Posted by Steve Middleton, MS, ATC, CSCS, CES, CKTP

The human body was designed for mobility, especially the musculoskeletal and myofascial systems. Yet, movement can often be a primary pain generator.

When normal movement occurs, reciprocal inhibition takes place to allow the muscles around a joint to act as a see-saw or pulley to move the bones. As the agonist of the movement shortens through concentric contraction, the antagonist of the movement must lengthen via eccentric contraction. The two muscles, along with synergists and stabilizers, work to provide a smooth, continuous movement.For example, the primary muscle for hip flexion is the psoas as it is the local, single joint muscle at the front of the hip. The gluteus maximus serves as the primary hip extensor as, again, it is the only single joint muscle located posteriorly. During the swing phase of the gait cycle, the psoas concentrically contracts to move the femur into flexion while the gluteus maximus eccentrically contracts to allow the movement to occur.At the time the foot contacts the ground, the muscles change roles as the femur changes direction. To propel the body forward, the gluteus maximus now performs a concentric contraction to pull the femur into extension. The psoas now switches to an eccentric contraction to stabilize the joint.

However, there are times when reciprocal inhibition can be detrimental to the body. One of the primary areas in athletes is medial tibial stress syndrome (MTSS aka “shin splint”) characterized by pain on the anterior portion of the tibia. This often occurs in runners or jumpers (i.e. basketball or volleyball) and is due to either a change in training surface or a remarkable increase in activity over a short period of time.

The majority of these activities require a heavy reliance on ankle plantarflexion mitigated by the triceps surae (soleus and gastrocnemius). Simply looking at the lower leg, the triceps surae comprises the bulk of the soft tissue. Through training, the body further increases the neuromuscular stimulation to this region which increases tone and activation potential. However, as tone increases to the posterior shin, it decreases to the anterior shin. The posterior muscles become dominant, the ankle is pulled into plantarflexion which stretches the anterior fibers (figure 1). The Golgi tendon and muscle spindle, sensing the increase in tension, increases tone to prevent plantarflexion from occurring. However, this increase tone, specifically in the anterior tibialis, tensions the periosteum of the tibia creating shearing forces and subsequent pain.

Most treatments focus on addressing the symptoms: ice massage and ultrasound for the anterior tibialis eventually progressing to stretching the anterior tibialis via ankle plantarflexion. While this does cause short-term symptom relief, it ultimately feeds into the dysfunctional pattern. The more relaxed the anterior tibialis becomes, there is an increase in the tonus of the triceps surae.

A better approach: reversing the reciprocal inhibition.

The tone of the triceps surae needs to be decreased and the tissue lengthened. The calcaneal tendon is one of the strongest structures in the body, responsible for lifting the weight of the body hundreds to thousands of times a day through normal walking. It does not respond well to standard static stretching.

Gua sha or instrument assisted soft tissue mobilization (IASTM) is the recommended treatment approach. With the patient prone, begin applying the technique to the calcaneal tendon (figure 2). As the fascia loosens, passively move the ankle into dorsiflexion to increase the length of the calcaneal tendon and its fascia.

Once the appropriate amount of petechiae has formed, continue to apply a passive stretch for 1-2 minutes to re-enforce the new length. Further inhibition of the triceps surae can be obtained via kinesiology taping. A “Y-strip” can be utilized to inhibit both heads of the gastrocnemius (figure 3). However, a single “I-strip” can also be used to inhibit either the medial or lateral head (the subject in figure 3 demonstrates calcaneal inversion and would benefit from an “I-strip” to inhibit the medial head).

Often, the inhibitory techniques are sufficient to correct the problems. If pain persists, the anterior tibialis may need to be addressed specifically. However, an inhibitory technique would not be benefical for the anterior structures. A facilitation technique would be (figure 4). If there is still localized pain after facilitating, then spacing techniques could also be utilized at 40-60% tension (not shown).

These techniques are very specific and highly affective in treating MTSS. If the patient does not respond to treatment or presents with bilateral symptoms, referral to a physician for a CT scan to rule out stress fractures would be encouraged.

References

1. Borgini, E. Stecco, A. Day, JA. Stecco, C. How much time is required to modify a fascial fibrosis? J Bodywork Mvmnt Therap. 2010. 14:318-325.
2. Cheung, JTM. Zhang, M. An, KN. Effects of plantar fascia stiffness on the biomechanical responses of the ankle-foot complex. Clin Biomech. 2004. 19:839-46.
3. Huijing, PA. Baan GC. Myofascial force transmission via extramuscular pathways occurs between antagonist muscles. Cells Tissues Organs. 2008. 188:400-14.
4. Kaczander, BI. Shapiro, J. Consider systemic causes of heel pain. Biomech. 2005. 12(2):59-61.
5. Kottke, FJ. Pauley, DL. Ptak, RA. The rationale for prolonged stretching for correction of shortening connective tissue. Arch Phys Medic Rehab. 47:345-52. 1966.
6. Liptan, GL. Fascia: a missing link in our understanding of the pathology of fibromyalgia. J Bodywork Mvmnt Therap. 2010. 14:3-12.
7. Looney, B. Srokose, T. Fernandez-de-las-Penas, C. Cleland, JA. Graston instrument soft tissue mobilization and home stretching for the management of plantar heel pain: a case series. J Manipulative Physio Ther. 2011. 34:138-142.
8. Mahowald, S. Legge, BS. Grady, JF. The correlation between plantar fascia thickness and symptoms of plantar fasciitis. J Am Podiatr Med Assoc. 2011. 101(5):385-389.
9. Moseley, AM. Herbert, RD. Nightingale, EJ. Taylor, DA. Evans, TM. Robertson, GJ. Gupta, SK. Penn, J. Passive stretching does not enhance outcomes in patients with plantarflexion contracture after cast immobilization for ankle fracture: a randomized controlled trial. Arch Phys Med Rehabil. 2005 86:1118-26.
10. Neuman, DA. Ankle and Foot. In: Neuman, DA. Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. St. Louis, MO:Mosby. 2002. 477-521.
11. Schleip, R. Duerselen, L. Vleeming, A. Naylor, IL. Lehmann-Horn, F. Zorn, A. Jaeger, H. Klingler, W. Strain hardening of fascia static stretching of dense fibrous connective tissues can induce a temporary stiffness increase accompanied by enhanced matrix hydration. J Bodywork Mvmnt Therap. 2012. 16:94-100.
12. Simmonds, N. Miller, P. Gemmel, H. A theoretical famework for the role of fascia in manual therapy. J Bodywork Mvmnt Therap.2012. 16:83-93.
13. Sutherland, DH. An electromuyographic study of the plantarflexors of the ankle in normal walking motion. J Bone Joint Surg. 48A:66-71. 1966.