Why Weak Glutes Aren’t A Reliable Predictor Of Low Back Pain
It seems we are constantly trying to find causes for low back pain with our patients.
Quite often we are caught up looking for biomechanical issues (which there often are) and avoiding other things that could influence a person’s pain.
One such instance is the possibility that weak glutes are a contributing factor.
I recall seeing one of my instructors demonstrate this (what I perceived to be) complicated movement test where my patient was lying prone and having them extend their leg. There was a specific pattern where the muscles in the low back down through the glutes and hamstrings were supposed to move.
This would be followed up with the comment: “your glutes aren’t firing”!
While I watched this all I could think was…”there’s no way I’m going to remember what order all of this goes in”!
But, when done with confidence and a really good explanation, it seemed to make sense to me, and the patient.
So, I worked through the low back, glutes, and hamstrings, and the patient felt better after the treatment.
I proceeded to pat myself on the back for a job well done!
However, the next time a patient came in for what I thought was the same issue, I couldn’t remember this specific pattern of movement and what it was supposed to tell me! Why couldn’t I get this!?
Well, in reality, I really didn’t have to and here’s why.
Limitations With Testing
There are a couple of tests used to see if the glutes are a contributing factor to low back pain, so let’s look at both of them.
The prone leg extension test1 is pretty commonly used to test for low back pain and lumbopelvic function (this is the one my instructor was demonstrating to me).
The pattern of movement you’re supposed to see is (if you were testing the right side) right glute max, right hamstring, left lumbar erector spinae, right lumbar erector spinae, left thoracolumbar erector spinae, then the right thoracolumbar erector spinae. A delay in glute max recruitment is supposed to show a dysfunctional pattern of movement.
There is a whole list of other patterns that are supposed to mean other things, but it’s a long list and more than I want to get into for the purposes of this post.
A study1 showed there was no consistent order of activation during the test and glute max was the last muscle to become activate with time ranging from 0.07 to 0.676 seconds in delay.
Now, these tests were done with proper EMG testing, so I have to wonder…how would we ever be able to properly assess this just using touch and vision!?
Another test we were taught was “Trendelenburg”, or “SLS” to assess for glute weakness possibly contributing to back pain.
With this test, a practitioner stands behind the patient and has them raise one leg so the hip is between 60°-90° of flexion. A positive test shows lateral pelvic tilt on the stance leg, which is supposed to represent glute weakness on that side.
One study 2 compared the differences between those with chronic low back pain vs. a control group using Trendelenberg. It actually showed the number of positive tests was no different between the groups. There was also no difference in glute med strength between those who scored a positive and negative test.
Since there was an equal number of positive and negative tests between both groups it showed this test is unreliable to differentiate between those with chronic low back pain and those without, nor was it reliable for demonstrating a difference in glute med strength.
Another study 3 actually injected a superior gluteal nerve block to see if there were any alterations in different movement variables. They found after the injection there was no difference in contralateral pelvic drop, hip adduction, or hip abduction due to reduced strength of the glutes post-injection.
The researchers found this surprising as an impaired gluteal nerve has always been associated with the SLS test.
So, in other words, lateral pelvic drop is not associated with weak glute med muscles in our patients who are dealing with chronic low back pain. It was even suggested that glute med strength of less than 10% of body weight is required to actually get a positive SLS.
The suggestion was also made that in order to maintain your stance during this test it is because of all muscles attaching to the greater trochanter working together combined with the mechanical force of the iliotibial band. This shows a positive SLS is more likely a global issue rather than a specific spine and pelvis issue.
In light of their findings they showed how this test could not distinguish between who was experiencing low back pain and who wasn’t, nor could it identify those who had weak glutes, and in fact demonstrated the test was probably due to some other issue altogether.
Another study 4 showed the presence of low back pain was a combination of higher BMI, signs of hip abductor problems, significant glute med weakness, gluteal tenderness, and a positive SLS (but the strength testing was admittedly not reliable in the study). However, this study showed something else that is probably far more significant which we will look into next.
It was unclear if glute med muscle weakness was the cause of the low back pain…or just a consequence of it.
Muscle Activation, Weakness, Or Protection?
Quite often when discussing this kind of thing and it’s relation to low back pain, the discussion can revolve around not only issues with the glutes, but also hamstring length and activation patterns between the two.
Inevitably when discussing “weak glutes” it’s due to an S.I. joint “dysfunction”, or this dysfunction is causing the weak glutes. But really, what is dysfunctional with the S.I. joint in this case?
They 5 described S.I joint dysfunction as; low back pain below L5, pain over the posterior aspect of SI joint around PSIS and buttock with or without above the knee leg pain. They used a combination of three SI joint provocation tests (posterior shear, compression, distraction, and sacral thrust) that showed good sensitivity and specificity (although the sensitivity rating was much higher).
When we look at the discussion around which muscles are “activating” with certain movements it is usually centered around the context of the pain-spasm-pain model which suggests pain results in increased muscle activity, in turn creating more pain.4
Or, the pain adaptation model which suggests pain reduces activation of muscles when active as agonists and increases activation of muscles when active as antagonists.6 They say this will reduce movement and ROM which would, in turn, prevent mechanical pain and further damage to the tissues.
The funny thing is that while both of these models are trying to prove the same thing, they end up contradicting each other quite a bit and neither of these ideas can predict how back pain will affect muscle activation.
There is lots of discussion around both increased and decreased muscle activation due to pain which results in disrupting motor control. However, this systematic review 6 argues that increases in muscle activation is an adaptation that occurs for various reasons, and those changes are mainly to avoid harmful stress placed on already injured structures, and to increase stability around the spine.
In each case, they looked at any changes that were task-dependent, related to an individual problem, and highly variable between each patient. This also shows those changes are functional since they are trying to reduce unpleasant stress and provide stabilization to the spine.
One common thread through most of the research cited is glute weakness in relation to back pain. However, it’s a bit of a chicken or the egg, is the weakness a result of reduced use because of pain, or did the weakness cause the pain? I’d venture to say it’s due to the reduced use.
While this can all sound maybe a little complicated and like word salad, when we look at everything we know about pain, what is this actually telling us?
One thing we know for sure that pain is ALWAYS a protection mechanism. So, if something in our body has a decreased ROM for a period of time in order to prevent stress in a sensitive area, this is just simply a way to protect that area. If those altered movements are also providing extra support to stabilize something, it’s actually doing this to protect the area! With this understanding we have to ask, does it really matter what order a muscle fires in (especially because we’d never be able to accurately assess this with just the human eye)? What we should be concerned with is calming those sensitized areas down, reassuring the patient they aren’t broken, and educating them as to why they’ll be okay. Then get them moving in pain-free full ranges again and help strengthen the area, build up that resilience!
- Lehman GJ, Lennon D, Tresidder B, Rayfield B, Poschar M. Muscle recruitment patterns during the prone leg extension. BMC Musculoskeletal Disorders. 2004 Dec 1;5(1):3.
- Penney T, Ploughman M, Austin MW, Behm DG, Byrne JM. Determining the Activation of Gluteus Medius and the Validity of the Single Leg Stance Test in Chronic, Nonspecific Low Back Pain. Archives of Physical Medicine & Rehabilitation [Internet]. 2014 Oct [cited 2020 Apr 17];95(10):1969–76. Available from: https://search.ebscohost.com/login.aspx?direct=true&db=s3h&AN=98597253&site=ehost-live
- Pohl MB, Kendall KD, Patel C, Wiley JP, Emery C, Ferber R. Experimentally reduced hip-abductor muscle strength and frontal-plane biomechanics during walking. Journal of athletic training. 2015 Apr;50(4):385-91.
- Cooper NA, Scavo KM, Strickland KJ, Tipayamongkol N, Nicholson JD, Bewyer DC, Sluka KA. Prevalence of gluteus medius weakness in people with chronic low back pain compared to healthy controls. European Spine Journal. 2016 Apr 1;25(4):1258-65.
- MassoudArab A, RezaNourbakhsh M, Mohammadifar A. The relationship between hamstring length and gluteal muscle strength in individuals with sacroiliac joint dysfunction. Journal of Manual & Manipulative Therapy. 2011 Feb 1;19(1):5-10.
- van Dieën JH, Selen LP, Cholewicki J. Trunk muscle activation in low-back pain patients, an analysis of the literature. Journal of electromyography and kinesiology. 2003 Aug 1;13(4):333-51.
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