Upper and Lower Crossed and Breathing for Volume

Here are a series of questions from a Northeastern Physical Therapy student that attended the Northeastern Sports Medicine and Performance Group 2nd Annual Boston Hockey Summit and Basketball Symposium. http://www.bsmpg.com/

Here is my Recap from the event, but I did not attend the Inspiratory training talk that the 2nd part of the post is referring to.

……….I know you are a big fan of Janda’s work, so my first question relates to his Lower Cross Syndrome. I also believe I remember you saying you believe everyone alive fits this to some degree. That being said, do you view this as more of a neurological adaptation in response to the position of the body’s center of mass or as a biomechanical phenomenon of anterior pelvic tilt where shortness prevails?

A key to understanding and appreciating Janda’s work, and without a doubt my understanding continues to evolve as I further my mentorships from Dr. Leibenson, Dr. Frank, and the DNS courses, is that it’s both. It’s neurological and biomechical. If we have to know which came first, the chicken or the egg, my opinion is that it’s more neurological. Unless you are born with these patterns, these issues can’t be biomechanical before neurological. Repetitive postures or poor youth development out of “normal” will send signals to the brain which will then create inhibition and facilitation for points of stability. When this neurology sets in, it then becomes biomechanics.

Poor biomechanics trigger the neural drive, but I don’t think instances of original poor biomechanics alone are what set in the Upper and Lower Crossed.  The biomechanical snapshot fits the definition, but not really the long term trigger.

You're screwed.

……….The reason I ask is because I remember you saying you put very little stock into a Thomas Test or Muscle Length testing because whether or not they can express that mobility during movement is of more importance.

The Thomas Test is important to look at after you see a limitation in multi-segmental extension. The thing is though is that when you see good MSE and split squat technique, you might still find a positive Thomas Test. I don’t think you should look at individual impairment tests as your umbrella evaluation. They are useful to break out and find the culprits.

This has got to be phony.

……….Also, if it were purely a biomechanical phenomenon that manifests in anterior pelvic tilt and a shortness of the anterior hip structures, than there would never be anybody in posterior pelvic tilt or with a flat lumbar spine and never a need to stretch the hamstrings to get length because when I think anterior pelvic tilt I think short hip flexors and lengthened hamstrings, due to the anterior rotation of innonminates. Is this “tightness” we get in the hamstrings, really due to neurological tension and stiffness as a means to prevent us from falling over due to our anterior weight shift at our hips or overcompensation of the hamstrings to control and stabilize the pelvis due to poor lower abdominal and glute function in controlling and posteriorly tilting the pelvis according to Sahrmann’s synergistic dominance?

So if the question is if you say all dysfunction is rooted in a Lower Crossed, then how do we see tight hamstrings and posterior pelvic tilts, then you have a good question. The answer is that when you attempt to function with a Lower-Crossed, you have options in how you react and how you cheat. I don’t know that these reactions are predictable ahead of time without screening or assessing movement. We can consider that the same “culprit” that we find from the SFMA can be the reason for DN MSF in one person and the reason for MSE in another person.

So in functioning with the Lower Crossed, one option is to continue in the basic pattern that would manifest in a dominant sway back position. But indeed that swayback position is an anterior weight shift. And that shift can be attenuated from forward head, rounded shoulders, and even stronger anterior pelvic tilt, or a posterior tilt, which then biomechanically shorten the hamstrings. Or it could simply be direct neural drive to the posterior chain hamstrings, calves, and deep plantar musculature to counteract the anterior weight shift. Try leaning forward. The first thing to turn on will be the calves. If you keep going, you will probably feel the hamstrings.

In a dynamic posture like gait, the Lower Crossed with limit stride reflexively from a lack of hip extension on the stance side. With a lack of hip extension, the swing side won’t swing as far and then set in an adaptive shortening.

So the posterior pelvic tilt or hamstring tone/length will always or at least typically be a reaction to the Lower Crossed anterior tilt and toned hip flexors.

I bet 21 for the guy, 19 for the girl. Both good control of the Lower Crossed.

……….I remember Bill Hartman referencing a study in his blog and when I talked to him about how core stability training decreased hamstring stiffness.  I would assume this was due to the fact that the proximal end of the hamstrings did not have to exert as much tension in controlling the pelvis posteriorly because the glutes and lower abs/obliques were doing more work.

I think this is exactly what he is inferring. Because anterior abdominals and glutes are inhibited, the hamstrings counter the dominant anterior tilt with tone. If the inhibited components are brought up, then the hamstrings will be detonified. It is all neurology from muscle spindles, GTO, and joint mechanoreceptors that tell the brain who should get turned on/up or off/down.

Why the hamstrings take over is probably rooted somewhere in human developmental ontology which basically means it’s all conjecture. I would theorize that the hamstrings aren’t really supposed to be hamstrings, and that is why they have different neural drive than the glutes.

I am guessing a World's Gym tank top.

……….For instance people who sit all day in a posterior pelvic tilt. Is there ways you distinguish between shortness and stiffness, or is there always stiffness and Lower Crossed with shortness of the posterior structures sometimes mixed in? The reason I ask all of these is because I firmly believe establishing optimal pelvic position and controlling the pelvis to be the most important aspect in rehab and good training as it is the centerpiece of the body and affects posture and movement up through the t-spine and upper extremity and down through the hip, knee, ankle and foot. How do you assess pelvic function and position?

Yes, the way to differentiate stiffness vs. shortness is active vs. passive motion. If there is more than a large difference (not sure there is research in this area – 10 degrees?) in active vs. passive, there is stiffness on the moving side of the joint. If active and passive are the same, and it is below the industry standard, then it would be short. I consider stiffness more of a principle than a measure though. Stiffness is always relative to all sides of a joint, and it may or may not impact the same way in different positions. There are also multiple muscles that can impact a joint’s presentation, and in claiming a muscle’s stiffness, multi-joint muscles may or may not act the same way with different sufficiencies.
I think of these issues in terms of movement. And no matter what you call the tissue, you attack whatever its presentation. As far as stiffness, it is a critical term to understand the neural feedback tissues send to the CNS that then guide biomechanical movement.

I assess pelvic function through the same means of the FMS and SFMA. In a painful spine or hip, there are local approaches that rely on pelvic landmarks for muscle energy or manipulation techniques, but

I just don’t think in terms of what “this” is supposed to be doing outside the context of the indicator movements of the FMS or SFMA. When you break out a pattern, if it takes you to the pelvis, it will often be via the hips or lumbar spine.

The pelvis’ supreme importance is not in question, but I don’t know that it has any of its “own” muscles. Its obliquities or function are guided by the lumbar spine and hips through osteopathic movement, at least as I see it.

WTF? Pelvic what?

……….During the BSMPG seminar, one of my professors, for Cardiopulmonary class, spoke about his research in developing a protocol to improve the inspiratory muscle performance in hockey players. I do not know if you saw itI know the importance you place in breathing and more particularly diaphragmatic breathing for health, performance, and activation of the inner core. His protocol called for maximal inspiration and he showed a video of an athlete breathing in maximally. What I noticed was paradoxical breathing, maximal drawing in of the abdominal musculature, superior migration of the upper thorax and sternum and tons of activity from the scalenes, SCM and upper trapezius. Do you think this can end up having any negative ramifications and that this can become a reflexive pattern if trained enough during tidal volume? I highly doubt taht you will get the same maximal inspiratatory volume training effect from not using accessory muscles excessively so would there be things you have to look out for and work on a corrective basis, especially in the core, t-spine, neck, scapula and shoulders, to prevent injury or dysfunction later on?

I did not see this presentation, but going off what you are saying, I would have some concerns with this approach.

The first thing I would consider is that I might expect this from someone with a cardiopulmonary background. His research and methods may be brilliant in terms of the measures that his discipline will find important. He may not be read on the deleterious effects of this type of high threshold strategy.

A question I would have would be does training this way expect to carry over to increased lung volumes without the high threshold strategies. Another question I would have is while volumes are high, is PaO2 after this type of breath vs. a diaphragmatic breath actually higher? This may be yet another great example of the research not lying, but not telling the whole story.

I think you are absolutely correct that enough of this pattern can supplant an appropriate motor pattern and cause dysfunction later on. The repetitions for a training effect would likely be enough to reprogram motor control.

This breathing pattern may be necessary under fatigue, and training the core under fatigue is a very interesting topic. It is also a topic that indirectly values HRV, basically so you don’t have to worry about core function under fatigue. If you recover quickly, the need for accessory respiratory musculature will not be as dominant.

If you try to stick this up your nose.......

  • September 6, 2010

Leave a Reply 5 comments

Robbie Bourke Reply

Great post Charlie.

Brent Wistrom Reply


Since this post related to breathing, I figured I’d send a few other breathing-related links/reads your way (all of which may have already been encountered by a number of your readers, so I apologize to any who may be rolling their eyes in a “been there, read that” manner right about now).

Perhaps if you have the time and inclination, you can peruse each of these at your leisure and potentially use it as fodder for future blog posts. While it may be difficult to give adequate coverage to the relative utility of all the various interventions discussed in these articles, as well as how they may or may not fit in based upon setting (early-stage PT, for high-level athletes with solid overall function, and other points on the continuum between those more extreme stops) and individual context, I have come to recognize that even the briefest of thoughts from you are overflowing with unmatched levels of insight and wisdom.




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