The Psoas Muscle in a Runner: An Endurance Savy Muscle ?

 We received a question yesterday from a doctor. We felt it was worthy of sharing. Here it is, followed by our response.

Doctor:  I do have a question about one of my athletes in particular.  He is a fairly good (All-State in IL) high school track distance runner that has some left sided femoral acetabular impingement.  He gets some capsular hip pain that also will ‘tighten up’ his low back during speed endurance/threshold running only.  Moderate and easy distance runs cause no problem and neither do track/speed workouts.  Only during speed endurance does he have issues.  Upon evaluation after these sessions he does seem to have some low back QL tightness, but joint mobility is fairly good in his lumbar spine.  He does show marked hypertonicity through his left hip joint.  I’m not quite sure the mechanism here- why he would only flare up with speed endurance running- any insights?
Thanks a bunch and I look forward to hearing from you!

The Gait Guys response:

 You state “only during speed endurance” does he have issues. We will assume you mean a long, hard anaerobic workout, which would tax type II b fibers. You also mention he has hypertonicity through his hip joint.  Since the psoas crosses this joint it should be considered in sprinting and long, hard endurance activities, especially if the patient is flexor dominant. The psoas major muscle is composed of type I, IIA and IIX muscle fibers. It has a predominance of type IIA muscle fibers. The fiber type composition of the psoas major muscle was different between levels of its origin starting from the first lumbar to the fourth lumbar vertebra. The psoas major muscle has dynamic and postural functions, which supports the fact that it is the main flexor of the hip joint (dynamic function) and stabilizer of the lumbar spine, sacroiliac and hip joints (postural function). The cranial part of the psoas major muscle has a primarily postural role, whereas the caudal part of the muscle has a dynamic role. This is all very much supported in this journal article here (link) (http://www.ncbi.nlm.nih.gov/pubmed/19930517) and making it work in an endurance capacity would certainly cause issues. Flexor dominance is a common scenario we see clinically, due to insufficient extensor activity (and decreased vestibulo and reticulo spinal drive to extensors) and increased cortico spinal drive (to the flexors, including the iliopsoas). This would fuel the “bail out” (lack of stability) of the lower abs. The anterior tippage of the pelvis would drive the femur posteriorly, binding the joint (the opposite of an anterior femoral glide).

Video footage and some pix of your athlete would provide more insight for us to help.

we are……The Gait Guys

The Psoas Muscle in a Runner: An Endurance Savy Muscle ?

 We received a question yesterday from a doctor. We felt it was worthy of sharing. Here it is, followed by our response.

Doctor:  I do have a question about one of my athletes in particular.  He is a fairly good (All-State in IL) high school track distance runner that has some left sided femoral acetabular impingement.  He gets some capsular hip pain that also will ‘tighten up’ his low back during speed endurance/threshold running only.  Moderate and easy distance runs cause no problem and neither do track/speed workouts.  Only during speed endurance does he have issues.  Upon evaluation after these sessions he does seem to have some low back QL tightness, but joint mobility is fairly good in his lumbar spine.  He does show marked hypertonicity through his left hip joint.  I’m not quite sure the mechanism here- why he would only flare up with speed endurance running- any insights?
Thanks a bunch and I look forward to hearing from you!

The Gait Guys response:

 You state “only during speed endurance” does he have issues. We will assume you mean a long, hard anaerobic workout, which would tax type II b fibers. You also mention he has hypertonicity through his hip joint.  Since the psoas crosses this joint it should be considered in sprinting and long, hard endurance activities, especially if the patient is flexor dominant. The psoas major muscle is composed of type I, IIA and IIX muscle fibers. It has a predominance of type IIA muscle fibers. The fiber type composition of the psoas major muscle was different between levels of its origin starting from the first lumbar to the fourth lumbar vertebra. The psoas major muscle has dynamic and postural functions, which supports the fact that it is the main flexor of the hip joint (dynamic function) and stabilizer of the lumbar spine, sacroiliac and hip joints (postural function). The cranial part of the psoas major muscle has a primarily postural role, whereas the caudal part of the muscle has a dynamic role. This is all very much supported in this journal article here (link) (http://www.ncbi.nlm.nih.gov/pubmed/19930517) and making it work in an endurance capacity would certainly cause issues. Flexor dominance is a common scenario we see clinically, due to insufficient extensor activity (and decreased vestibulo and reticulo spinal drive to extensors) and increased cortico spinal drive (to the flexors, including the iliopsoas). This would fuel the “bail out” (lack of stability) of the lower abs. The anterior tippage of the pelvis would drive the femur posteriorly, binding the joint (the opposite of an anterior femoral glide).

Video footage and some pix of your athlete would provide more insight for us to help.

we are……The Gait Guys

The impact force in heel-toe running initiates vibrations of soft-tissue compartments of the leg that are heavily dampened by muscle activity. ….Relative to heel-strike, the maximum vibration intensity occurred significantly later in the fatigued condition. Thus, the protective mechanism of muscle tuning seems to be reduced in a fatigued muscle and the risk of potential harm to the tissue may increase. J Biomech. 2011 Jan 4;44(1):116-20. Epub 2010 Sep 16.Order this article from Elsevier Ltd   !!!!Tissue vibration in prolonged running. Friesenbichler B, Stirling LM, Federolf P, Nigg BM. Source Human Performance Laboratory, Faculty of Kinesiology, University of Calgary, 2500 University Dr NW, Calgary, Alberta, Canada. berndf@kin.ucalgary.ca

Tissue vibration in prolonged running.

Gait Gaff Time.

(Gaff: verb tr. (to stand or take the gaff) To receive severe criticism; to endure hardship.

The Foot Slap Gait Style:  

This is a funny little video that shows a few important points.

Remember, our purpose here is to help train your eyes to the important things.  We used to use slow/stop frame digital gait software programs to slow down the person to look for particular components of failure in the gait or running cycle. After many years of doing this, we found more and more that even before we could fire up the video camera and software that we had trained our eye to see these deficits.  This is because, there are multiple clues in every gait compensation.  There is head movement (which we will discuss in this case), there is arm swing (is it equal and symmetrical, topics we have posted research articles on in the last 48 hours on this blog), torso rotation, hip lateral sway in the frontal plane, violations of sagittal knee progression, and then the always difficult multiplanar foot and ankle motions as well as so many other parameters we consider.  So, when one component goes wrong, with enough experience and skill, one can make predictions as to what is wrong.  And, the more flaws (correlative compensations) that are noted, the higher the predictive value of the assumption.  Now, many will say to us that there is no way one can do this, and that is ok.  To each his/her own.  But, after decades of doing this, as with anything, a skill is developed and an art to doing it begins to take shape, as we will see here (without stop frame, without foot mapping devices etc).  One begins to form a mental algorithm to the process.  We always start with, “is the head silent in the vertical, frontal and sagital plane?”.  When a person’s gait is off, the head is almost never silent in space.  And arm swing also begins an assymetrical pendulum effect.  This could be called an energy conservation mode (as talked about in the article on the blog entitled, Dynamic Arm Swing in Human Walking, (http://www.ncbi.nlm.nih.gov/pubmed/19640879) where it was determined that normal arm swinging required minimal shoulder torque, while volitionally holding the arms still required 12% more metabolic energy. Among measures of gait mechanics, vertical ground reaction moment was most affected by arm swinging and increased by 63% without it.

  So, as  you do this more and more you will develop the skills of observation to improve the art form of assessing one’s gait.  But remember this KEY POINT *** what you see is mere information gathering, it is not always and frequently ever, the problem that you see.  You are seeing their compensation pattern around some neurologic, orthopedic or biomechanical problems…..things that are making a silent pristine gait impossible.  You MUST then, take this information and correlate it to your clinical findings in terms of neuro-orthopedic-biomechanical limitations during your exam.  Things like, joint range limitations, muscle weakness, instabilities and the like. So, you are trying to take what you see, and what you find, and develop a logical algorithm as to where their problem lies and one that tells a logical mechanical story as to the gait pattern you are seeing.  For example, a person comes to see you with a lurching forward of their body mass onto the right leg, abruptly skipping over the heel strike phase of gait on the right causing a slap of the right forefoot onto the ground.  One option of thought COULD be a deficit in the right tibialis anterior, that being eccentrically weak in that muscle thus delivering an abrupt right foot drop type gait.  But your examination on the table, your CLINICAL examination, shows a LEFT hallux limitus with dorsiflexion range shy of the key 45 degrees needed for normal toe off.  You then have a clinical epiphany that they are leaving the left foot quickly and prematurely because THEY HAVE NO OTHER CHOICE because it hurts to load that first MTP joint on the left.  You then go down, determine the joint is limited in range, it is painful, there is a pinch callus on the medial hallux and the extensor hallucis longus and brevis are weak.  Gait analysis is done. What you saw, was not the problem, it was their compensation.  Now, you have to try and fix the problem and the compensations…….and treatment begins.

OK, soap box aside………

lets build on that skill set we are trying to develop, the powers of observation and what they COULD mean.

THE SKUNK FU GAIT:

The first thing we see is, the Sagittal head bob.…..each step there is a propulsive head anterior oscillation and then dropping downwards at the end. This can mean there is an apropulsive problem in midstance such as loss of ankle rocker but that is not so in this case, the ankle rocker is great.  The head drop in this case coincides with successive heel strikes each time.  This in essence means that they are dropping from a height each time.  How can this be ? The little fella is on flat ground ! (more on this in a minute).  This could mean a lack of core maintenance in the late midstance phase of gait (heel rise-toe off) and subsequent movement onto the next heel strike.  This can come from overstriding, as in this case, but it can also come from an aggressive forward lean in a person’s gait style (like walking into a strong head wind).  In this case, we have a more reasonable ASSUMPTION, it comes back to the “falling from a height issue”. In this case, lack of adequate anterior compartment lower limb strength (tibialis anterior and the long and short toe extensors, EDL, EDB, EHL, EHB) allows PEPE to move from heel strike to foot flat in an uncontrolled and abrupt fashion.  When this occurs, pronation (even the normal amount of pronation) occurs fast.  And we know that when a person moves from supination to pronation there is a drop in height of the arch and thus a drop in the body (try this to prove the point, …..stand up straight, look in a mirror and begin raising up your toes and then dropping them.  If you do it right, each rise of the toes should raise the arch (The Windlass Effect), and each fall should drop the arch demonstrated in the mirror by a rise and fall of the head vertically.)  And so here you have the height differential in this case.  So, in a nutshell, PEPE is over-striding (as evidenced by his also aggressive arm swing), and falling hard from  heel strike abruptly into foot flat, a double whammy !  There is basically zero eccentric phase activity of the lower anterior compartment musculature and so the foot accelerated to the ground from its starting peak height at heel strike.  The poor fella probably has a raging anterior shin splint condition because of this but you would be hard to tell from the smile on the little stinkers face.  …………but remember, prove your facts on the table……who knows, maybe he has posterior column spinal cord disease, but an examination will have to be done to confirm your findings and suspicions.  In this case, we highly recommend an upwind exam table and plenty of air fresheners. 

we remain,…  The Gait Guys

Hip internal rotation

Q: why do The Gait Guys test for internal hip rotation loss with the client supine and leg straight ?
A: because this is as close as you can get to representing midstance phase of gait where they are converting from external rotation at rearfoot strike to moving through the pronatory phase where internal limb rotation is paramount. A loss on the table is a key exam finding ! it must be listened to.

* key……the leg is straight at zero degress of leg raise……ie. the leg is flush on the table. if you lift the leg…..you have effectively put them more in early midstance…..ideally you would love to drop them a bit further into hip extension to see if you can get the internal rotation with hip extension which would represent the approach to toe off.

Q: so what are the internal hip rotators you would check functionally then to find out who is inhibited (& could be related to loss of the range ?)
A: lower TVA, anterior G. Med, TFL, v. lateralis, rectus femoris, lateral hamstrings, coccygeal g. maximus, iliocostalis T/L paraspinals…….to start with. Find me one that is weak and i will show you one that might get them more internal hip rotation.

Arm Swing privides clues to gait pathology

Arm swing provides clues to gait pathology. We always talk about arm swing as a compensation mechanism. Here arm swing is used to increase hip extension in individuals that want to limit rotation of the lumbar spine.

 

http://www.ncbi.nlm.nih.gov/pubmed/21181483

get the article !

 

Eur Spine J. 2011 Mar;20(3):491-9. Epub 2010 Dec 24.

Gait adaptations in low back pain patients with lumbar disc herniation: trunk coordination and arm swing.

Huang YP, Bruijn SM, Lin JH, Meijer OG, Wu WH, Abbasi-Bafghi H, Lin XC, van Dieën JH.

Source

Department of Orthopaedics, First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 35005, People’s Republic of China.

Abstract

Patients with chronic non-specific low back pain (LBP) walk with more synchronous (in-phase) horizontal pelvis and thorax rotations than controls. Low thorax-pelvis relative phase in these patients appears to result from in-phase motion of the thorax with the legs, which was hypothesized to affect arm swing. In the present study, gait kinematics were compared between LBP patients with lumbar disc herniation and healthy controls during treadmill walking at different speeds and with different step lengths. Movements of legs, arms, and trunk were recorded. The patients walked with larger pelvis rotations than healthy controls, and with lower relative phase between pelvis and thorax horizontal rotations, specifically when taking large steps. They did so by rotating the thorax more in-phase with the pendular movements of the legs, thereby limiting the amplitudes of spine rotation. In the patients, arm swing was out-of phase with the leg, as in controls. Consequently, the phase relationship between thorax rotations and arm swing was altered in the patients.

Arm Swing Matters !

Arm swing matters! “The data thus suggest that the motor cortex makes an active contribution, through the corticospinal tract, to the ongoing EMG activity in arm muscles during walking.” Appropriate afferent feedback loops (from the joints in the upper and lower extremities) are necessary for the brain to run this motor engram; so if gait is altered, so are those feedback loops. You are witnessing a CORTICAL phenomenon! It’s about a lot more than pronation!

http://www.ncbi.nlm.nih.gov/pubmed/20123782

get the article !!!

J Physiol. 2010 Mar 15;588(Pt 6):967-79. Epub 2010 Feb 1.

Corticospinal contribution to arm muscle activity during human walking.

Barthelemy D, Nielsen JB.

Source

Department of Exercise and Sport Science, University of Copenhagen, Blegdamsvej 3, DK-2200 Copenhagen, Denmark.

Abstract

When we walk, our arm muscles show rhythmic activity suggesting that the central nervous system contributes to the swing of the arms. The purpose of the present study was to investigate whether corticospinal drive plays a role in the control of arm muscle activity during human walking. Motor evoked potentials (MEPs) elicited in the posterior deltoid muscle (PD) by transcranial magnetic stimulation (TMS) were modulated during the gait cycle in parallel with changes in the background EMG activity. There was no significant difference in the size of the MEPs at a comparable level of background EMG during walking and during static PD contraction. Short latency intracortical inhibition (SICI; 2 ms interval) studied by paired-pulse TMS was diminished during bursts of PD EMG activity. This could not be explained only by changes in background EMG activity and/or control MEP size, since SICI showed no correlation to the level of background EMG activity during static PD contraction. Finally, TMS at intensity below the threshold for activation of corticospinal tract fibres elicited a suppression of the PD EMG activity during walking. Since TMS at this intensity is likely to only activate intracortical inhibitory interneurones, the suppression is in all likelihood caused by removal of a corticospinal contribution to the ongoing EMG activity. The data thus suggest that the motor cortex makes an active contribution, through the corticospinal tract, to the ongoing EMG activity in arm muscles during walking.