18 I Spring 2018 www.anjc.info Legislative Update Legal Ease Chiro Assist TECHNIQUE Council REHABILITATION Council Legal Q&A S C H O L ARSHIP WI N N E R S By Dr. Kenneth T. Cieslak Doctors of Chiropractic, as well as other healthcare and fitness profes- sionals, commonly incorporate flexi- bility exercises into our patient educa- tion and rehabilitation protocols, with the distinct goals of producing greater ranges of motion and decreasing the incidence of injury. This is often based upon the long held beliefs that stretching, whether in active or passive forms, is an effective method for lengthening muscle to allow for greater mobility and better movement. But what if our previously held ideas about stretching were not entirely correct? What if flexibility training does not lead to an actual change in muscle length, but works through some other mechanism? These are questions that are controversial, but that need to be answered if we are to improve upon our abilities to provide the best possible care to our patients and maximize treatment outcomes. Stretching is often categorized into two realms: static stretching (Figure 1) and active (dynamic) stretching. It can be further sub-divided into single person, or partner-assisted methods, such as active-isolated stretching (AIS) and post-isometric relaxation (PIR). The primary goals of stretching often center around increasing joint range of motion, and decreasing risk of injury. This has been discussed frequently in literature (Thacker, 2004; Small, 2008). There is ample evidence that various forms of stretching all lead to an increase in joint range of motion and tissue extensibility (McHugh, 2010). What is less clear is exactly how this mechanism occurs and how permanent this phenomenon is. Before we delve into the literature on flexibility training, let us briefly review muscle and tendon structure. Muscles are composed of structural proteins that have the ability to form cross- bridges and shorten or lengthen under tension. These contractile units are bound together into fascicles, which then come together to form muscle bellies. At each level, fascial connective tissue (endomysium, perimysium, and epimysium) separates and binds these entities together to create a strong tissue structure capable of withstanding many newtons of force. Fascial tissue itself is incredibly strong, and has very minimal ability to stretch. In a mathematical modeling study by Chaudhry (2008), it was hypothesized that a minimum force of 925 kg is necessary to create even a 1 percent deformation of the IT Band. While the iliotibial band is significantly thicker than the fascia that surrounds and invests most muscles, it highlights the structural integrity of this tissue, and the likelihood that it would influence the ability of a muscle to stretch as well. Furthermore, tendons are also invested with a similar fascial network (Witvrouw, 2007). As it pertains to the possible mechanisms whereby stretching exerts its positive clinical effects, the literature suggests it may be due to the following tissue characteristics: visco-elastic deformation; plastic deformation; thixotrophy; and alter- ations in stretch tolerance. Viscoelastic deformation describes the inherent characteristic of most biolog- ical tissues in which a certain degree of “elasticity” is possible. It is dependent upon both the rate and magnitude of loading, and is often transient in nature, with the tissue being capable of returning to its pre-tensioned state. Plastic deformation refers to a permanent change in the shape or extensibility of a tissue in response to an external force. It typically results from a load applied to take a tissue beyond its elastic limit, and may lead to a loss of tissue integrity. An example is when a shoulder capsule becomes permanently loosened secondary to a shoulder dislocation. In most instances, plastic deformation is not a desirable outcome. Thixotrophy refers to the ability of a tissue to change its viscous properties in response to pressure and tempera- ture (Schleip, 2003). This is a likely mechanism behind such therapies as massage, and this also tends to be transient in nature. Alteration of stretch tolerance is the process wherein tissue extensibility increases as a result of an individual’s ability to tolerate increasing levels of tissue tension and perceive it as non-threatening. (Magnusson, 1996; Weppler, 2010). This mechanism is primarily neurophyiological, and current literature suggests it may the primary driver of the immediate effects we see in response to most stretching protocols. When a tissue exhibits a rapid change in extensibility, or increase in joint range of motion, it is usually due to one or more of the previously mentioned mechanisms. It is unlikely that the muscle actually increased in length to any degree greater than 1-2 percent, but rather “relaxed” enough to temporarily allow for a greater range of motion (Halbertsma, 1994; Ylinen, 2009; Weppler, 2010; Law, 2009). These effects often last less than 24 hours. For a muscle to change its functional length in the long term, it has to undergo either myofibrillogenesis, or add sarcomeres in series (sarcomero- genesis). Both of these processes are structural changes that require at least several weeks to occur. In a study on rabbits, Takahashi (2014) found that a continuous stretch load of 7-10 days was needed to add sarcomeres in series. An example of this process would be a teenager who has undergone a sudden growth spurt, and is no longer able to touch his toes, until his muscles structurally lengthen to adapt to this change in bone length. Again, this is a slow process, and cannot explain the sudden changes in muscle length we see in response to