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Facilitating change through active rehabilitation techniques
Journal of Bodywork & Movement Therapies (2013) 17, 531e540
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.elsevier.com/jbmt
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Facilitating change through active rehabilitation techniques M. Wallden, MSc Ost Med, BSc (Hons) Ost Med, DO, ND Primal Lifestyle Ltd., United Kingdom
Over the last century, the large focus of rehabilitative healthcare has been on passive techniques; what can “I” as the therapist do “to you” as the patient, in order to help you feel better? However, with a growing understanding, both of the neurophysiology and of motivational concepts, it has become clear that active rehabilitation is essential in the effective long-term resolution of pain and biomechanical dysfunction (Lederman, 1997), as well as in the empowerment of the patient (Liebenson, 1999). As this understanding has grown, a raft of interventions have arisen, from self-stretching targeting muscles and fascia, self-mobilization of the joints, muscle activation, core stability, and strength training, right the way through to more ballistic forms of performance conditioning (Fig. 1). In this paper, a logical sequence of rehabilitation is presented, along with a more in-depth review of Panjabi’s model of joint stability (Panjabi, 1992), which should allow clinicians and patients to understand better where they may be in the rehabilitative process and what path they can follow to return to full function. This coherent chronological rehabilitative formula, detailing techniques ranging from stretching, through to ballistic, e-concentric loading protocols, are potentially important for full rehabilitation for both athletes and for the everyday patient. As a brief summary, the proposed model for the rehabilitative sequence is as follows: E-mail address: [email protected]. 1360-8592/$ - see front matter ª 2013 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jbmt.2013.09.004
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Received 2 September 2013; accepted 2 September 2013
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Figure 1 Adapted from Lederman (1997), A) describes the process when a passive technique is applied to a patient; the effect being largely mediated at the cord level and therefore short-term in effect. B) describes the process when a patient is actively engaged in the rehabilitative process, where new patterns of movement can be coached and formed as motor programs.
An underlying premise of this approach is the recognition that everyone is an athlete, with an athletic requirement to meet; whether that requirement is simply to resist and move in a field of gravity, or whether they have more specific demands based on job, vocation or activities of daily living. There are several hidden factors that may “trip-up” the rehabilitative process too, which will also be touched on to raise clinical awareness of them, to ensure they don’t surreptitiously de-rail the patient’s return to full function.
neural subsystem regarding joint position which, in turn allows the nervous system to activate the musculature appropriately to control joint movement and stability; thereby minimizing stress on the passive subsystem.
Before the first assessment Prior to assessment, it may be useful to review a second model: Panjabi’s (1992) model of joint stability (see below). As much as this is already well understood and regularly described in previous editorials, it is useful to examine it one more time in order to gain clarity on what the therapeutic goal is in this context (Fig. 2). The model informs us that for optimal joint function each of the 3 key subsystems must be functional and working in harmony; the passive subsystem, the active subsystem and the neural subsystem. In a simplistic view of the model, the “passive” subsystem comprises the joints and connective tissues containing an abundance of mechanoreceptors which feedback to the
Figure 2 Panabi’s model of joint stability. Often the passive subsystem is considered to be distinct from the musculature, but there are passive tissues associated with and embedded within the muscular system; some of which are trainable.
The active subsystem The active subsystem may be further divided into inner unit musculature and outer unit musculature. The inner unit muscles, described in detail elsewhere (Wallden, 2013) contain a preponderance of type 1, tonic muscle fibres, which have differentiated into these slower twitch, postural fibres due to being activated by tonic motoneurons. In turn, the tonic motoneurons have behaved “tonically” as opposed to phasically, based on how they were utilized during infant development (Fig. 3). The outer unit muscles contain a preponderance of type 2 muscle fibres, which have differentiated into these faster twitch, mobiliser fibres due to being activated by phasic motoneurons. In turn, the phasic motoneurons have behaved “phasically”, phasing on and off, as opposed to holding consistent tone, based on how they were utilized during infant development. (Kuno, 1989). The “inner” inner unit Interestingly, much of the focus in the field of motor control in recent years has been the “inner unit” or local stability musculature which have a low threshold to stimulus and
533 therefore both fire ahead of the outer unit musculature (the “feedforward mechanism”), and are also more prone to inhibition from aberrant neural stimuli, such as pain (see Wallden, 2013 for more discussion & further references). However, less attention has been focused on the mechanoreceptive role of the passive subsystem; which, in one way, can be interpreted as the “inner” inner unit. As far back as 1972, Wyke identified that the outer part of the joint capsule is densely packed with type 1 mechanoreceptors which communicate directly with the inner unit musculature. Conversely, the inner part of the joint capsule is richly innervated with type 2 mechanoreceptors, which communicate with the outer unit musculature (Fig. 4). Of course, when a joint moves, the outer part of the joint, being furthest from the axis of rotation, will be stretched first. This means that subtle motion at the joint will excite the inner unit musculature first and increase tone, stabilizing the joint. If a greater stretch occurs due to a greater range of motion at the joint, the outer unit musculature will become stimulated providing, greater rigidity around the joint with larger leverages to resist that stress.
Figure 3 Muscles can be loosely categorized into tonic and phasic, with differing characteristics. These are listed in the table above, but should not be considered universal as there are many exceptions, especially to the lengthen/weaken: shorten/tighten category.
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that it responds to movement with hydration and elasticity and to lack of movement with dehydration and crystallization (Schleip and Mu ¨ller, 2013). In addition the fascia has smooth muscle cells embedded within it meaning that it will reflect the underlying autonomic tone; a parasympathetic dominance will facilitate more relaxed fascia, while reciprocally sympathetic dominance will facilitate greater tension in the fascia (Barnes, 1997). Other aspects of the passive system lesser discussed may include hydration of the joints and discs, viscera as viscous (non-compressible) functional stability units, blood as a connective tissue, and connective tissues infiltration and integration into muscular tissue; not just as an apparently discrete entity, such as endomysium, but also as components of the contractile unit itself such as the series and parallel elastic components (discussed further below).
Figure 4 Stretch to type 1 mechanoreceptors excites the tonic motoneurons stimulating inner-unit function, while a larger stretch to the type 2 mechanorecepors excites the phasic motoneurons and outer-unit function. In this way, the mechanoreceptors in the outer joint capsule can be seen as the precursor to inner-unit function. From a rehabilitation perspective, this helps to inform the clinician that to isolate inner unit musculature, smaller, subtle movement is likely to be most effective.
A more detailed view, which is useful in many instances to overcome clinical road-blocks, is to understand more about the range of connective tissues that offer stability, and how these both influence and can be influenced by various neural factors, and how this may selectively affect function of the muscular system.
The passive subsystem In terms of total afferent drive, it has been reported that the mechanoreceptive population may account for as much as 70% of all inbound information to the brain (Stecco et al., 2007). This information is typically associated with stretch or pressure, stimulating the mechanoreceptors within the fascia and connective tissues, stimulating a reciprocal contraction of the musculature, depending on degree of stretch (discussed above under The active subsystem). Connective tissues, having a lower density of elastin to collagen and a much lower blood supply than active tissues, such as muscle, tend to be more susceptible to injury than muscle; and, once damaged, will typically take longer to heal. Many professions work directly with the joints to mobilize and manipulate them as it has been shown that such mechanoreceptive stimulation appears to help in reducing pain and improving function by blocking nociceptor activity, inhibiting overactive muscles associated with that segmental level and optimizing joint play. Until recently, the fascia was relatively ignored as part of the passive subsystem, but it has been brought increasingly into the awareness of the rehabilitation and performance communities by the work of many, and Schleip in particular (Schleip et al., 2012). What is of importance here is that the tension of the fascia is not only related to muscle tone, but the fascia also has crystalline properties meaning
The neural subsystem The neural subsystem is undoubtedly complex, so this discussion is kept simple for practical purposes. The nervous system both receives sensory and sends out motor information; functioning in the adult primarily as a “sensory-motor” system (as opposed to in a young infant, where for the first 3 months or so after birth it is primarily motor-sensory). In other words, throughout most of our lives the information going out to the muscles (the active subsystem) is only as accurate as the information coming in to the central nervous system (or neural subsystem). In a sensory-motor based system such as the human being, compromised information due to injury, pain, deconditioning, impaired proprioception, aberrant neural stimuli, such as (inhibition, facilitation, trigger point development, limbic-emotional drives, viscero-somatic inputs) must, by definition, detrimentally affect motor output. Examples here may include a situation such as a flat foot where the plantar fascia has undergone creep due to overpronation. This means that as the foot kinematically moves into pronation, the mechanoreceptors in the plantar fascia and plantar aspects of the joints of the mid-foot will not be stimulated until it is “too late” and the foot has overpronated. Plantar fascia that has not undergone creep will be stretched as the foot begins to pronate, stimulating the embedded mechanoreceptors, resulting in activation of the anti-pronation (supinator) musculature. Similarly, at the spinal level, the posterior ligamentous system of the spine may undergo creep due to poor ergonomics, such as sitting in end-range lumbar flexion for prolonged durations. This means that whereas under normal circumstances when the spine reaches approximately 45 of forward flexion the mechanoreceptors would send an inhibitory neural drive to the cord to shut-off the lumbar extensors and engage the transversus abdominis; in this instance, as the spine moves into flexion, the preinduced creep in the posterior ligamentous system would mean that the mechanoreceptors are not stimulated until deeper into the flexion movement (say, 55 ) which poses greater risk to spinal structures, such as discs, due to compressive loading from the increased lever arm in tandem with the late shut-off of the lumbar erectors (Hashemirad et al. 2010).
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Initial assessment Correct adverse neurological inputs In this author’s clinical experience, the following observations in this section would seem to be useful as guidelines: Posture may be used as a quick-screen overview. Optimal postural findings indicate a minimized risk of adverse neurological factors, but do not indicate their absence. Functional movement screening, including gait analysis and other key movement patterns such as squatting, lunging, bending and so on, provides a more comprehensive assessment. Optimal postural findings in conjunction with optimal movement assessment indicate a significantly decreased risk of adverse neurological factors, though is still not a thorough, foolproof finding as many clients (athletes, or those with good kinesthetic awareness in particular), may exhibit difficult-to-spot compensation patterns, leading to false-negative conclusions. It is, however, extremely rare in clinical practice to find either optimal postural, or optimal movement screenings. In postural screening, commonly what can be observed are gross muscle imbalances expressed as one of the following: Upper-crossed syndrome Lower-crossed syndrome Layered (stratification) syndrome . and any of these may be accompanied by a sway posture, which is where the pelvis can be observed in the lateral view to have swayed ahead of the plumb-line. In movement screening, what is often observed are signs of poor movement skill, facilitation of certain muscle groups, deconditioning, inhibition or poor stabilization. Examples of poor movement skill may include someone who attempts to pick up or move a load in an arm-dominant fashion, instead of utilizing their body as an integrated unit (expression of load mobilization should typically follow a legsetrunkearms sequence). This is poor, or inefficient motor sequencing. Deconditioning of the core musculature may result in the above arm-dominant sequencing, but other examples of deconditioning commonly observed are quadriceps dominance in squat or lunge movements due to deconditioning of the gluteus maximus. Inhibition is often seen in the gluteus medius and is expressed as a Trendelenburg pattern, or compensated Trendelenburg; in the transversus abdominis, and is expressed as oblique dominance or rectus abdominis dominance; in the serratus anterior and is expressed as scapula winging; or in the vastus medialis obliquus, often as a result of pain inhibition or a simple lack of stabilization requirement at the knee in ADL’s e often expressed as retropatellar pain.
Facilitation may be seen in certain muscle groups, usually as a result of trigger-points, tender points and compensatory motor patterns. Common examples of facilitation include hitching of the shoulder during arm abduction due to facilitation (often accompanied by trigger points) in the scapula elevator musculature (upper trapezius and levator scapulae); or winging of the scapula (inhibition of serratus anterior) due to facilitation of the pectoralis minor. Trigger points are commonly found in facilitated tissues. Other adverse neurological inputs can include pain, viscero-somatic reflexes, central sensitization, trigger point formation, facilitation and inhibition (among others).
Correct lengthetension relationships As mentioned above, the major muscle imbalances, as well as other aberrant posture may be the cause or effect of dysfunctional lengthetension relationships. Without any other apparent adverse neurological inputs, it is likely that lengthetension relationships may be held through habit and facilitation of neural pathways. Lengthetension relationships should always be addressed first by stretching shorter, more facilitated musculature that may be inhibiting longer, apparently weaker musculature (such as a pectoralis minor inhibiting a serratus anterior). Janda showed in 1972 that when the lumbar erectors, for example, are short and facilitated, they will fire even when the patient is attempting to perform a sit up from the floor, where they should be quiescent. However, after stretching the lumbar erectors, they become electromyographically silent and more neural drive is allowed to reach the key muscles involved in the situp movement, such as rectus abdominis (Janda, 1978). Hence, as a clinical strategy, it would seem important to stretch tight, potentially facilitated musculature before addressing apparently weaker, longer musculature as it may simply be inhibited.
Correct chronic joint adaptations Arguably, a joint, being a passive structure, cannot be “held” out of position in and of itself without a preceding lengthetension imbalance creating chronic adaptations in the joint capsule. Picture a life size plastic skeleton with rubberized joint capsules and now try to create a joint adhesion, a facet lock, or a pelvic torsion*. It really is not going to happen easily without a muscular system to hold it out of place. *Of course there may be some exceptions to this statement, but it appears none that have been conclusively validated. What, most probably, creates a majority of changes to joint play are chronic (long-term) length-tension imbalances in the surrounding musculature creating contracture of the connective tissues on one side of the joint and, reciprocally, creep* on the opposite side of the joint. In this instance, it is the chronicity of the length-tension imbalance of the musculature that ultimately dictates the severity of the joint dysfunction. *Contracture can be defined as a permanent shortening of a muscle or joint usually in response to prolonged
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Simply put, the information going out, can only be as good as the information coming in. The human functions as a biocomputer with the motor control being entirely dependent on the information coming in to the system.
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536 hypertonia, while creep can be defined as the tendency of a solid material to move slowly or deform permanently under the influence of mechanical stresses (Fig. 5).
higher centres; the process of progressing from a “conscious competent” to becoming an “unconscious competent” (Wallden, 2013).
Stimulate & condition tonic motoneurons & inner unit musculature
Re-assess
Since tonic motoneurons are predominant to the inner unit musculature, it is important that once the joint mechanics, lengthetension relationships and other neurological inputs are optimized, the inner unit should be stimulated actively. This process is used to help re-establishment of new, more functional motor patterns, through active engagement of the motor cortex to help facilitate the neural pathways to the tissue. Subsequent repetition of these targeted, isolated exercises is designed to help the process to become increasingly reflexive, requiring less and less activation of the executive
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Of course, reassessment is often a continuous clinical process, but if the patient hasn’t been through this process, this is a key time for reassessment to evaluate whether the patient is ready to move to higher, more functional loading interventions.
Condition phasic motoneurons & outer unit musculature While conditioning the tonic motoneurons and inner unit musculature calls for subtle techniques, such as breathwork, Feldenkrais, Alexander Technique, motor control methodologies and so on. Conditioning of the phasic motor neurons and outer unit musculature is built on that important foundation and spans across a broad range of conditioning, from common clinical rehabilitation approaches, through to ballistic, sports-specific and injury prevention strategies. Loosely, beyond what is often termed “stability”, rehabilitation can, and ideally should, move into “strength” and “power” phases. These phases can be further subdivided many times, however, for the purposes of this piece, only strength-endurance and strength-hypertophy will be focused upon as subdivisions of the Strength category; with e-concentric loading and perturbation loading as subdivisions in the Power category.
Strength Strength training is a term often used distinctively from endurance training. The purpose of strength training is clearly to build strength in the targeted tissue(s); whereas endurance training may either increase or decrease strength depending on the base level of conditioning of the individual.
Figure 5 A) When muscle balance is equal either side of the joint, the joint maintains its instantaneous axis of rotation, balance is maintained in the joint capsule and passive subsystem, and cumulative microtrauma to the joint is minimized. B) When muscle imbalance is present, one side of the joint undergoes compressive stresses, and the other side traction stresses which, across time, result in contracture on the former and creep on the latter side of the joint. Adapted from Comerford and Mottram (2001).HYPERLINK
Strength-endurance Strength-endurance training, or “extensive” training, is classified as resistance training with loads of up to 50% of the maximum load the individual can lift or move, which typically means they will be able to perform 12 or more repetitions of that exercise; and thereby targets a combination of the type 1 and type 2a fibres. For example, if one were to pick up a dumbbell and press it above one’s head, but can only do this 8 times before becoming fatigued, this load is too heavy for strength-endurance training. From this perspective then, strength-endurance training can be important in building postural strength and in learning (or re-learning) new movement patterns, such as a squat, or a deadlift (bend) movement pattern. Strength (hypertrophy) training Strength training covers a broad range, from loads that can be lifted only once, through to loads that can be lifted hundreds of times, however, classically strength training
tends to cover the range of loads that can be lifted from 6 to 12 times before fatigue (Baechle and Earle, 2000). Within this range, research has indicated that loads lifted in the 8e12 rep range (ie which can be lifted 8e12 times before fatigue halts further repetitions) is the optimal zone for inducing hypertrophy (Baechle and Earle, 2000) (Fig. 6). Why would the clinician want to introduce hypertrophy training to their client, is there any benefit in terms of rehabilitation? The answer to this is yes, but only at the right time in the rehabilitation process. If the clinician were to load a patient too early with the kinds of loads that induce a strong hypertrophy stimulus, there is a good chance that this would reinforce faulty and compensatory outer-unit dominant motor patterns. For example, prescribing a deadlift with hypertrophy loading variables for a patient whose inner unit is not firing will just reinforce their outer unit dominance, such as rectus abdominis dominance or lumbar erector firing and trigger point development. There are
537 several potential reasons why hypertrophy training is important in rehabilitation. Firstly, by its very nature, hypertrophy training is stimulating a growth and repair process, including an increase in growth hormone and in receptors for such hormones (Poliquin, 2006) setting up an optimal anabolic environment for tissue repair. Secondly, intrinsic, or inner unit musculature, becomes inhibited in the presence of nociceptive drives. For example, Hides et al. (1996) demonstrated that within 24 h of the onset of pain the lumbar multifidus had apparently “shrunken” on the symptomatic side and the symptomatic level to, on average, 69% of the cross sectional area of the contralateral multifidus. What is known is that atrophy cannot occur that quickly. Instead, this is explained by neural inhibition of the muscle. Hence, if the pain can be managed effectively and the intervention is early enough, the cross sectional area of the multifidus (in this instance) may be “recovered” simply by the activation techniques commonly taught in manual therapy circles. However, the
Figure 6 This diagram summarizes the typical effects of training with loads at a certain repetition range. Along the base of the diagram are numbers indicating the number of repetitions the exerciser can complete before fatigue. The heavier the load the lower the number of repetitions achievable (and, in strength & conditioning, this generally means the higher the number of sets, and the longer the required rest period between sets). The opposite can be seen at the other end of the repetition range e higher reps Z less sets Z shorter rest periods between sets. What is useful to understand is that the hypertrophy effect of training is greatest in the 8e12 rep range’ hypertrophy gains being represented by the diamond in the middle of the diagram.
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538 issue here is that if the pain has been present for longer than 2 weeks, the process of atrophy will have begun. Hence, loss of cross-sectional area in the muscle for patients whose pain has exceeded 2 weeks duration will be a combination of both inhibition of the muscle and atrophy of the muscle tissue. Across time, this leads to a clear “mothballing” appearance on MRI. Consequently, introducing a low level, activation technique will certainly help with facilitating the neural pathway and improving crosssectional area through simple contraction, but to reverse the atrophy requires a hypertrophy stimulus; and to produce a hypertrophy stimulus requires loading at the 8e12 rep-max level (a weight or load that can only be lifted 8e12 times before complete fatigue). Thirdly, one of the known mechanisms of joint stabilization is the hydraulic amplifier effect of muscle contraction, creating cross-sectional expansion of the muscle within its fascial sheath e the epimysium (Lee, 2004). This increased intra-epimyseal pressure causes an increased stiffness of the muscle, which means that where that muscle crosses one or more joints, those joints will be more stable the more hypertrophied the muscle. Additionally, this intra-epimyseal pressure doesn’t just create stiffness, but also produces an erectile force lifting the spine (for example) upward. Of course, the stiffness produced in the epimysium is thereby transferred via the surrounding fascia into adjacent and interconnecting musculature in a kind of activeepassiveeactive stability process. Lastly, and perhaps most importantly, although muscle is classified as being the “active” subsystem in joint stability, it can also be viewed, as in point three above, as part of the passive subsystem due to its integration with the fascia. An additional mechanism, where muscles’ function traverses
M. Wallden into the role of the passive subsystem is where it comes to both the series elastic components and the parallel elastic components of the muscle. Between each sarcomere (the functional contractile unit within the muscle) there is a series elastic component (SEC), while down the lateral aspect of each sarcomere can be found parallel elastic components (PEC). Combined, these SEC’s and PEC’s behave like springs, giving the muscle a passive, spring-like resistance to stretch (and recoil when it is stretched). It is the number of sarcomeres in parallel, plus the size of these sarcomeres, that determines the stiffness of the muscle (Sahrmann, 2002). Somewhat intuitively, the greater the stiffness of the muscle, the greater “passive” protection is offered to the joint by the muscle. Somewhat counterintuitively, the greater the stiffness of the muscle, the less prone it is to injury itself (Hunter, 2005), as with more and stronger “springs” between and around its contractile elements, it’s less likely to be overstretched (Fig. 7) When a muscle is trained with loads that induce a growth response, the process accounting for the growth is largely attributed to hypertrophy (an enlargement of the sarcomeres and their respective “springs” the SEC’s and PEC’s), while there is also some evidence there may be hyperplasia (an increase in the number of sarcomeres in parallel). Either way, whether there are just larger springs, or larger springs and more of them, the stiffness of the muscle will be increased and underlying joint more protected. Why is this important? The neural component of joint stability; the nervous system, has a response time that is too slow for some stimuli. If a patient recovering from a whiplash, for example, where the passive subsystem has been traumatized, was given a rehabilitation program which focuses on
Figure 7 A) Depicts sarcomeres both in series going horizontally across the image and in parallel going vertically down the image, illustrating schematically their actinemyosin interdigitation. B) Depicts sarcomeres, in series, at a lower magnification. C) Depicts sarcomeres in series at a higher magnification illustrating both their series elastic components between the sarcomeres and their parallel elastic components down the lateral border of the sarcomeres (in red).
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Power Why would the clinician want to introduce power training to a client? Is there any benefit for non-athletes? Firstly, it is important to address the issue of exactly who is an athlete and who is not. Anyone who is alive and moving has an athletic requirement; especially those who live in a gravitational field! Hence it is entirely feasible and correct to define everyone as an athlete. The rationale for conditioning at the power level is much the same as the rationale for training to induce strength-hypertrophy; because the average person may well encounter “power” requirements in activities of daily living, such as the examples described above in the Strength section. Power can be defined as the time rate of doing work, where work is the product of force exerted on an object and the distance the object moves in the direction in which force is exerted (Baechle and Earle, 2000). Force is calculated by the equation: force Z mass acceleration. Hence, power training is simply the movement (force) of loads (mass) under conditions of acceleration; an “explosive” or high-speed form of strength training. How is this relevant to rehabilitation? Power training does not induce hypertophy nearly as much as strength training, so the benefit is different. Power training performed concentrically, also does not convey significant protective benefit to the passive subsystem of the joints, as linear directional acceleration is usually a higher-centre decision, under conscious control and is therefore appropriately stabilized by the nervous system (neural subsystem) and inner-unit (active subsystem) musculature. What is often poorly anticipated by the nervous system, however, are non-linear accelerations, such as the pull of dog on its lead, or a horse while leading it out, or change of direction decelerations, such as “jarring” in the car, or on step. While, as described above, these may sometimes happen too quickly for the nervous system to respond, in other instances, a pot-hole may be seen at the last minute, but it is too late to avoid hitting it, or the dog may give an indication it is about to
lurch off. This gives the patient crucial milliseconds to prepare and brace for the impending force. E-concentric loading As described above, e-concentric loading, in this context, can be defined as the process by which a muscle contraction rapidly switches from eccentric to concentric. This is the more common way that a muscle is utilized in functional movement patterns. A concentriceeccentric movement pattern is primarily used for “start speed” or “start strength” such as exploding out of the blocks for a sprinter, or doing a standing long jump, but as soon as that athlete starts to move, then most of the power is generated by e-concentric processes. To train for these potential scenarios described in the section above, e-concentric loading is a useful tool to condition the nervous system and build both an appropriate response and effective muscular power to protect the underlying passive subsystem. Essentially it is about effectively controlling the deceleration, in order that the body can accelerate back out of the movement pattern towards neutral. This optimally prepares the body to accept loads and so would be important in the training of those in contact sports, combat sports, or those who may crash, or fall as part of their pursuits. Hence it is good and important conditioning for life in general; teaching the body how to effectively handle rapid loading and unloading. Perturbation loading Perturbation training is similar to e-concentric training, but is typically more random in its application and therefore trains versatility in the body’s response to loading. Perturbation may be conducted using very light loads, such as those induced by swinging a tennis ball at the end of a sock in a circle above your head, then moving the arm position to different angles and inclinations so as to change the angle of the forces being induced through the shouldereneckecore. Other tools, such as the Bodyblade, which works with rhythmical or oscillatory forces, working with controlled falling, with the Swiss ball, or partner work, involving a form of controlled wrestling can be utilized to train perturbation. The forces involved in this rapid change in direction can be significant and hence can train the patient to be able to effectively anticipate, tolerate, absorb and dissipate aberrant forces more efficiently in activities of daily living. Other examples of perturbation and e-concentric training can be viewed at https://www.youtube.com/user/ primallifestyleltd.
Summary The proposal in this paper is to view the body from the perspective of a skeleton whose bones cannot be magically held out of alignment without some alteration to the tone of the musculature holding that skeleton. The question then becomes what controls may affect the function of the muscular system; the answer to which is the neural system. This leads onto the next question, what can influence the neural system, and here there are many possibilities from overuse of a given neural pathway creating facilitation of that pathway, versus underuse of a
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the inner unit musculature of the neck, that program may be successful in rebuilding postural stability, but it may confer no real benefit in many dynamic real-life scenarios, such as, receiving an unexpected jolt from a pothole while driving down the road; getting a sudden tug on the dog on a lead who has just spotted a squirrel in the bushes; or missing a step while carrying a child down an unfamiliar stair-case. These are all everyday examples of situations where the function of the neural and active systems, just won’t be effective, and therefore the stress is transferred into the passive system; but if the passive system is already compromised, damaged or has undergone creep, then injury (or reinjury) is the likely outcome. Since the passive system, by its nature, has a poor blood supply and long healing duration e often measured in months and years, rather than days and weeks for the active system e it strategically therefore makes sense to concentrate efforts on building “passive” support through hypertrophy training which could feasibly start within 6e8 weeks post-accident depending on the success of pain management and progress in establishing inner-unit function.
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540 pathway (perhaps to an antagonistic muscle) resulting in inhibition of that pathway. What else may cause either up-regulation (facilitation) or down-regulation (inhibition) of the neural system thereby affecting the musculature, which holds the skeleton? Some of the possibilities here include trigger points and tender points, emotional holding patterns, viscerosomatic reflexes, pain inhibition and so on. Once these causative mechanisms are identified and begin to be addressed, the next consideration is the chronicity of the various holding patterns and how, across time, this may have resulted in creep or contracture to the underlying passive tissues, such as ligaments, fascia and joint capsules. Such chronicity, it should be noted, will also affect the accuracy of the neural feedback from mechanoreceptors within these passive tissues, thereby potentially perpetuating aberrant muscular tone. Having addressed the joint mechanics, the objective is to rebuild the function of the muscular system in the way that nature builds it in the first instance; by stimulating the inner-unit, tonic musculature first, and then to build upon that the outer-unit more phasic musculature afterwards. Re-visiting this process, in this sequence, is important as the neural properties of the inner unit musculature are such that its lower threshold to stimulus makes it more prone to influence from aberrant neural stimuli at the cord, such as pain or visceral afferent drives, or descending from the higher centres, such as limbic-emotional drives. By considering patients as athletes and training them to develop both hypertrophy in relevant musculature and to tolerate loads that are fast, multidirectional and sometimes unpredictable, they are provided with the broadest set of tools to both perform to their optimum and to minimize risk of future injury or re-injury.
References Baechle, T., Earle, R., 2000. Essentials of Strength Training and Conditioning, second ed. Human Kinetics, Champaign, IL. Barnes, M., 1997. The basic science of myofascial release: morphologic change in connective tissue. J. Bodywork Mov. Ther. 1 (4), 231e238.
M. Wallden Comerford, M., Mottram, S., 2001. Functional stability retraining: principles and strategies for managing mechanical dysfunction. Man. Ther. 6 (1), 3e14. Hashemirad, F., Talebian, S., Olyaei, G., Hatef, B., 2010. Compensatory behaviour of the postural control system to flexion-relaxation phenomena. J. Bodywork Mov. Ther. 14 (2). Hides, J., Carolyn, A., Richardson, C., Jull, G., 1996. Multifidus muscle recovery is not automatic after resolution of acute, first episode low back pain. Spine 21, 2763e2769. Hunter, G., 2005. Hamstring strain in professional football. In: Football Association Medical Society Non-league Conference, Lilleshall, UK, October 2005. Janda, V., 1978. Muscles, central nervous motor regulation and back problems. In: Korr, M. (Ed.), Neurobiologic Mechanisms in Manipulative Therapy. Plenum Press, New York, pp. 27e41. Kuno, M., 1989. A hypothesis for neural control for the speed of muscle contraction in the mammal. Adv. Biophys. 17, 69e95. Lederman, E., 1997. Fundamentals of Manual Therapy. Churchill Livingstone, Edinburgh, p. 105. Lee, D., 2004. The Pelvic Girdle. Churchill Livingstone. Liebenson, C., 1999. Motivating pain patients. J. Bodywork Mov. Ther. 3 (3), 143e146. Panjabi, M., 1992. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J. Spinal Disord. Tech. 5 (4), 382e389. Poliquin, C., 2006. The German Body Comp Program. Poliquin Performance Center, East Greenwich, RI. Sahrmann, S., 2002. Diagnosis and Treatment of Movement Impairment Syndromes. Mosby. Schleip, L., Findley, T., Chaitow, L., Huiging, P., 2012. Fascia: the Tensional Network of the Human Body: the Science and Clinical Applications in Manual and Movement Therapy. Churchill Livingstone. Schleip, R., Mu ¨ller, D.G., January 2013. Training principles for fascial connective tissues: scientific foundation and suggested practical applications. J. Bodywork Mov. Ther. 17 (1), 103e115. Stecco, C., Gagey, O., Belloni, A., et al., 2007. Anatomy of the deep fascia of the upper limb. Second part: study of innervation. Morphologie 91, 38e43. Wallden, M., April 2013. The primal nature of core function: in rehabilitation & performance conditioning. J. Bodywork Mov. Ther. 17 (2), 239e248. Wyke, B., 1979. Neurological mechanisms in the experience of pain. Acupunct. Electrother. Res. 4, 27e35.
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Facilitating change through active rehabilitation techniques M. Wallden, MSc Ost Med, BSc (Hons) Ost Med, DO, ND Primal Lifestyle Ltd., United Kingdom
Over the last century, the large focus of rehabilitative healthcare has been on passive techniques; what can “I” as the therapist do “to you” as the patient, in order to help you feel better? However, with a growing understanding, both of the neurophysiology and of motivational concepts, it has become clear that active rehabilitation is essential in the effective long-term resolution of pain and biomechanical dysfunction (Lederman, 1997), as well as in the empowerment of the patient (Liebenson, 1999). As this understanding has grown, a raft of interventions have arisen, from self-stretching targeting muscles and fascia, self-mobilization of the joints, muscle activation, core stability, and strength training, right the way through to more ballistic forms of performance conditioning (Fig. 1). In this paper, a logical sequence of rehabilitation is presented, along with a more in-depth review of Panjabi’s model of joint stability (Panjabi, 1992), which should allow clinicians and patients to understand better where they may be in the rehabilitative process and what path they can follow to return to full function. This coherent chronological rehabilitative formula, detailing techniques ranging from stretching, through to ballistic, e-concentric loading protocols, are potentially important for full rehabilitation for both athletes and for the everyday patient. As a brief summary, the proposed model for the rehabilitative sequence is as follows: E-mail address: [email protected]. 1360-8592/$ - see front matter ª 2013 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jbmt.2013.09.004
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Received 2 September 2013; accepted 2 September 2013
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Figure 1 Adapted from Lederman (1997), A) describes the process when a passive technique is applied to a patient; the effect being largely mediated at the cord level and therefore short-term in effect. B) describes the process when a patient is actively engaged in the rehabilitative process, where new patterns of movement can be coached and formed as motor programs.
An underlying premise of this approach is the recognition that everyone is an athlete, with an athletic requirement to meet; whether that requirement is simply to resist and move in a field of gravity, or whether they have more specific demands based on job, vocation or activities of daily living. There are several hidden factors that may “trip-up” the rehabilitative process too, which will also be touched on to raise clinical awareness of them, to ensure they don’t surreptitiously de-rail the patient’s return to full function.
neural subsystem regarding joint position which, in turn allows the nervous system to activate the musculature appropriately to control joint movement and stability; thereby minimizing stress on the passive subsystem.
Before the first assessment Prior to assessment, it may be useful to review a second model: Panjabi’s (1992) model of joint stability (see below). As much as this is already well understood and regularly described in previous editorials, it is useful to examine it one more time in order to gain clarity on what the therapeutic goal is in this context (Fig. 2). The model informs us that for optimal joint function each of the 3 key subsystems must be functional and working in harmony; the passive subsystem, the active subsystem and the neural subsystem. In a simplistic view of the model, the “passive” subsystem comprises the joints and connective tissues containing an abundance of mechanoreceptors which feedback to the
Figure 2 Panabi’s model of joint stability. Often the passive subsystem is considered to be distinct from the musculature, but there are passive tissues associated with and embedded within the muscular system; some of which are trainable.
The active subsystem The active subsystem may be further divided into inner unit musculature and outer unit musculature. The inner unit muscles, described in detail elsewhere (Wallden, 2013) contain a preponderance of type 1, tonic muscle fibres, which have differentiated into these slower twitch, postural fibres due to being activated by tonic motoneurons. In turn, the tonic motoneurons have behaved “tonically” as opposed to phasically, based on how they were utilized during infant development (Fig. 3). The outer unit muscles contain a preponderance of type 2 muscle fibres, which have differentiated into these faster twitch, mobiliser fibres due to being activated by phasic motoneurons. In turn, the phasic motoneurons have behaved “phasically”, phasing on and off, as opposed to holding consistent tone, based on how they were utilized during infant development. (Kuno, 1989). The “inner” inner unit Interestingly, much of the focus in the field of motor control in recent years has been the “inner unit” or local stability musculature which have a low threshold to stimulus and
533 therefore both fire ahead of the outer unit musculature (the “feedforward mechanism”), and are also more prone to inhibition from aberrant neural stimuli, such as pain (see Wallden, 2013 for more discussion & further references). However, less attention has been focused on the mechanoreceptive role of the passive subsystem; which, in one way, can be interpreted as the “inner” inner unit. As far back as 1972, Wyke identified that the outer part of the joint capsule is densely packed with type 1 mechanoreceptors which communicate directly with the inner unit musculature. Conversely, the inner part of the joint capsule is richly innervated with type 2 mechanoreceptors, which communicate with the outer unit musculature (Fig. 4). Of course, when a joint moves, the outer part of the joint, being furthest from the axis of rotation, will be stretched first. This means that subtle motion at the joint will excite the inner unit musculature first and increase tone, stabilizing the joint. If a greater stretch occurs due to a greater range of motion at the joint, the outer unit musculature will become stimulated providing, greater rigidity around the joint with larger leverages to resist that stress.
Figure 3 Muscles can be loosely categorized into tonic and phasic, with differing characteristics. These are listed in the table above, but should not be considered universal as there are many exceptions, especially to the lengthen/weaken: shorten/tighten category.
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that it responds to movement with hydration and elasticity and to lack of movement with dehydration and crystallization (Schleip and Mu ¨ller, 2013). In addition the fascia has smooth muscle cells embedded within it meaning that it will reflect the underlying autonomic tone; a parasympathetic dominance will facilitate more relaxed fascia, while reciprocally sympathetic dominance will facilitate greater tension in the fascia (Barnes, 1997). Other aspects of the passive system lesser discussed may include hydration of the joints and discs, viscera as viscous (non-compressible) functional stability units, blood as a connective tissue, and connective tissues infiltration and integration into muscular tissue; not just as an apparently discrete entity, such as endomysium, but also as components of the contractile unit itself such as the series and parallel elastic components (discussed further below).
Figure 4 Stretch to type 1 mechanoreceptors excites the tonic motoneurons stimulating inner-unit function, while a larger stretch to the type 2 mechanorecepors excites the phasic motoneurons and outer-unit function. In this way, the mechanoreceptors in the outer joint capsule can be seen as the precursor to inner-unit function. From a rehabilitation perspective, this helps to inform the clinician that to isolate inner unit musculature, smaller, subtle movement is likely to be most effective.
A more detailed view, which is useful in many instances to overcome clinical road-blocks, is to understand more about the range of connective tissues that offer stability, and how these both influence and can be influenced by various neural factors, and how this may selectively affect function of the muscular system.
The passive subsystem In terms of total afferent drive, it has been reported that the mechanoreceptive population may account for as much as 70% of all inbound information to the brain (Stecco et al., 2007). This information is typically associated with stretch or pressure, stimulating the mechanoreceptors within the fascia and connective tissues, stimulating a reciprocal contraction of the musculature, depending on degree of stretch (discussed above under The active subsystem). Connective tissues, having a lower density of elastin to collagen and a much lower blood supply than active tissues, such as muscle, tend to be more susceptible to injury than muscle; and, once damaged, will typically take longer to heal. Many professions work directly with the joints to mobilize and manipulate them as it has been shown that such mechanoreceptive stimulation appears to help in reducing pain and improving function by blocking nociceptor activity, inhibiting overactive muscles associated with that segmental level and optimizing joint play. Until recently, the fascia was relatively ignored as part of the passive subsystem, but it has been brought increasingly into the awareness of the rehabilitation and performance communities by the work of many, and Schleip in particular (Schleip et al., 2012). What is of importance here is that the tension of the fascia is not only related to muscle tone, but the fascia also has crystalline properties meaning
The neural subsystem The neural subsystem is undoubtedly complex, so this discussion is kept simple for practical purposes. The nervous system both receives sensory and sends out motor information; functioning in the adult primarily as a “sensory-motor” system (as opposed to in a young infant, where for the first 3 months or so after birth it is primarily motor-sensory). In other words, throughout most of our lives the information going out to the muscles (the active subsystem) is only as accurate as the information coming in to the central nervous system (or neural subsystem). In a sensory-motor based system such as the human being, compromised information due to injury, pain, deconditioning, impaired proprioception, aberrant neural stimuli, such as (inhibition, facilitation, trigger point development, limbic-emotional drives, viscero-somatic inputs) must, by definition, detrimentally affect motor output. Examples here may include a situation such as a flat foot where the plantar fascia has undergone creep due to overpronation. This means that as the foot kinematically moves into pronation, the mechanoreceptors in the plantar fascia and plantar aspects of the joints of the mid-foot will not be stimulated until it is “too late” and the foot has overpronated. Plantar fascia that has not undergone creep will be stretched as the foot begins to pronate, stimulating the embedded mechanoreceptors, resulting in activation of the anti-pronation (supinator) musculature. Similarly, at the spinal level, the posterior ligamentous system of the spine may undergo creep due to poor ergonomics, such as sitting in end-range lumbar flexion for prolonged durations. This means that whereas under normal circumstances when the spine reaches approximately 45 of forward flexion the mechanoreceptors would send an inhibitory neural drive to the cord to shut-off the lumbar extensors and engage the transversus abdominis; in this instance, as the spine moves into flexion, the preinduced creep in the posterior ligamentous system would mean that the mechanoreceptors are not stimulated until deeper into the flexion movement (say, 55 ) which poses greater risk to spinal structures, such as discs, due to compressive loading from the increased lever arm in tandem with the late shut-off of the lumbar erectors (Hashemirad et al. 2010).
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Initial assessment Correct adverse neurological inputs In this author’s clinical experience, the following observations in this section would seem to be useful as guidelines: Posture may be used as a quick-screen overview. Optimal postural findings indicate a minimized risk of adverse neurological factors, but do not indicate their absence. Functional movement screening, including gait analysis and other key movement patterns such as squatting, lunging, bending and so on, provides a more comprehensive assessment. Optimal postural findings in conjunction with optimal movement assessment indicate a significantly decreased risk of adverse neurological factors, though is still not a thorough, foolproof finding as many clients (athletes, or those with good kinesthetic awareness in particular), may exhibit difficult-to-spot compensation patterns, leading to false-negative conclusions. It is, however, extremely rare in clinical practice to find either optimal postural, or optimal movement screenings. In postural screening, commonly what can be observed are gross muscle imbalances expressed as one of the following: Upper-crossed syndrome Lower-crossed syndrome Layered (stratification) syndrome . and any of these may be accompanied by a sway posture, which is where the pelvis can be observed in the lateral view to have swayed ahead of the plumb-line. In movement screening, what is often observed are signs of poor movement skill, facilitation of certain muscle groups, deconditioning, inhibition or poor stabilization. Examples of poor movement skill may include someone who attempts to pick up or move a load in an arm-dominant fashion, instead of utilizing their body as an integrated unit (expression of load mobilization should typically follow a legsetrunkearms sequence). This is poor, or inefficient motor sequencing. Deconditioning of the core musculature may result in the above arm-dominant sequencing, but other examples of deconditioning commonly observed are quadriceps dominance in squat or lunge movements due to deconditioning of the gluteus maximus. Inhibition is often seen in the gluteus medius and is expressed as a Trendelenburg pattern, or compensated Trendelenburg; in the transversus abdominis, and is expressed as oblique dominance or rectus abdominis dominance; in the serratus anterior and is expressed as scapula winging; or in the vastus medialis obliquus, often as a result of pain inhibition or a simple lack of stabilization requirement at the knee in ADL’s e often expressed as retropatellar pain.
Facilitation may be seen in certain muscle groups, usually as a result of trigger-points, tender points and compensatory motor patterns. Common examples of facilitation include hitching of the shoulder during arm abduction due to facilitation (often accompanied by trigger points) in the scapula elevator musculature (upper trapezius and levator scapulae); or winging of the scapula (inhibition of serratus anterior) due to facilitation of the pectoralis minor. Trigger points are commonly found in facilitated tissues. Other adverse neurological inputs can include pain, viscero-somatic reflexes, central sensitization, trigger point formation, facilitation and inhibition (among others).
Correct lengthetension relationships As mentioned above, the major muscle imbalances, as well as other aberrant posture may be the cause or effect of dysfunctional lengthetension relationships. Without any other apparent adverse neurological inputs, it is likely that lengthetension relationships may be held through habit and facilitation of neural pathways. Lengthetension relationships should always be addressed first by stretching shorter, more facilitated musculature that may be inhibiting longer, apparently weaker musculature (such as a pectoralis minor inhibiting a serratus anterior). Janda showed in 1972 that when the lumbar erectors, for example, are short and facilitated, they will fire even when the patient is attempting to perform a sit up from the floor, where they should be quiescent. However, after stretching the lumbar erectors, they become electromyographically silent and more neural drive is allowed to reach the key muscles involved in the situp movement, such as rectus abdominis (Janda, 1978). Hence, as a clinical strategy, it would seem important to stretch tight, potentially facilitated musculature before addressing apparently weaker, longer musculature as it may simply be inhibited.
Correct chronic joint adaptations Arguably, a joint, being a passive structure, cannot be “held” out of position in and of itself without a preceding lengthetension imbalance creating chronic adaptations in the joint capsule. Picture a life size plastic skeleton with rubberized joint capsules and now try to create a joint adhesion, a facet lock, or a pelvic torsion*. It really is not going to happen easily without a muscular system to hold it out of place. *Of course there may be some exceptions to this statement, but it appears none that have been conclusively validated. What, most probably, creates a majority of changes to joint play are chronic (long-term) length-tension imbalances in the surrounding musculature creating contracture of the connective tissues on one side of the joint and, reciprocally, creep* on the opposite side of the joint. In this instance, it is the chronicity of the length-tension imbalance of the musculature that ultimately dictates the severity of the joint dysfunction. *Contracture can be defined as a permanent shortening of a muscle or joint usually in response to prolonged
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Simply put, the information going out, can only be as good as the information coming in. The human functions as a biocomputer with the motor control being entirely dependent on the information coming in to the system.
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536 hypertonia, while creep can be defined as the tendency of a solid material to move slowly or deform permanently under the influence of mechanical stresses (Fig. 5).
higher centres; the process of progressing from a “conscious competent” to becoming an “unconscious competent” (Wallden, 2013).
Stimulate & condition tonic motoneurons & inner unit musculature
Re-assess
Since tonic motoneurons are predominant to the inner unit musculature, it is important that once the joint mechanics, lengthetension relationships and other neurological inputs are optimized, the inner unit should be stimulated actively. This process is used to help re-establishment of new, more functional motor patterns, through active engagement of the motor cortex to help facilitate the neural pathways to the tissue. Subsequent repetition of these targeted, isolated exercises is designed to help the process to become increasingly reflexive, requiring less and less activation of the executive
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Of course, reassessment is often a continuous clinical process, but if the patient hasn’t been through this process, this is a key time for reassessment to evaluate whether the patient is ready to move to higher, more functional loading interventions.
Condition phasic motoneurons & outer unit musculature While conditioning the tonic motoneurons and inner unit musculature calls for subtle techniques, such as breathwork, Feldenkrais, Alexander Technique, motor control methodologies and so on. Conditioning of the phasic motor neurons and outer unit musculature is built on that important foundation and spans across a broad range of conditioning, from common clinical rehabilitation approaches, through to ballistic, sports-specific and injury prevention strategies. Loosely, beyond what is often termed “stability”, rehabilitation can, and ideally should, move into “strength” and “power” phases. These phases can be further subdivided many times, however, for the purposes of this piece, only strength-endurance and strength-hypertophy will be focused upon as subdivisions of the Strength category; with e-concentric loading and perturbation loading as subdivisions in the Power category.
Strength Strength training is a term often used distinctively from endurance training. The purpose of strength training is clearly to build strength in the targeted tissue(s); whereas endurance training may either increase or decrease strength depending on the base level of conditioning of the individual.
Figure 5 A) When muscle balance is equal either side of the joint, the joint maintains its instantaneous axis of rotation, balance is maintained in the joint capsule and passive subsystem, and cumulative microtrauma to the joint is minimized. B) When muscle imbalance is present, one side of the joint undergoes compressive stresses, and the other side traction stresses which, across time, result in contracture on the former and creep on the latter side of the joint. Adapted from Comerford and Mottram (2001).HYPERLINK
Strength-endurance Strength-endurance training, or “extensive” training, is classified as resistance training with loads of up to 50% of the maximum load the individual can lift or move, which typically means they will be able to perform 12 or more repetitions of that exercise; and thereby targets a combination of the type 1 and type 2a fibres. For example, if one were to pick up a dumbbell and press it above one’s head, but can only do this 8 times before becoming fatigued, this load is too heavy for strength-endurance training. From this perspective then, strength-endurance training can be important in building postural strength and in learning (or re-learning) new movement patterns, such as a squat, or a deadlift (bend) movement pattern. Strength (hypertrophy) training Strength training covers a broad range, from loads that can be lifted only once, through to loads that can be lifted hundreds of times, however, classically strength training
tends to cover the range of loads that can be lifted from 6 to 12 times before fatigue (Baechle and Earle, 2000). Within this range, research has indicated that loads lifted in the 8e12 rep range (ie which can be lifted 8e12 times before fatigue halts further repetitions) is the optimal zone for inducing hypertrophy (Baechle and Earle, 2000) (Fig. 6). Why would the clinician want to introduce hypertrophy training to their client, is there any benefit in terms of rehabilitation? The answer to this is yes, but only at the right time in the rehabilitation process. If the clinician were to load a patient too early with the kinds of loads that induce a strong hypertrophy stimulus, there is a good chance that this would reinforce faulty and compensatory outer-unit dominant motor patterns. For example, prescribing a deadlift with hypertrophy loading variables for a patient whose inner unit is not firing will just reinforce their outer unit dominance, such as rectus abdominis dominance or lumbar erector firing and trigger point development. There are
537 several potential reasons why hypertrophy training is important in rehabilitation. Firstly, by its very nature, hypertrophy training is stimulating a growth and repair process, including an increase in growth hormone and in receptors for such hormones (Poliquin, 2006) setting up an optimal anabolic environment for tissue repair. Secondly, intrinsic, or inner unit musculature, becomes inhibited in the presence of nociceptive drives. For example, Hides et al. (1996) demonstrated that within 24 h of the onset of pain the lumbar multifidus had apparently “shrunken” on the symptomatic side and the symptomatic level to, on average, 69% of the cross sectional area of the contralateral multifidus. What is known is that atrophy cannot occur that quickly. Instead, this is explained by neural inhibition of the muscle. Hence, if the pain can be managed effectively and the intervention is early enough, the cross sectional area of the multifidus (in this instance) may be “recovered” simply by the activation techniques commonly taught in manual therapy circles. However, the
Figure 6 This diagram summarizes the typical effects of training with loads at a certain repetition range. Along the base of the diagram are numbers indicating the number of repetitions the exerciser can complete before fatigue. The heavier the load the lower the number of repetitions achievable (and, in strength & conditioning, this generally means the higher the number of sets, and the longer the required rest period between sets). The opposite can be seen at the other end of the repetition range e higher reps Z less sets Z shorter rest periods between sets. What is useful to understand is that the hypertrophy effect of training is greatest in the 8e12 rep range’ hypertrophy gains being represented by the diamond in the middle of the diagram.
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538 issue here is that if the pain has been present for longer than 2 weeks, the process of atrophy will have begun. Hence, loss of cross-sectional area in the muscle for patients whose pain has exceeded 2 weeks duration will be a combination of both inhibition of the muscle and atrophy of the muscle tissue. Across time, this leads to a clear “mothballing” appearance on MRI. Consequently, introducing a low level, activation technique will certainly help with facilitating the neural pathway and improving crosssectional area through simple contraction, but to reverse the atrophy requires a hypertrophy stimulus; and to produce a hypertrophy stimulus requires loading at the 8e12 rep-max level (a weight or load that can only be lifted 8e12 times before complete fatigue). Thirdly, one of the known mechanisms of joint stabilization is the hydraulic amplifier effect of muscle contraction, creating cross-sectional expansion of the muscle within its fascial sheath e the epimysium (Lee, 2004). This increased intra-epimyseal pressure causes an increased stiffness of the muscle, which means that where that muscle crosses one or more joints, those joints will be more stable the more hypertrophied the muscle. Additionally, this intra-epimyseal pressure doesn’t just create stiffness, but also produces an erectile force lifting the spine (for example) upward. Of course, the stiffness produced in the epimysium is thereby transferred via the surrounding fascia into adjacent and interconnecting musculature in a kind of activeepassiveeactive stability process. Lastly, and perhaps most importantly, although muscle is classified as being the “active” subsystem in joint stability, it can also be viewed, as in point three above, as part of the passive subsystem due to its integration with the fascia. An additional mechanism, where muscles’ function traverses
M. Wallden into the role of the passive subsystem is where it comes to both the series elastic components and the parallel elastic components of the muscle. Between each sarcomere (the functional contractile unit within the muscle) there is a series elastic component (SEC), while down the lateral aspect of each sarcomere can be found parallel elastic components (PEC). Combined, these SEC’s and PEC’s behave like springs, giving the muscle a passive, spring-like resistance to stretch (and recoil when it is stretched). It is the number of sarcomeres in parallel, plus the size of these sarcomeres, that determines the stiffness of the muscle (Sahrmann, 2002). Somewhat intuitively, the greater the stiffness of the muscle, the greater “passive” protection is offered to the joint by the muscle. Somewhat counterintuitively, the greater the stiffness of the muscle, the less prone it is to injury itself (Hunter, 2005), as with more and stronger “springs” between and around its contractile elements, it’s less likely to be overstretched (Fig. 7) When a muscle is trained with loads that induce a growth response, the process accounting for the growth is largely attributed to hypertrophy (an enlargement of the sarcomeres and their respective “springs” the SEC’s and PEC’s), while there is also some evidence there may be hyperplasia (an increase in the number of sarcomeres in parallel). Either way, whether there are just larger springs, or larger springs and more of them, the stiffness of the muscle will be increased and underlying joint more protected. Why is this important? The neural component of joint stability; the nervous system, has a response time that is too slow for some stimuli. If a patient recovering from a whiplash, for example, where the passive subsystem has been traumatized, was given a rehabilitation program which focuses on
Figure 7 A) Depicts sarcomeres both in series going horizontally across the image and in parallel going vertically down the image, illustrating schematically their actinemyosin interdigitation. B) Depicts sarcomeres, in series, at a lower magnification. C) Depicts sarcomeres in series at a higher magnification illustrating both their series elastic components between the sarcomeres and their parallel elastic components down the lateral border of the sarcomeres (in red).
Facilitating change through rehabilitation
Power Why would the clinician want to introduce power training to a client? Is there any benefit for non-athletes? Firstly, it is important to address the issue of exactly who is an athlete and who is not. Anyone who is alive and moving has an athletic requirement; especially those who live in a gravitational field! Hence it is entirely feasible and correct to define everyone as an athlete. The rationale for conditioning at the power level is much the same as the rationale for training to induce strength-hypertrophy; because the average person may well encounter “power” requirements in activities of daily living, such as the examples described above in the Strength section. Power can be defined as the time rate of doing work, where work is the product of force exerted on an object and the distance the object moves in the direction in which force is exerted (Baechle and Earle, 2000). Force is calculated by the equation: force Z mass acceleration. Hence, power training is simply the movement (force) of loads (mass) under conditions of acceleration; an “explosive” or high-speed form of strength training. How is this relevant to rehabilitation? Power training does not induce hypertophy nearly as much as strength training, so the benefit is different. Power training performed concentrically, also does not convey significant protective benefit to the passive subsystem of the joints, as linear directional acceleration is usually a higher-centre decision, under conscious control and is therefore appropriately stabilized by the nervous system (neural subsystem) and inner-unit (active subsystem) musculature. What is often poorly anticipated by the nervous system, however, are non-linear accelerations, such as the pull of dog on its lead, or a horse while leading it out, or change of direction decelerations, such as “jarring” in the car, or on step. While, as described above, these may sometimes happen too quickly for the nervous system to respond, in other instances, a pot-hole may be seen at the last minute, but it is too late to avoid hitting it, or the dog may give an indication it is about to
lurch off. This gives the patient crucial milliseconds to prepare and brace for the impending force. E-concentric loading As described above, e-concentric loading, in this context, can be defined as the process by which a muscle contraction rapidly switches from eccentric to concentric. This is the more common way that a muscle is utilized in functional movement patterns. A concentriceeccentric movement pattern is primarily used for “start speed” or “start strength” such as exploding out of the blocks for a sprinter, or doing a standing long jump, but as soon as that athlete starts to move, then most of the power is generated by e-concentric processes. To train for these potential scenarios described in the section above, e-concentric loading is a useful tool to condition the nervous system and build both an appropriate response and effective muscular power to protect the underlying passive subsystem. Essentially it is about effectively controlling the deceleration, in order that the body can accelerate back out of the movement pattern towards neutral. This optimally prepares the body to accept loads and so would be important in the training of those in contact sports, combat sports, or those who may crash, or fall as part of their pursuits. Hence it is good and important conditioning for life in general; teaching the body how to effectively handle rapid loading and unloading. Perturbation loading Perturbation training is similar to e-concentric training, but is typically more random in its application and therefore trains versatility in the body’s response to loading. Perturbation may be conducted using very light loads, such as those induced by swinging a tennis ball at the end of a sock in a circle above your head, then moving the arm position to different angles and inclinations so as to change the angle of the forces being induced through the shouldereneckecore. Other tools, such as the Bodyblade, which works with rhythmical or oscillatory forces, working with controlled falling, with the Swiss ball, or partner work, involving a form of controlled wrestling can be utilized to train perturbation. The forces involved in this rapid change in direction can be significant and hence can train the patient to be able to effectively anticipate, tolerate, absorb and dissipate aberrant forces more efficiently in activities of daily living. Other examples of perturbation and e-concentric training can be viewed at https://www.youtube.com/user/ primallifestyleltd.
Summary The proposal in this paper is to view the body from the perspective of a skeleton whose bones cannot be magically held out of alignment without some alteration to the tone of the musculature holding that skeleton. The question then becomes what controls may affect the function of the muscular system; the answer to which is the neural system. This leads onto the next question, what can influence the neural system, and here there are many possibilities from overuse of a given neural pathway creating facilitation of that pathway, versus underuse of a
PREVENTION & REHABILITATION: REHABILITATION
the inner unit musculature of the neck, that program may be successful in rebuilding postural stability, but it may confer no real benefit in many dynamic real-life scenarios, such as, receiving an unexpected jolt from a pothole while driving down the road; getting a sudden tug on the dog on a lead who has just spotted a squirrel in the bushes; or missing a step while carrying a child down an unfamiliar stair-case. These are all everyday examples of situations where the function of the neural and active systems, just won’t be effective, and therefore the stress is transferred into the passive system; but if the passive system is already compromised, damaged or has undergone creep, then injury (or reinjury) is the likely outcome. Since the passive system, by its nature, has a poor blood supply and long healing duration e often measured in months and years, rather than days and weeks for the active system e it strategically therefore makes sense to concentrate efforts on building “passive” support through hypertrophy training which could feasibly start within 6e8 weeks post-accident depending on the success of pain management and progress in establishing inner-unit function.
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540 pathway (perhaps to an antagonistic muscle) resulting in inhibition of that pathway. What else may cause either up-regulation (facilitation) or down-regulation (inhibition) of the neural system thereby affecting the musculature, which holds the skeleton? Some of the possibilities here include trigger points and tender points, emotional holding patterns, viscerosomatic reflexes, pain inhibition and so on. Once these causative mechanisms are identified and begin to be addressed, the next consideration is the chronicity of the various holding patterns and how, across time, this may have resulted in creep or contracture to the underlying passive tissues, such as ligaments, fascia and joint capsules. Such chronicity, it should be noted, will also affect the accuracy of the neural feedback from mechanoreceptors within these passive tissues, thereby potentially perpetuating aberrant muscular tone. Having addressed the joint mechanics, the objective is to rebuild the function of the muscular system in the way that nature builds it in the first instance; by stimulating the inner-unit, tonic musculature first, and then to build upon that the outer-unit more phasic musculature afterwards. Re-visiting this process, in this sequence, is important as the neural properties of the inner unit musculature are such that its lower threshold to stimulus makes it more prone to influence from aberrant neural stimuli at the cord, such as pain or visceral afferent drives, or descending from the higher centres, such as limbic-emotional drives. By considering patients as athletes and training them to develop both hypertrophy in relevant musculature and to tolerate loads that are fast, multidirectional and sometimes unpredictable, they are provided with the broadest set of tools to both perform to their optimum and to minimize risk of future injury or re-injury.
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