Hip Biomechanics: Part 5 of 6

Sagittal Plane Functional Biomechanics

Thus far we have discussed the hip biomechanics mostly in the frontal plane.  The sagittal plane mechanics are much less complex since the axis of movement is in the frontal plane (the axis is directed horizontally through the femoral heads and pelvis) and the body weight for the most part rests on this same plane (unlike the frontal plane mechanics where the body weight is a moment arm away from the center of the hip rotation).  One of the main reasons the mechanics are a little less complicated for the most part is due to the fact that even with the pelvic obliquity that occurs during gait cycles of swing and stance, the body weight still remains largely over this trans-femoral head axis. 

In the sagittal plane the prime movers are the abdominas and gluteals (flexion and extension of the hip respectively) with some help from the ilopsoas for hip flexion perpetuation. The calf compartment is also  helpful as is arm swing.  The hip flexor synergistic muscles are the quadriceps and abdominals while the hip extensor synergist is mainly the hamstring group.  This is certainly simplified since transaxial rotation through a vertical oriented axis does occur as a coupled motion and thus we cannot talk about sagittal plane movements, or even frontal plane movements for that matter, without at least considering the effects of movement generation or stabilization by the hip intrinsics (gemelli, oburators, quadratus femoris, piriformis). 

The greatest body function in the sagittal plane is gait and many of the body’s compensations and conditions stem from alterations in hip joint function through this movement negotiation through the sagittal space.  For the therapist, clinician or trainer the greatest problem can be the body’s numerous back-up systems which compensate and share normal or abnormal loading.

The basis of gait evaluation needs to be based from a holistic perspective.  Gait cannot be evaluated without consideration of the entire organism. A minor functional limitation in the first metatarsophalangeal (MTP) joint can significantly impact hip, pelvic and spinal biomechanics.  The best and simplest example of this is the clinical scenario of hallux limitus.  We will entertain the equally devastating functional hallux limitus later on in the chapter but the point to note here is that a minor loss of the last few degrees of the normal MTP joint dorsiflexion (45-60 degrees is necessary, patient specific) can be devastating to sagittal plane motion of the body.  Even a loss of the last 5 degrees of this normal range, although appearing relatively normal on an examination and possibly without symptoms (ie. early stages of progression into a more noticable hallux limitus), can impact normal and efficient toe off.  If toe off is early, even to a small degree, then the stance phase will be abbreviated via early heel rise.  If heel rise is early this creates a functional change in the kinetic chain, both open chain and closed chain.  There are many closed chain changes that will occur. One such change might be toe off propulsion forces being imparted through a more flexed tibiofemoral joint (knee) which will impart both translatory shear forces in the sagittal plane and torsional forces through the joint, both causing potential maceration effects on the menisci.  However, perhaps the easiest functional changes to understand are the changes at the hip.  It is well known on EMG studies that hip flexion is both an active and passive motion during gait.  The active flexion of the hip is generated largely by iliopsoas concentric contraction.  However, this is not the first mechanism to generate hip flexion.  In fact, hip flexion is first generated passively through engagement of the kinetic chain.  The first movement of the swing phase is rotational or torsional activation of the oblique pelvis through core activiation of the abdominal muscle group.  Through activation of the internal and external abdominal obliques and transversus abdominus, in addition to activation of their synergists and cocontration of their antagonistic stabilizers, the obliqued pelvis is rotated.  Better said, the trailing leg’s lagging pelvis is moved forward by contract of the synergistic oblique activation.  This forward movement generates a sagittal momentum and movement of the toe off leg.  Once movement is generated then the iliopsoas activates concentrically to perpetuate hip flexion.  In other words, the ilopsoas is not an initiator of hip flexion, rather, a perpetuator.  When hallux limitus limits the stride length via early generation of heel rise the pelvic obliquity is limited.  As a result, the degree of initial swing phase leg movement is less from the generation of pelvis de-rotation via abdominal activation and more through ill-directed iliopsoas hip flexion.  Thus, as hip flexion still needs to occur, the iliopsoas is called upon to compensate; it now becomes a hip flexion initiator as well as its previous function of hip flexion perpetuator.  This demand is minimal but with repetitive demand thousands of steps per day, the iliopsoas eventually looses its ability to continue these compensations, as does its now over burdened synergists.  The result is either hypertrophy, inhibition, hypertonicity, spasm, shortening, insertional tendonitis, origin tendonitis or a combination thereof but make no mistake, such burden will eventually cause dysfunction within the muscle itself or within its synergists or antagonistic pair.  The scenario may result in either joint dysfunction at the lumbar spine near the muscle’s origin, at the sacroiliac joint over which it crosses, or at the hip joint proper.  The ensuing joint derangement or dysfunction is complex and creates numerous compensation patterns locally and globally since the main function of the muscle is to create hip flexion, external rotation, and abduction in the open kinetic chain and trunk flexion and trunk internal rotation in the closed kinetic chain. In a nutshell, the loss of dorsiflexion of the hallux, even to a minor degree, must be made up somewhere in the sagittal plane.  If it is not immediately made up for at the more proximal joints (1st metatarsal-midfoot joint, talo-navicular, ankle mortise-tibiotalar, or knee) the hip will undoubtedly change its function as described above to compensate, it is well suited to do so.  Keep in mind that such compensations may be better suited at the ankle, knee or hip depending on the degree of hip ante/retrotorsion or tibial internal/external torsion if present but none the less these compensations have consequences to changes in function of muscles either eccentrically, isometrically or concentrically or by recruiting assistance from synergists or antagonistic groups.  Additionally, a person with a very flexible midtarsal joint may stop the more proximal compensations via restoration of the necessary first ray (first toe) complex dorsiflexion at that more immediately proximal joint complex. 

Shawn and Ivo (yup, that is Dr. Allen thinking he is a bad ass in the picture above, clay pigeon shooting and a cubano……. thinks he is Clint Eastwood or something. Regardless, don’t mess with The Gait Guys !).