Corrective ExerciseMuscular Impairments

The Foot and Ankle: The Foundation of the Human Movement System

Understanding that the foot and ankle complex has the greatest contributing factor to the Human Movement System, any arthrokinomatic dysfunction or muscular imbalance, such as a decrease in control over the medial longitudinal arch, can result in an altered mechanical approach to the HMS leading to a possible cumulative injury cycle(Clark et al, 2011). The medial longitudinal arch is a “load-bearing and shock-absorbing structure of the foot,” as described by Neumann.  This arched configuration provides the bones the ability to receive and diminish the excessive loads that are placed on the body during impact situations, such as running and jumping.  During neutral stance on healthy feet, the connective tissue of the longitudinal arch is optimal to support the body weight without the integration of intrinsic and extrinsic muscles of the foot (Neumann, 2011).  When the longitudinal arch is not able to support the pressure of the body weight, this can result in “flat feet” or Pes Planus.   A person with pes planus, lacks the ability of the foot to dissipate loads, and requires intrinsic and extrinsic muscles of the foot to engage to help compensate for the lack of tension in the connective tissue.  Neumann states that even during standing that the client may develop fatigue and overuse symptoms, such as “shin splints,” bone spurs and plantar fasciitis.  Hyperpronation, as defined by Khamis et al(2006), is “the rear foot pronation that is excessive, prolonged, and as a result, causing the foot to remain in maximum pronation, too late or never resupinate in terminal stance for push off (Khamis et al, 2006)”.   The kinematic dysfunction of the foot will throw the tibia into internal rotation which puts the hip into internal rotation and a flexed position, causing genu valgum (knock knees) and increasing the Q-Angle of the hip joint.  This kinetic dysfunction places the hip into anterior pelvic tilt and lordosis of the spine. A lack of posterior glide to the talus commonly appears in subjects that experience an injury to the ankle joint such as a lateral ankle sprain.  The result of the injury is commonly a decreased posterior glide of the talus resulting in a limited range of dorsiflexion.   This limited range of motion in the HMS in regards to dorsiflexion creates a shortened muscle complex primarily the gastrocnemius and the soleus (Denegar, Fonseca, Hertel, 2002).  According to the Journal of Orthopaedic & Sports Physical Therapy, in addition to the lack of posterior glide on the talus, restricted motion at the tibiofibular, subtalar, or midtarsal joint, or any combination of the previous, could also limit ankle dorsiflexion.   The lengthened or weakened muscles that will be affected is the dorsiflexor of the anterior tibialis.  The weakened anterior tibialis muscle eccentrically decelerates plantar flexion at heel strike and decelerates pronation at forefoot (NASM Unit 3).  This excessive pronation of the subtalar joint will create a dysfunction in the HMS that could possible lead to pronation distortion syndrome and affecting the proper arthokinematics of the Lateral Subsystem (Clark and Lucett 2011).   Possible arthrokinomatic dysfunctions would be increased knee adduction, knee internal rotation that may lead to possible plantar fasciitis, patellar tendonitis, and posterior tibialis tendonitis (shin splints) (Clark and Lucett, 2011).     References:   Clark, Michael, and Scott Lucett. NASM Essentials of Corrective Exercise Training. Philadelphia, PA: Lippincott Williams & Wilkins, 2010. Pr Denegar, C., Hertel, J., & Fonseca, J. (2002). The effect of lateral ankle sprain on dorsiflexion range of motion, posterior talar glide, and joint laxity. Journal of Orthopaedic and Sports Physical Therapy, 32(4), 171. Clark, Michael and Scott Lucett, NASM Functional  Anatomy Presentation, Unit 3 Handout.  Print. Khamis, Sam and Yizhar, Ziva, Effect of feet hyperpronation on pelvic alignment in a standing position,  Gait and Motion Analysis Laboratory, Dana Children’s Hospital, Tel Aviv, Israel, September 14, 2005.  

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