Category Archives: AT Program

A Blog Inspired By and Dedicated to Runners

 

by Joshua J. Stone, MA, ATC, NASM-CPT, CES, PES, FNS

I have been looking for something to blog. No idea surfaced that said, “Yes, that is a great blog idea.” That was until yesterday’s tragic Boston Marathon bombing. Runners are a rare breed. You cannot keep them down. A runner’s passion for sport, resilience to challenge, and unique characteristic to rise above is unparalleled by any other athlete. I am not a runner. In fact I am the antithesis of a runner. I go in to anaphylactic shock just hearing the word aerobic exercise, but have many friends who are passionate runners. I dedicate this blog to my running friends, competitors of the Boston Marathon, the friends and family of those impacted by yesterday’s events, and runners everywhere from the competitive to non-competitive. I will keep it true to my blog site and remain sports medicine focused. I hope you find the information useful.

Running is one of the most popular recreational sports in the US. Race events can be found in almost every town. My town – Champaign, IL – has 2 events in the next 4 weeks. Some estimates say 20% of the population is runners and 10% of these people participate in race events. The benefits of exercise are well documented. Running has shown to build confidence and character, reduce stress and improve mood. However, the due to their very nature – the unwillingness stop – running does bring about an increased incidence of musculoskeletal injury.

You don’t need to be an astrophysicist to know running injury is secondary to cumulative overload. Running injuries are multifactorial; neuromuscular imbalance, poor arthrokinematics and other things such as age, nutritional status and environment are to blame. From a biomechanical point of view frontal plane knee adduction moments play a significant role in lower extremity injury. Q-angle – a measure of knee alignment – can indicate risk for running injury. An increased Q-angle can be a result of many neuromusculoskeletal inefficiencies from poor muscular hip control to limited ankle dorsiflexion and excessive forefoot pronation.

Running brings about many injuries, but the most common are Patellofemoral Syndrome, Iliotibial Band Syndrome, Medial Tibial Stress Syndrome / Tibial Stress Fracture, Achilles Tendinitis, Plantar Fasciitis, and Sacroiliac Joint Pain. What is interesting is that all of these injuries can be caused by biomechanical breakdown and neuromusculoskeletal inefficiency. The good is the dysfunctional patterns are identifiable, preventable and correctable. Below is a sample 15 minute injury prevention program from a blog I wrote in Sept 2012. Yes, 15 minutes is all you need to prevent many running injuries.

Step 1: Decrease neurological drive to hypertonic tissue – 3 minutes

  • Self-Myofascial Release (foam roll) or Manual Trigger Point Therapy
    • Gastrocnemius/Soleus – 60 seconds
    • Adductors – 60 sec
    • TFL/IT-band – 60 sec

Step 2: Lengthen hypertonic muscle or joint tissue – 3 minutes

  • Static stretch or joint mobilization
    • Gastrocnemius/Soleus Stretch – 1 set @ 30 sec
    • Kneeling Hip Flexor Stretch – 1 set @ 30 sec
    • Adductor stretch – 1 set @ 30 sec
    • Posterior joint mobilizations at the ankle – 90 seconds

Step 3: Increase neurological drive to hypotonic tissue – ~ 6 minutes:

  • Exercise: Isolated Strengthening or positional isometrics
    • Resisted Ankle Dorsiflexion – 2 sets x 15 reps (slow) (2 minutes)
    • Resisted Hip Abduction and External Rotation- 2 sets x 15 reps (slow) (2 minutes)
    • Resisted Hip Extension – 2 sets x 15 reps (slow) (2 minutes)

Step 4: Integrated Dynamic Functional Movement – ~ 3 minutes

  • Box step-up with overhead dumbbell press – 2 sets x 15 reps (slow)

Beyond the correction of movement dysfunction there are alternatives to treat running injuries which are effective and gaining popularity. This table highlights a few.

Prolotherapy This has been around since the late 1800’s, but has since become popular. The basis of prolotherapy is that it expedites healing by increasing fibroblastic activity and collagen repair.
Autologous Blood Blood is the medium that carries tissue repairing materials to injury sites. However, sometimes, blood cannot deliver adequate amounts of material to the injured area. Thus, injections directed right at the injury site deliver tissue repairing material.
PRP Like autologous blood, Platelet Rich Plasma (PRP) is injection of a concentrated mix of tissue repairing blood components, specifically platelets, which facilitate tissue repair healing.
Bone Marrow Aspirate Concentrate Despite the negative press and belief that stem cells are only derived from an unborn fetus, stem cells do come from other sources – such as bone marrow. By taking stem cells from bone marrow and injecting in to damaged areas will facilitate tissue repair.
ESWT Extracorporeal Shock Wave Therapy might best be known as lithotripsy. Lithotripsy is a procedure in which sound waves blast and destroy kidney stones. ESWT is the use of sound waves to destroy calcific tendons and ligaments.

I prefer preventing and rehabilitating injury through correcting neuromuscular inefficiencies and dysfunctional movement. The problem with the above treatments is that they are treatments. If an injury is caused by dysfunctional movement patterns and those patterns are not corrected it is likely the above treatments will simply serve as a Band-Aid because the true problem was not fixed.

If the person(s) responsible for the Boston Marathon bombing were looking to put fear in people, they chose the wrong population to target. Runners are the most stubborn and prideful athletes. No means yes, and yes means do more. If you took a graphical representation of marathon registration numbers from last night through the end of this week I would bet you’d find a spike, rather than a decline. Social media is exploding with a rise of the runner. A quote from a friends Facebook page: “If you’re trying to defeat the human spirit, marathoners are the wrong group to target” –unknown. Other movements like, wear a race shirt tomorrow, donations, and wear yellow and blue (Boston Marathon colors) have already begun. So, thank you runners for inspiring this blog post!

Find more of Josh’s work here.

Mechanotransduction: Why Does Rehabilitation Work?

by Joshua Stone, Guest Blogger

Find more of Josh’s work at Athletic Medicine.

You have an athlete with a stress fracture. The physician prescribes active rest and places the athlete in a non-weight bearing boot. Sound familiar? Suppose I told you the better option is to place some load on that bone and non-weight bearing is not recommended. Would you think I am nuts? Maybe I can convince you otherwise. Let me explain but, before you read the next paragraph and decide to leave the page, bear with me. What follows this introductory piece may provide insight to further understanding of injury pathophysiology and could revolutionize the future of rehabilitation science.

In January 2013 the Annals of Human Genetics published an article that demonstrated AchillesTendinopathy is associated with gene polymorphism (Abrahams, et al., 2013). I am not a geneticist by any stretch of the imagination, so pardon my basic explanation. COL51A is a gene that encodes the development and organization of Type V collagen. Type V collagen is a collagen that is distributed in tissues as a component of extracellular matrix and composed of one pro alpha 2 (V) and two pro alpha 1 (V) chains. This collagen can be found in ligaments, tendons, and connective tissue. COL51A plays an integral role in development and maintenance of connective tissue. Abrahams, et al. (2013) demonstrated that polymorphisms occur in the COL51A gene causing altered structure of collagen resulting in tendionpathy.

I state the aforementioned because it is time for athletic trainers to begin taking a deeper look at pathophysiology and more importantly, to utilize this understanding in the development of our rehabilitation and treatment guidelines. Some of you may already be cognizant of this, but these revolutionary approaches to treatment and rehabilitation are already coming to light. Let me introduce the concepts of cellular signaling, mechanotransduction, and mechanotherapy.

Mechanotransduction and the Processes of:

Mechanotransduction ( described by Khan 2009) is the process whereby mechanical load initiates biochemical signals that leads to gene upregulation, protein synthesis and ultimately structural change (Khan 2009). Load causes perturbation to cells that initiates signaling pathways, where mRNA is sent to the endoplasmic reticulum for gene encoding. If you recall from college physiology, proteins are created by ribosomes following this transcription. These proteins are the new collagen and are extruded from the extracellular matrix and delivered to the damaged tissue. This is why eccentric training heals tendinopathy.

This process is not limited to damaged connective tissue. The mechanical load induces cellular signaling in all tissue – nervous, muscular, connective, bone and cartilage (Khan, 2009). In muscle, load stimulates upregulation of mechanogrowth factor and ultimately hypertrophy. Chrondrocytes are sensitive to load and are fed through load. Load applied to osteocytes deep within bone stimulates bone lining cells and facilitates healing to expedite fracture repair.

Review of cool supporting studies: 

Joseph, et al., (2012) stated that tendinopathic tendon is less stiff and loses ability to transfer energy. Joseph goes on to state that load creates a viscoelastic response in the Achilles tendon that increases stiffness and decreased hysteresis. Fragala et al., (2011) demonstrated leukocyte β2-adrenergic receptor expression changed in response to heavy resistance exercise. Flück, et al., (2008) evaluated tenascin-C,  a protein responsible for tissue remodeling that is expressed only in damaged tissue and regulated by mechanical load. They found that mice deficient of tenascin-C had diminished muscle tissue healing and conclude that tenascin-C is needed for reducing and healing of musculoskeletal injuries.

Scott, et al., (2008), demonstrated physiological load induces an osteogenic response that stimulates anabolic cellular activity in bone. In the Journal of Sport Rehabilitation – published by the one and only Human Kinetics – stated “the notion that deep friction massage may provide mechanical stimulation for healing is intriguing, especially given the context in which Cyriax, advocated this “mechanotherapy” as early as 1984…. While this is difficult to study in a human model, there is some poignant animal evidence that tendon massage indeed stimulates tissue adaptation at the cellular level.” (Joseph, et al., 2012). Durieux, et al., (2009) assessed regulation of focal adhesion kinase in mechano-regulated differentiation of slow-oxidative muscle. Focal adhesion kinase initiates cellular signaling and ultimately migration of cells and is required during development. The authors found that focal adhesion kinase is part of the signaling pathway that governs repair of striated muscle.

Conclusion:

Is a non-weight bearing walking boot the best treatment option for a stress fracture? It appears it is not. Based on the data discussed here, the practitioner must utilize an intricate balance between rest and mechanical loading of bone to obtain optimal healing. In order to heal damaged tissue we must use exercise as a repair stimulus – mechanotherapy.

The body of evidence exists and is continuing to grow. It is recommended athletic trainers and rehabilitation specialists take time to understand the pathophysiology of injury and the biochemical processes that elicits healing. In the very near future you will need to understand the biochemical events that promote tissue repair. The knowledge gained will dictate rehabilitation protocols needed for specific injuries.

References:

Abrahams Y, Laguette MJ, Prince S, and Collins M. Polymorphisms within the COL5A1 3′-UTR That Alters mRNA Structure and the MIR608 Gene are Associated with Achilles Tendinopathy. Ann Hum Genet. (Epub – ahead of print) Jan 2013.

Khan, K M, and Scott, A. Mechanotherapy: How Physical Therapists’ Prescription of Exercise Promotes Tissue Repair.  Br J Sports Med. 2009;43:247–251.

Joseph, MF, Lillie, KR, Bergeron, DJ, and Denegar, CR. Measuring Achilles tendon mechanical properties: A reliable, noninvasive method. J Strength Cond Res. 26(8): 2017–2020, 2012.

Fragala, M. S., Kraemer, W. J., Mastro, A. M., Denegar, C. R., Volek,  J. S., Hakkinen, K.,  Anderson, J.M.,  Lee, E. C., and Maresh, C. M. Leukocyte β2-Adrenergic Receptor Expression in Response to Resistance Exercise. Med. Sci. Sports Exerc. Vol. 43, No. 8, pp. 1422–1432, 2011.

Fluck M, Mund SI, Schittny JC, Klossner S, Durieux AC, et al. (2008) Mechano-regulated tenascin-C orchestrates muscle repair. Proc Natl Acad Sci U S A 105: 13662–13667.

Scott, A., Khan, K.M.,  Duronio, V, Hart, D.A. Mechanotransduction in Human Bone In Vitro Cellular Physiology that Underpins Bone Changes with Exercise. Sports Med. 2008; 38 (2): 139-160.

Joseph, MF, Taft, K, Moskwa, M, and Denegar, CR. Deep Friction Massage to Treat Tendinopathy: A Systematic Review of a Classic Treatment in the Face of a New Paradigm of Understanding.Journal of Sport Rehabilitation. 2012, 21, 343-353.

Durieux AC, D’Antona, G, Desplaches, D,  Freyssenet, D, Klossner, S, Bottinelli, R, and Fluck, M. Focal adhesion kinase is a load-dependent governor of the slow contractile and oxidative muscle phenotype. Jof Physiol.  2009;587:14. 3703–3717