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Whip it: Heel whip running gait analysis

Updated: Sep 8, 2019

“Heel Whip” and torsional forces in recreational runners

By Iris Saar, Masters of Exercise Science candidate, Concordia University of Chicago, April 2019



The research on the vast topic of running gait is ever evolving, as noted by the various perspectives to the analysis - be it physiological, biomechanics or demographic (for example, Eritrean runner show superior running economy over European runners in research[1]). In my recent observations on the subject, I reviewed the running gait cycle in the absence of a faulty biomechanical mechanism. As I advance my explorations, the review on potential alterations in running gait in the presence of pathologies is asked for as it is either the cause, or the result of altered ostheokinemtics and / or arthrokinemtics. It is particularly fascinating to observe the complex relationships between the kinematics and their effect on the musculoskeletal system. Sometimes, it can even be progressed into the research of myofascial tissues and how those are altering their functions due to pathological or impaired arthrokinematics (since fascial tissues might have contractile abilities). Dysfunctions in impact sports are expressed as responsive to external ground reaction forces that transmit from the foot (Talocrural joint) superiorly through the entire skeletal system. Two distinct physical forces are existent in this setting- ground reaction force (vertical) and torsional forces. Both are noted in their greatest magnitude during the stance phase, or the initial phase, of the running gait cycle (Figure 1: running gait cycle)



Figure 1: running gait cycle[2]

Ground reaction force can be described by Newton’s third law of “For every action there is an equal and opposite reaction.[3] In application to running, it is the production of force when the foot is hitting the ground and the transmission of into a vertical line of force (known in abbreviation as GRF)[4]. It also translated into a horizontal line of force which brings the thorax forward.

Torsional force can be described as two parallel forces act along an axis. Compression and tension both peak when maximal twisting occurs[5]. Torsion is beneficial to the runner as it contains and releases elastic energy due its rotational motion; however has its toll in the resistance required from the Talocrural joint to stabilize the foot and prevent it from pronating excessively, or “whipping” laterally or medially.

As the stance phase of the running gait displays the peak forces, it is where the torsional force can be measured. “Free moment[6] is a term associated with the peak torsion measured at this point and is anything but free; it is the magnitude of force produced in order to resist the toe-out motion, caused by the torsional friction (and the vertical ground force) acted upon the (tibia) bone. The purpose of this case study is to observe the constellation of torsion and lower extremity dysfunctions, specifically a dysfunction called “Heel whip” (HW)[7].

HW as described in this case study is observed as functional (that is, not caused by congenital or structural deformity) dysfunction. Such dysfunctions may lead to various injuries, more specifically to this case study are running related musculoskeletal injuries. The most prevalent ones are medial tibia stress syndrome, Achilles tendinopathy and plantar fasciitis, followed by patellofemoral syndrome[8]. If we could proactively identify (lower extremities) dysfunctions and relate those to potential consequent injuries, the often neglected pre-hab period in athletic training might become more apparent and assist in reducing the rate and magnitude of such injuries.

HW consists of an excessive eversion, relative lack of dorsiflexion and abduction (overall pronation) of the Talocrural and other joints of the shank and foot. It is not uncommon and tends to display more among females7. It can be assumed that under normal gait conditions the moment of dorsiflexion will be greater, comparing to an HW gait in which the moment might be reduced due to the longer line of force under normal gait. The “whip” termination describes the rapid motion of lateral or medial deviation of the talus from the midline in the transverse plane. Superiorly in the frontal plane, it is associated with to knee valgus[9] and has an average range (on both deviations) of approximately 6 degrees[10]. When occurs medially, it is also referred to as an “Adductory twist”, an excessive pronation created again due to lack of dorsiflexion at the Talocrural joint. It has been associated with increased risk for Tibial stress syndrome and can also be seen distally, at the mid tarsal joint which abducts to allow for greater range of motion[11].

HW may be described as a compensatory pattern[12] or as a dysfunction by its own merit. The literature is scarce on the topic and this might be a point for future study, along with other future applications (see later discussion).

Heel whip and how it presents during the running gait

The following video demonstrates the HW during running gait of a recreational runner and discusses six key positions along the lower extremities. Lateral and posterior views are available. Anterior filming was not accessible due to technical limitations; nevertheless the faulty biomechanics is shown at is outmost through posterior view.



The five key positions selected for this analysis are as follows, listed and discussed in a proximal-distal order:

A. Hip extension (Table 1): at the Coxal joint

B. Medial hip rotation (Table 2): at the Sacroiliac joint

C. Knee flexion (Table 3): at the Tibiofemoral joint

D. External Tibial torsion (Table 4): at the Tibiofemural and proximal Tibiofibular joints

E. “Heel whip” (Table 5): Abduction of the foot- Medial rotation of the heel and pronation (subtalar eversion and dorsiflexion) at the Talocrural, subtalar and Talocalcanealnavicular joints

A: Hip extension at the Coxal joint

The hip extension peaks during terminal stance into swing, creating propulsion. This contraction of the prime movers (Gluteus Maximus and Bicep femoris) as well as the synergists helps accelerate the runner by concentrically contracting. To cite Newton’s second law, “Force equals mass times acceleration”3, the more force the agonists produce, the faster and the runner can become or the higher the velocity will be. The optimal ROM for the purpose of acceleration, or sprinting in running, is still being studied. It may be assumed that a higher degree of hip extension is the result of a similar, precedential hip flexion during initial stance. It was found that a higher degree of hip flexion can assist in track & field races[13] as shown in Figure 3: Professional runner’s hip extension, in which the world record holder in the 10 seconds sprint displays an impressive hip extension stance in the pre-swing phase.

Figure 2: case study hip extension Figure 3: Professional runner’s hip extension[14]


Hip extension- Usain Bolt

B: Medial hip rotation at the Sacroiliac joint

Medial rotation of the hip differs between the genders[15] as females tend to show greater rotation. Apparent during terminal swing into stance, the hip medially rotates to allow for the later hip flexion and to allow the lengthening of the stride which contributes to velocity. Apart from being a functional part of the running gait, excessive medial rotation has been linked to Patellofemoral pain[16] and is related in part of relative weakness or under-activity of the abductors[17]. Since the Gluteus medius is responsible for both medial and lateral hip rotation, it might become short and over active (see later discussion: Corrective Exercises). The literature mentions two major factors to affect medial rotation- one as the angle between the neck of the femur and the acetabulum and the second as asymmetry in the Sacroiliac joint[18] (SI). The dysfunction analyzed in this case study is distal and inferior to the SI joint, which might become a substantial, if not exclusive, in the Tibial torsion of the runner. The SI asymmetry shown in Figure 4: hip hike and medial hip rotation may be described as a “hip hike” (elevation) or opposing “hip drop” (depression) from PSIS to PSIS. This refers inferiorly to the Tibiofemoral joint, contributing to the external rotation of the Tibia which becomes even greater to the ground reaction forces.

Figure 4: hip hike and medial hip rotation


Hip hike

C: Knee flexion at the Tibiofemoral joint

Knee flexion takes place at the 60% mark of the gait cycle, or during mid-swing and is greater among elite runners as mentioned earlier (and perhaps help increase propulsion). The angle of the flexion will determine the placement of the foot relative to the center of mass. Excessive flexion can position the foot further away (“over-striding”) or limit the propulsion if the flexion is not adequate. Greater knee flexion reduces the energy requirements during swing (by reducing knee flexion during swing), therefore considered more economical in the overall running economy[19]. The runner in this case study presented an average ROM of 57⁰ at knee flexion (Figure 5: knee flexion ROM ).

Figure 5: knee flexion ROM


Knee flexion

D: External Tibial torsion at the Tibiofemoral and proximal Tibiofibular joints

The tibia is located medially to the Fibula however has a substantial degree of rotating laterally; under rotary forces, it can range in 25⁰ [20]. As explained earlier, torsional force shifts the tibia along its (longitudinal) axis. It appears as the rate of lateral (external) torsion increases with age, as with gender (females show more lateral torsion than males, especially in the tibiofibular articulation)[21]. Another interesting distinguishing factor has been found to be ethnic; Japanese people who sit in a cross-legged position have shown more medial rotation of the tibia, relatively to a Caucasian control group[22]. From the musculoskeletal perspective, it is interesting to note that the Bicep femoris is the only agonist. Perhaps due to its lateral location relative to the other hamstrings muscles it pulls the tibia externally. Early childhood pathologies such as Osgood Schlatter disease have been shown to increase the angle of torsion, even later in life[23]. Other than synergistic muscles (among them, the Tensor fascia latae) assisting during the pre-activity of knee flexion, the Bicep femoris operates alone in laterally rotating the Tibia and is therefore considered over-active, according to the (see later discussion) predictive model of lower extremity dysfunctions, developed by Dr. Brent Brookbush[24]. Initial contact rotates the tibia at the highest rate and short muscles in the ITB region can contribute to an even higher rate, as seen in a study where runners with ITB syndrome presented more external rotations of the Tibia, comparing to a control group[25]. See Figure 6: comparison of left and right limbs Tibial torsion during initial swing for a case-study image of Tibial torsion in an external rotation, measured at approximately 45⁰ and compared to the other (right) limb measured at 23⁰.

Figure 6: comparison of left and right limbs Tibial torsion during initial swing





Posterior view: Left and right limbs Tibial torsion

E: “Heel whip”- Abduction of the foot: Medial rotation of the heel and pronation (subtalar eversion and dorsiflexion) at the Talocrural, subtalar and Talocalcanealnavicular joints

HW is the main point of interest in this case study and lower extremity dysfunction analyzed. It can be seen as a consequential motion or compensatory pattern of asymmetrical (and unstable) sacroiliac joint movement, an inadequate angel of knee flexion and hip extension and a relatively high rate of Tibial torsion. More distally, there is a combination of Talcrural joint movements consisting the overall abduction of the foot: the Calcaneus which medially rotates the eversion of the foot both in the subtalar and Talocalcanealnavicular joints and dorsiflexion in the later phase of the HW. In this aspect, I am aligning with the “top down” approach towards such dysfunctions, assuming the source is more proximal. However, I will identify some muscles known to be agonist for eversion as short and over active as this dysfunction is more integrative than isolated in type, in my opinion. Surprisingly, the literature is scarce in studying HW during running in spite of the dysfunction apparent in many recreational and competitive runners. Perhaps since it is considered a “normal” movement however the extent, as shown in this case study, varies and can be predictive (or subsequent) to repetitive overuse injuries. The range of the motion is shown in Figure 7: Heel Whip and compared to the right limb.

Figure 7: Heel Whip


Heel whip

Posterior view: Left and right limbs heel whip

Kinematic mechanism

In order to discuss the altered mechanism that materializes the HW it is important to acknowledge the “top down” and the “bottom up” approaches seen in the literature. That is, the hips can be viewed to dictate the kinematics of the feet, however it is not clear if this mechanism works in its entirety or weather the feet have some independency in lower extremity dysfunctions. The latter relates to the “bottom up” perspective. The analysis of the dysfunction in this case study is based on the works of Dr. Brent Brookbush, specifically the predictive model of lower extremity movement impairment24 and therefor will identify the muscles involved in this dysfunction based on their tonic / phasic state. Before laying out a chart of the muscles involved, the kinematic mechanism of the dysfunction will be discussed as follows: Heel whip occurs at the transition from stance phase to swing phase. Various evidence exist regarding the root cause of HW, and it might be related to forces developed during stance phase and the excessive movement that is occurring due to the recoiled, or elastic stored energy in both the muscles and the myofascial sheets. Weakness in the Talocrural region may not provide the Tibia with enough support to resist the said ground reaction force and laterally rotate the shank. The torsional force rotating the Tibia and consequently the foot has been shown to relate to the magnitude of friction the foot has with the ground during the “Free moment” (see synopsis). The higher the friction, the more ground reaction force produced and therefor the cost of energy to resist this force is increased[26]. If the limb, in general, is not strong enough to (resist) stabilize, either uni or bilaterally, HW occurs together with Tibia torsion.

The role of dorsiflexion in the Tibial torsion is important, since relative lack of (normal ROM of dorsiflexion in healthy adults is approximately 34.7⁰, weight bearing[27]) constricts the Tibia from moving forward and maintain stride length. This can be explained by too short and over active calves which limit dorsiflexion in their inability to reach optimal ROM. Pronation, which has been explained as the combination of foot eversion, abduction and lack of dorsiflexion, is an additional expression of the HW. Interestingly, the runner in this case study does not show excessive pronation with the HW, which brings up the question of the autonomy of foot in determining movement deviations (since pronation isn’t necessarily linked to the dysfunction). HW might also be influenced by the angle between the Tibial tuberosity and the Patella or the Q angle; an increased Q angle in four cadavers was linked to higher lateral forces[28], which might suggest that the Tibia laterally rotates also due to the structural setting of the ASIS, patella and Tibial tuberosity. Excessive external rotation of the knee (over 60⁰) has also been linked to HW and in my perspective it is part of the kinetic chain reaction following the Sacroiliac asymmetry during the runner’s impaired gait. This may be linked to knee valgus, due to an internally rotated femur (and again, changes in Q angle).

Corrective exercises

HW may be controlled by cautious selection of corrective exercises. The Brookbush model of lower extremity movement impairment24 suggests the methodic identification of relevant joint actions and the tonic / phasic state of the respective muscles crossing those joints. It is worth mentioning that HW, among other dysfunctions, can be seen prior to impact sports through the overhead squat assessment[29]

*Vastus medialis obliques has altered function do to its role as knee stabilizer.

The main muscles shown to be over active are the lateral Gastrocnemius, which is a multi-joint muscle as it crosses both the knee and ankle and is a strong external rotator of the Tibia. The short head of the Bicep femoris, with its insertion on the Fibula, is another external rotator since it inserts inferiorly to the knee. The Tensor fascia lata (TFL), as its name suggest, tenses the lateral thigh through the ITB as a connecting medium and when over active, can increase the external rotation. Among the underactive muscles are the Gluteus maximus is underactive as it posteriorly rotates the opposing side of the medially rotated and elevated SI joint. The Tibialis anterior is responsible for both inversion and dorsiflexion, which when limited can increase the Tibial external torsion.

Corrective exercises application emphasizes the need for toning down the overactive muscles prior to lengthening. Self-administered release is appropriate and can be advanced into active release/ lengthening to follow by static release (i.e. stretching the muscles for adequate time, between 30-120 seconds). Static release also can also be progressed into active and dynamic stretch.

The long and underactive muscles can lead to dominance of synergists and need to be activated. This can be done through “Isolated activation”, which minimizes the recruitment of synergists (and is a topic of research by itself) and focuses on a single-joint movement[30]. Activated exercises may be loaded or resistive, and progressed later into integrated exercises which involve multi-joints movements.

The following videos demonstrate two corrective exercises for the HW dysfunction.

Video links for corrective exercises

1. Video 1: self-administrated static release of the TFL



2. Video 2: isolated activation of the Gluteus maximus



Conclusions and future applications

The magnitude in which the contractile state of the skeletal muscles effect the joint action is significant, as noted by the HW dysfunction analyzed in this article. Prime movers can be classified as short and over active, or long and under active and reach a degree of hypertonic or phasic state. The predictive model and references of related research relay on the perspective that it is the musculature which constraints or enables the kinematics. However an osteokinematic analysis might see this as secondary to congenital or early-life deformities. In this case, a different set of assumptions should be used to diagnose, treat and potentially prevent the altered mechanism. In addition, researching the fascial connections and their contribution to movement impairment can potential add a level of understanding and corrective exercises design (one question is whether reduced Elastin in the fascial tissues inhibits movement?).

Through the perspective of corrective exercises, HW might seem to be modifiable in favor of a more economical running gait or optimal gait in ADL. However, gait retraining has not been proved efficient when such dysfunctions are structural or neurologically impaired. Modifying such gait will require changes in brain stimulation or in some cases, surgical intervention. HW seems to also be progressive with age and a contributor to conditions such as osteoarthritis and Patellofemoral maltracking and pain. As a runner who demonstrates the dysfunction, I have been searching for a narrow cause for quite a while. Various thesis and articles do bring up HW as a topic of research; however I was not successful in finding a narrow and decisive definition of the dysfunction. Circling back to the SI joint, I tend to believe it is the regional area of the kinetic chain impairment which may establish the HW, be it structural, muscular or both. Identifying HW at a younger age through easy to implement assessment such as the overhead squat, might assist in designing gait retraining protocols to reduce the risk for long term and progressive injuries and pathologies such as osteoarthritis, and might benefit runners who wish to engage in the sport for a longer term.



References

[1] Santos-Concejero, J., Oliván, J., Maté-Muñoz, J. L., Muniesa, C., Montil, M., Tucker, R., & Lucia, A. (2015). Gait-cycle characteristics and running economy in elite Eritrean and European runners. International journal of sports physiology and performance, 10(3), 381-387.


[2] Dugan, S. A., & Bhat, K. P. (2005). Biomechanics and analysis of running gait. Physical Medicine and Rehabilitation Clinics, 16(3), 603-621.


[3] Tait, Peter Guthrie. (1899) Newton's laws of motionLondon, A. & C. Black,


[4] Illustrated Dictionary of Podiatry and Foot Science by Jean Mooney © 2009 Elsevier Limited


[5] Jensen, G. M. (1980). Biomechanics of the lumbar intervertebral disk: a review. Physical therapy, 60(6), 765-773.


[6] Ferber, R., & Macdonald, S. L. (2018). Running mechanics and gait analysis. Human Kinetics.


[7] Souza, R. B., Hatamiya, N., Martin, C., Aramaki, A., Martinelli, B., Wong, J., & Luke, A. (2015). Medial and lateral heel whips: prevalence and characteristics in recreational runners. PM&R, 7(8), 823-830.


[8] Lopes, A. D., Hespanhol, L. C., Yeung, S. S., & Costa, L. O. P. (2012). What are the main running-related musculoskeletal injuries?. Sports medicine, 42(10), 891-905.


[9] Ahmad, O. F., Ghosh, P., Stanley, C., Karp, B., Hallett, M., Lungu, C., & Alter, K. (2018). Electromyographic and Joint Kinematic Patterns in Runner’s Dystonia.


[10] Krackow, K. (2008). The measurement and analysis of axial deformity at the knee. Home Stryker Center, unit 1.


[11] Tweed, J. L., Campbell, J. A., & Avil, S. J. (2008). Biomechanical risk factors in the development of medial tibial stress syndrome in distance runners. Journal of the American Podiatric Medical Association, 98(6), 436-444.


[12] Singh, A. K. (2012). Bionic Feet. Int. J. of Computer & Organization Trends, 12, 216-242.


[13] Hewlett, B. K. (2013). Relationships between hip range of motion, sprint kinematics and kinetics in track and field athletes (Doctoral dissertation, Auckland University of Technology).


[14] Image access: https://www.hpi-ibji.com/blog/2016/3/7/stop-jumping-to-outrageously-high-boxes-seriously-stop-it


[15] Ferber, R., Davis, I. M., & Williams Iii, D. S. (2003). Gender differences in lower extremity mechanics during running. Clinical biomechanics, 18(4), 350-357.


[16] Souza RB, Powers CM. Predictors of hip internal rotation during running: an evaluation of hip strength and femoral structure in women with and without patellofemoral pain. Am J Sports Med. 2009;37(3):579-87.


[17] Fredericson, M., Cookingham, C. L., Chaudhari, A. M., Dowdell, B. C., Oestreicher, N., & Sahrmann, S. A. (2000). Hip abductor weakness in distance runners with iliotibial band syndrome. Clinical Journal of Sport Medicine, 10(3), 169-175.


[18] Cibulka, M. T., Sinacore, D. R., Cromer, G. S., & Delitto, A. (1998). Unilateral hip rotation range of motion asymmetry in patients with sacroiliac joint regional pain. Spine, 23(9), 1009-1015.


[19] Clermont, C. A., Osis, S. T., Angkoon Phinyomark, & Ferber, R. (2017). Kinematic Gait Patterns in Competitive and Recreational Runners. Journal of Applied Biomechanics, 33(4), 1–9.


[20] Zarins, B., Rowe, C. R., Harris, B. A., & Watkins, M. P. (1983). Rotational motion of the knee. The American journal of sports medicine, 11(3), 152-156.


[21] Mullaji, A. B., Sharma, A. K., Marawar, S. V., & Kohli, A. F. (2008). Tibial torsion in non-arthritic Indian adults: A computer tomography study of 100 limbs. Indian Journal of Orthopaedics, 42(3), 309–313.


[22] Nagamine R, Miyanishi K, Miura H, Urabe K, Matsuda S, Iwamoto Y. Medial torsion of the tibia in Japanese patients with osteoarthritis of the knee. Clin Orthop Relat Res 2003;408:218-24


[23] Gigante, A., Bevilacqua, C., Bonetti, M. G., & Greco, F. (2003). Increased external tibial torsion in Osgood-Schlatter disease. Acta Orthopaedica Scandinavica, 74(4), 431


[24] Brookbush, B. (2015). Predictive Model of Lower Extremity Movement Impairment. URL: https://brentbrookbush.com/articles/postural-dysfunction-movement-impairment/lower-leg-dysfunction/. Last access date: April 30th, 2019.


[25] Noehren B, Davis I, Hamill J. ASB clinical biomechanics award winner 2006 prospective study of the biomechanical factors associated with iliotibial band syndrome. Clin Biomech (Bristol, Avon). 2007;22(9):951–956.


[26] Holden, J. P., & Cavanagh, P. R. (1991). The free moment of ground reaction in distance running and its changes with pronation. Journal of biomechanics, 24(10), 887-897.


[27] Baggett, B. D., & Young, G. (1993). Ankle joint dorsiflexion. Establishment of a normal range. Journal of the American Podiatric Medical Association, 83(5), 251-254.


[28] Gross, K. D. (2006). The relationship of foot alignment to hip and knee conditions (Order No. 3215011). Available from ProQuest Dissertations & Theses Global.


[29] Hirth, C. J. (2007). Clinical movement analysis to identify muscle imbalances and guide exercise. Athletic Therapy Today, 12(4), 10-14.


[30] Brookbush, B. Introduction to activation exercises. URL: https://brentbrookbush.com/articles/corrective-exercise-articles/activation/introduction-to-activation-exercise/, last access date: May 1st, 2019.

“Heel Whip” and torsional forces in recreational runners

By Iris Saar, Masters in Exercise Science candidate, Concordia university of Chicago

April 2019

The research on the vast topic of running gait is ever evolving, as noted by the various perspectives to the analysis - be it physiological, biomechanics or demographic (for example, Eritrean runner show superior running economy over European runners in research[1]). In my recent observations on the subject, I reviewed the running gait cycle in the absence of a faulty biomechanical mechanism. As I advance my explorations, the review on potential alterations in running gait in the presence of pathologies is asked for as it is either the cause, or the result of altered ostheokinemtics and / or arthrokinemtics. It is particularly fascinating to observe the complex relationships between the kinematics and their effect on the musculoskeletal system. Sometimes, it can even be progressed into the research of myofascial tissues and how those are altering their functions due to pathological or impaired arthrokinematics (since fascial tissues might have contractile abilities). Dysfunctions in impact sports are expressed as responsive to external ground reaction forces that transmit from the foot (Talocrural joint) superiorly through the entire skeletal system. Two distinct physical forces are existent in this setting- ground reaction force (vertical) and torsional forces. Both are noted in their greatest magnitude during the stance phase, or the initial phase, of the running gait cycle (Figure 1: running gait cycle)

Figure 1: running gait cycle[2]

Ground reaction force can be described by Newton’s third law of “For every action there is an equal and opposite reaction.[3] In application to running, it is the production of force when the foot is hitting the ground and the transmission of into a vertical line of force (known in abbreviation as GRF)[4]. It also translated into a horizontal line of force which brings the thorax forward.

Torsional force can be described as two parallel forces act along an axis. Compression and tension both peak when maximal twisting occurs[5]. Torsion is beneficial to the runner as it contains and releases elastic energy due its rotational motion; however has its toll in the resistance required from the Talocrural joint to stabilize the foot and prevent it from pronating excessively, or “whipping” laterally or medially.

As the stance phase of the running gait displays the peak forces, it is where the torsional force can be measured. “Free moment[6] is a term associated with the peak torsion measured at this point and is anything but free; it is the magnitude of force produced in order to resist the toe-out motion, caused by the torsional friction (and the vertical ground force) acted upon the (tibia) bone. The purpose of this case study is to observe the constellation of torsion and lower extremity dysfunctions, specifically a dysfunction called “Heel whip” (HW)[7].

HW as described in this case study is observed as functional (that is, not caused by congenital or structural deformity) dysfunction. Such dysfunctions may lead to various injuries, more specifically to this case study are running related musculoskeletal injuries. The most prevalent ones are medial tibia stress syndrome, Achilles tendinopathy and plantar fasciitis, followed by patellofemoral syndrome[8]. If we could proactively identify (lower extremities) dysfunctions and relate those to potential consequent injuries, the often neglected pre-hab period in athletic training might become more apparent and assist in reducing the rate and magnitude of such injuries.

HW consists of an excessive eversion, relative lack of dorsiflexion and abduction (overall pronation) of the Talocrural and other joints of the shank and foot. It is not uncommon and tends to display more among females7. It can be assumed that under normal gait conditions the moment of dorsiflexion will be greater, comparing to an HW gait in which the moment might be reduced due to the longer line of force under normal gait. The “whip” termination describes the rapid motion of lateral or medial deviation of the talus from the midline in the transverse plane. Superiorly in the frontal plane, it is associated with to knee valgus[9] and has an average range (on both deviations) of approximately 6 degrees[10]. When occurs medially, it is also referred to as an “Adductory twist”, an excessive pronation created again due to lack of dorsiflexion at the Talocrural joint. It has been associated with increased risk for Tibial stress syndrome and can also be seen distally, at the mid tarsal joint which abducts to allow for greater range of motion[11].

HW may be described as a compensatory pattern[12] or as a dysfunction by its own merit. The literature is scarce on the topic and this might be a point for future study, along with other future applications (see later discussion).

Heel whip and how it presents during the running gait

The following video demonstrates the HW during running gait of a recreational runner and discusses six key positions along the lower extremities. Lateral and posterior views are available. Anterior filming was not accessible due to technical limitations; nevertheless the faulty biomechanics is shown at is outmost through posterior view.

Hyperlink 1: Heel whip running gait video link

The five key positions selected for this analysis are as follows, listed and discussed in a proximal-distal order:

A. Hip extension (Table 1): at the Coxal joint

B. Medial hip rotation (Table 2): at the Sacroiliac joint

C. Knee flexion (Table 3): at the Tibiofemoral joint

D. External Tibial torsion (Table 4): at the Tibiofemural and proximal Tibiofibular joints

E. “Heel whip” (Table 5): Abduction of the foot- Medial rotation of the heel and pronation (subtalar eversion and dorsiflexion) at the Talocrural, subtalar and Talocalcanealnavicular joints

Table 1: Hip extension at the Coxal joint

The hip extension peaks during terminal stance into swing, creating propulsion. This contraction of the prime movers (Gluteus Maximus and Bicep femoris) as well as the synergists helps accelerate the runner by concentrically contracting. To cite Newton’s second law, “Force equals mass times acceleration”3, the more force the agonists produce, the faster and the runner can become or the higher the velocity will be. The optimal ROM for the purpose of acceleration, or sprinting in running, is still being studied. It may be assumed that a higher degree of hip extension is the result of a similar, precedential hip flexion during initial stance. It was found that a higher degree of hip flexion can assist in track & field races[13] as shown in Figure 3: Professional runner’s hip extension, in which the world record holder in the 10 seconds sprint displays an impressive hip extension stance in the pre-swing phase.

Figure 2: case study hip extension Figure 3: Professional runner’s hip extension[14]

Table 2: Medial hip rotation at the Sacroiliac joint

Medial rotation of the hip differs between the genders[15] as females tend to show greater rotation. Apparent during terminal swing into stance, the hip medially rotates to allow for the later hip flexion and to allow the lengthening of the stride which contributes to velocity. Apart from being a functional part of the running gait, excessive medial rotation has been linked to Patellofemoral pain[16] and is related in part of relative weakness or under-activity of the abductors[17]. Since the Gluteus medius is responsible for both medial and lateral hip rotation, it might become short and over active (see later discussion: Corrective Exercises). The literature mentions two major factors to affect medial rotation- one as the angle between the neck of the femur and the acetabulum and the second as asymmetry in the Sacroiliac joint[18] (SI). The dysfunction analyzed in this case study is distal and inferior to the SI joint, which might become a substantial, if not exclusive, in the Tibial torsion of the runner. The SI asymmetry shown in Figure 4: hip hike and medial hip rotation may be described as a “hip hike” (elevation) or opposing “hip drop” (depression) from PSIS to PSIS. This refers inferiorly to the Tibiofemoral joint, contributing to the external rotation of the Tibia which becomes even greater to the ground reaction forces.

Figure 4: hip hike and medial hip rotation

Table 3: Knee flexion at the Tibiofemoral joint

Knee flexion takes place at the 60% mark of the gait cycle, or during mid-swing and is greater among elite runners as mentioned earlier (and perhaps help increase propulsion). The angle of the flexion will determine the placement of the foot relative to the center of mass. Excessive flexion can position the foot further away (“over-striding”) or limit the propulsion if the flexion is not adequate. Greater knee flexion reduces the energy requirements during swing (by reducing knee flexion during swing), therefore considered more economical in the overall running economy[19]. The runner in this case study presented an average ROM of 57⁰ at knee flexion (Figure 5: knee flexion ROM ).

Figure 5: knee flexion ROM

Table 4: External Tibial torsion at the Tibiofemoral and proximal Tibiofibular joints

The tibia is located medially to the Fibula however has a substantial degree of rotating laterally; under rotary forces, it can range in 25⁰ [20]. As explained earlier, torsional force shifts the tibia along its (longitudinal) axis. It appears as the rate of lateral (external) torsion increases with age, as with gender (females show more lateral torsion than males, especially in the tibiofibular articulation)[21]. Another interesting distinguishing factor has been found to be ethnic; Japanese people who sit in a cross-legged position have shown more medial rotation of the tibia, relatively to a Caucasian control group[22]. From the musculoskeletal perspective, it is interesting to note that the Bicep femoris is the only agonist. Perhaps due to its lateral location relative to the other hamstrings muscles it pulls the tibia externally. Early childhood pathologies such as Osgood Schlatter disease have been shown to increase the angle of torsion, even later in life[23]. Other than synergistic muscles (among them, the Tensor fascia latae) assisting during the pre-activity of knee flexion, the Bicep femoris operates alone in laterally rotating the Tibia and is therefore considered over-active, according to the (see later discussion) predictive model of lower extremity dysfunctions, developed by Dr. Brent Brookbush[24]. Initial contact rotates the tibia at the highest rate and short muscles in the ITB region can contribute to an even higher rate, as seen in a study where runners with ITB syndrome presented more external rotations of the Tibia, comparing to a control group[25]. See Figure 6: comparison of left and right limbs Tibial torsion during initial swing for a case-study image of Tibial torsion in an external rotation, measured at approximately 45⁰ and compared to the other (right) limb measured at 23⁰.

Figure 6: comparison of left and right limbs Tibial torsion during initial swing

Posterior view: Left and right limbs Tibial torsion

Table 5: “Heel whip”- Abduction of the foot: Medial rotation of the heel and pronation (subtalar eversion and dorsiflexion) at the Talocrural, subtalar and Talocalcanealnavicular joints

HW is the main point of interest in this case study and lower extremity dysfunction analyzed. It can be seen as a consequential motion or compensatory pattern of asymmetrical (and unstable) sacroiliac joint movement, an inadequate angel of knee flexion and hip extension and a relatively high rate of Tibial torsion. More distally, there is a combination of Talcrural joint movements consisting the overall abduction of the foot: the Calcaneus which medially rotates the eversion of the foot both in the subtalar and Talocalcanealnavicular joints and dorsiflexion in the later phase of the HW. In this aspect, I am aligning with the “top down” approach towards such dysfunctions, assuming the source is more proximal. However, I will identify some muscles known to be agonist for eversion as short and over active as this dysfunction is more integrative than isolated in type, in my opinion. Surprisingly, the literature is scarce in studying HW during running in spite of the dysfunction apparent in many recreational and competitive runners. Perhaps since it is considered a “normal” movement however the extent, as shown in this case study, varies and can be predictive (or subsequent) to repetitive overuse injuries. The range of the motion is shown in Figure 7: Heel Whip and compared to the right limb.

Figure 7: Heel Whip

Posterior view: Left and right limbs heel whip

Kinematic mechanism

In order to discuss the altered mechanism that materializes the HW it is important to acknowledge the “top down” and the “bottom up” approaches seen in the literature. That is, the hips can be viewed to dictate the kinematics of the feet, however it is not clear if this mechanism works in its entirety or weather the feet have some independency in lower extremity dysfunctions. The latter relates to the “bottom up” perspective. The analysis of the dysfunction in this case study is based on the works of Dr. Brent Brookbush, specifically the predictive model of lower extremity movement impairment24 and therefor will identify the muscles involved in this dysfunction based on their tonic / phasic state. Before laying out a chart of the muscles involved, the kinematic mechanism of the dysfunction will be discussed as follows: Heel whip occurs at the transition from stance phase to swing phase. Various evidence exist regarding the root cause of HW, and it might be related to forces developed during stance phase and the excessive movement that is occurring due to the recoiled, or elastic stored energy in both the muscles and the myofascial sheets. Weakness in the Talocrural region may not provide the Tibia with enough support to resist the said ground reaction force and laterally rotate the shank. The torsional force rotating the Tibia and consequently the foot has been shown to relate to the magnitude of friction the foot has with the ground during the “Free moment” (see synopsis). The higher the friction, the more ground reaction force produced and therefor the cost of energy to resist this force is increased[26]. If the limb, in general, is not strong enough to (resist) stabilize, either uni or bilaterally, HW occurs together with Tibia torsion.

The role of dorsiflexion in the Tibial torsion is important, since relative lack of (normal ROM of dorsiflexion in healthy adults is approximately 34.7⁰, weight bearing[27]) constricts the Tibia from moving forward and maintain stride length. This can be explained by too short and over active calves which limit dorsiflexion in their inability to reach optimal ROM. Pronation, which has been explained as the combination of foot eversion, abduction and lack of dorsiflexion, is an additional expression of the HW. Interestingly, the runner in this case study does not show excessive pronation with the HW, which brings up the question of the autonomy of foot in determining movement deviations (since pronation isn’t necessarily linked to the dysfunction). HW might also be influenced by the angle between the Tibial tuberosity and the Patella or the Q angle; an increased Q angle in four cadavers was linked to higher lateral forces[28], which might suggest that the Tibia laterally rotates also due to the structural setting of the ASIS, patella and Tibial tuberosity. Excessive external rotation of the knee (over 60⁰) has also been linked to HW and in my perspective it is part of the kinetic chain reaction following the Sacroiliac asymmetry during the runner’s impaired gait. This may be linked to knee valgus, due to an internally rotated femur (and again, changes in Q angle).

Corrective exercises

HW may be controlled by cautious selection of corrective exercises. The Brookbush model of lower extremity movement impairment24 suggests the methodic identification of relevant joint actions and the tonic / phasic state of the respective muscles crossing those joints. It is worth mentioning that HW, among other dysfunctions, can be seen prior to impact sports through the overhead squat assessment[29]

*Vastus medialis obliques has altered function do to its role as knee stabilizer.

The main muscles shown to be over active are the lateral Gastrocnemius, which is a multi-joint muscle as it crosses both the knee and ankle and is a strong external rotator of the Tibia. The short head of the Bicep femoris, with its insertion on the Fibula, is another external rotator since it inserts inferiorly to the knee. The Tensor fascia lata (TFL), as its name suggest, tenses the lateral thigh through the ITB as a connecting medium and when over active, can increase the external rotation. Among the underactive muscles are the Gluteus maximus is underactive as it posteriorly rotates the opposing side of the medially rotated and elevated SI joint. The Tibialis anterior is responsible for both inversion and dorsiflexion, which when limited can increase the Tibial external torsion.

Corrective exercises application emphasizes the need for toning down the overactive muscles prior to lengthening. Self-administered release is appropriate and can be advanced into active release/ lengthening to follow by static release (i.e. stretching the muscles for adequate time, between 30-120 seconds). Static release also can also be progressed into active and dynamic stretch.

The long and underactive muscles can lead to dominance of synergists and need to be activated. This can be done through “Isolated activation”, which minimizes the recruitment of synergists (and is a topic of research by itself) and focuses on a single-joint movement[30]. Activated exercises may be loaded or resistive, and progressed later into integrated exercises which involve multi-joints movements.

The following videos demonstrate two corrective exercises for the HW dysfunction.

Video links for corrective exercises

1. Video 1: self-administrated static release of the TFL Static release of TFL video

2. Video 2: isolated activation of the Gluteus maximus activation of the Gluteus maximus video

Conclusions and future applications

The magnitude in which the contractile state of the skeletal muscles effect the joint action is significant, as noted by the HW dysfunction analyzed in this article. Prime movers can be classified as short and over active, or long and under active and reach a degree of hypertonic or phasic state. The predictive model and references of related research relay on the perspective that it is the musculature which constraints or enables the kinematics. However an osteokinematic analysis might see this as secondary to congenital or early-life deformities. In this case, a different set of assumptions should be used to diagnose, treat and potentially prevent the altered mechanism. In addition, researching the fascial connections and their contribution to movement impairment can potential add a level of understanding and corrective exercises design (one question is whether reduced Elastin in the fascial tissues inhibits movement?).

Through the perspective of corrective exercises, HW might seem to be modifiable in favor of a more economical running gait or optimal gait in ADL. However, gait retraining has not been proved efficient when such dysfunctions are structural or neurologically impaired. Modifying such gait will require changes in brain stimulation or in some cases, surgical intervention. HW seems to also be progressive with age and a contributor to conditions such as osteoarthritis and Patellofemoral maltracking and pain. As a runner who demonstrates the dysfunction, I have been searching for a narrow cause for quite a while. Various thesis and articles do bring up HW as a topic of research; however I was not successful in finding a narrow and decisive definition of the dysfunction. Circling back to the SI joint, I tend to believe it is the regional area of the kinetic chain impairment which may establish the HW, be it structural, muscular or both. Identifying HW at a younger age through easy to implement assessment such as the overhead squat, might assist in designing gait retraining protocols to reduce the risk for long term and progressive injuries and pathologies such as osteoarthritis, and might benefit runners who wish to engage in the sport for a longer term.

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