delays or timing differences going to make a difference? Can we really affect a change in what amounts to differences in a second or less? Not likely.

Bottom line? This test is not really that helpful—and it certainly doesn’t correlate automatically to gait, standing, lifting, or other functionally relevant activities that call for pelvic control/stabilization (which is the job of the hip muscles in these scenarios, not the trunk muscles). Therefore, this test does not assess ‘lumbopelvic function’ in any meaningful way.

Filed Under: Article Reviews

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