Concepts and Principles of Movement

After reviewing this chapter, the reader will be able to discuss:

1 The components of and differences among the three models of the movement system.

2 How the muscular, nervous, and skeletal systems are affected by repeated movements and sustained postures.

3 How repeated movements and sustained postures contribute to the development of musculoskeletal pain syndromes.

4 The concept of relative flexibility, its relationship to muscle stiffness, and its implications in the role of exercise to stretch muscles.

5 The role of a joint’s directional susceptibility to movement in the development of a musculoskeletal pain syndrome.

Kinesiologic Model

Composition of the Model

This text discusses musculoskeletal pain syndromes arising from tissue alterations that are caused by movement. Movement is considered a system that is made up of several elements, each of which has a relatively unique basic function necessary for the production and regulation of movement. Various anatomic and physiologic systems are components of these basic elements (Figure 2-1). To understand how movement induces pain syndromes, the optimal actions and interactions of the multiple anatomic and physiologic systems involved in motion must be considered. The optimal function and interaction of the elements and their components are depicted in the following kinesiologic model.

Figure 2-1 The kinesiologic model.

The elements of the model are (1) base, (2) modulator, (3) biomechanical, and (4) support. The components that form the base element, the foundation on which movement is based, are the muscular and skeletal systems. The components of the modulator element regulate movement by controlling the patterns and characteristics of muscle activation. The modulator element of motion is the nervous system, because of its regulatory functions (described in the sciences of neurophysiology, neuropsychology, and physiologic psychology). Components of the biomechanical element are statics and dynamics. Components of the support element include the cardiac, pulmonary, and metabolic systems. These systems play an indirect role because they do not produce motion of the segments but provide the substrates and metabolic support required to maintain the viability of the other systems.

Every component of the elements is essential to movement because of the unique contributions of each; however, equally essential is the interaction among the components. Each has a critical role in producing movement and is also affected by movement. For example, muscular contraction produces movement, and movement helps maintain the anatomic and physiologic function of muscle. Specifically, movement affects properties of muscle, such as tension development, length, and stiffness, as well as the properties of the nervous, cardiac, pulmonary, and metabolic systems. (The changes in these properties are discussed in detail later in this chapter.)

Clinical Relevance of the Model

Optimal function of the movement system is maintained when there is periodic movement and variety in the direction of the movement of specific joints. For example, a posture should not be sustained for longer than 1 hour, based on studies of the effects of sustained forces. McGill and associates have shown that 20 minutes in a position of sustained flexion can induce creep in the soft tissues, requiring longer than 40 minutes for full recovery.⁴¹ Two types of effect on soft tissues from sustained forces are described: (1) time-dependent deformation of soft tissues, and (2) soft tissue adaptations involving protein synthesis.²³ A study by Light and colleagues demonstrates that 1 hour per day of sustained low-load stretching produces significant improvement in range-of-knee extension in patients with knee flexion contractures when compared with high-load stretching produced during short duration.³⁷ The implication is that short duration stretching produces temporary deformation of soft tissues, but 1 hour of stretching may be a sufficient stimulus for long-term soft-tissue adaptations. When there is variety in the stresses and directions of movement of a specific joint, the supporting tissues are more likely to retain optimal kinesiologic behavior (defined as precision in movement) than when there is constant repetition of the same specific movement or maintenance of the same specific position.

Pathokinesiologic Model

Composition of the Model

Pathokinesiology is described by Hislop as the distinguishing clinical science of physical therapy, and it is defined as the study of anatomy and physiology as they relate to abnormal movement.²⁵ Based in part on word construction and in part on clarification of causative factors, pathokinesiology emphasizes abnormalities of movement as a result of pathologic conditions. The pathokinesiologic model (Figure 2-2) depicts the role of disease or injury as producing changes in the components of movement, which result in abnormalities of movement. In the Nagi model of disablement,⁴⁵ disease leads to impairments that cause functional limitations with the possible end result of disability. Impairments are defined as any abnormality of the anatomic, physiologic, or psychologic system. Therefore abnormalities of any component system or of any movement are considered impairments.

Figure 2-2 The pathokinesiologic model.

In the pathokinesiologic model, a pathologic disease such as rheumatoid arthritis, produces lesions in the skeletal components because of the degenerative changes in joints. The degenerative joint changes cause alterations in movement of the joint and possibly in movements involved in functions such as ambulating or self-care activities. This model suggests that in addition to the changes in skeletal components, such as joint structures and movement characteristics, there are also changes in the neurologic, biomechanical, cardiopulmonary, and metabolic components. Depending on the severity of the movement impairments, the consequence can be disability.

Clinical Relevance of the Model

In the pathokinesiologic model, the pathologic abnormality is the source of component impairments, which then causes movement impairments, functional limitations, and often disability. Because of the interaction of the component systems as depicted in the model, identifying the secondary changes in each system is as important as understanding the primary pathologic effect on a system component. For example, in the case of hemiparesis, the movement dysfunction is the result of an abnormality involving the nervous system. Factors contributing to movement dysfunction include but are not limited to (1) an inability of the central nervous system to recruit and drive motor units at a high frequency,⁵⁶ (2) the co-activation of antagonistic muscles,¹³ (3) a secondary atrophy of muscles that compromise contractile capacity,⁷ (4) the stiffness of the muscle,⁵⁷ (5) a loss of range of motion from contracture,²¹ (6) the biomechanical alterations that are the result of insufficient and inappropriate timing of muscular activity,^12,51 and (7) an internal sensory disorganization.¹² In addition, the alterations of metabolic demands during activity and the aerobic conditioning of the patient must all be considered as contributing factors in the movement impairment. The degree of involvement of each of these factors and their influence on function varies from patient to patient. Physical examination formats should address all these factors and their relative importance to the patient’s functional problem. Decisions that lead to the formation of the management program must be based on the potential for remediation of each of the contributing factors and ranked according to their relative importance to the functional outcome of the patient.

Kinesiopathologic Model

Rationale for the Model

A common belief is that movement impairments are the result of pathologic abnormalities, but the thesis of this text is that movements performed in daily activities can also cause impairments that eventually lead to pathologic abnormalities. Therefore a different model is proposed to characterize the role of movement in producing impairments and abnormalities. The empirical basis of this model stems from observations that repetitive movements and sustained postures affect musculoskeletal and neural tissue. The cumulative effect of repetitive movements is tissue damage, particularly when the movements deviate from the optimal kinesiologic standard for movement. Human movements involve similar internal and external forces as do mechanical systems.⁴⁹ In mechanical systems, maintaining precise movement is of such importance that the science of tribology is devoted to the study of factors involved in movement interactions. Tribology is defined as the study of the mechanisms of friction, lubrication, and wear of interacting surfaces that are in relative motion.¹ Based on the similarities of biomechanical and mechanical systems, the premise for ensuring the efficiency and longevity of the components of the human movement system is maintaining precise movement of rotating segments. Although the adaptive and reparative properties of biological tissues permit greater leeway in maintaining their integrity than do nonbiologic materials, it is reasonable to assume that maintaining precise movement patterns to minimize abnormal stresses is highly desirable.

A useful criterion for assessing precise or balanced movement is observing the path of instantaneous center of rotation (PICR) during active motion (Figure 2-3). The instantaneous center of rotation (ICR) is the point around which a rigid body rotates at a given instant of time.⁴⁸ The PICR is the path of the ICR during movement. In many joints the PICR is not easily analyzed and radiologic methods are necessary to depict the precision of the motion (Figure 2-4). These radiologic methods use movements that are performed passively and under artificial conditions. The joints in which the PICR is difficult to observe clinically include those of the knee and spine. The PICR of the scapulothoracic (Figure 2-5) and glenohumeral (Figure 2-6) joints can be observed visually, but it cannot be easily quantified.

Figure 2-3 As the knee moves from flexion to extension, successive instantaneous centers can be mapped, which is known as the instant center pathway. In the normal knee, the pathway is semicircular and located in the femoral condyle. (Modified from Rosenberg A, Mikosz RP, Mohler CG: Basic knee biomechanics. In Scott WN, editor: The knee, St Louis, 1994, Mosby.)

Figure 2-4 PICR of the knee. Line drawn perpendicular from the instantaneous center to the joint surface is normally parallel to the joint surface, indicative of a sliding motion between surfaces. (Modified from Rosenberg A, Mikosz RP, Mohler CG: Basic knee biomechanics. In Scott WN, editor: The knee, St Louis, 1994, Mosby.)

Figure 2-6 PICR of the glenohumeral joint.

Figure 2-5 PICR of the scapulothoracic joint.

Knowledge of the PICR and range of motion of the joint both guide observations and judgments about movement. Although it is rarely referred to specifically, the observation of the PICR is the guideline that physical therapists use to judge whether the joint motion is normal or abnormal. Anatomic and kinesiologic factors that determine the PICR and the pattern of joint movement are (1) the shape of joint surfaces, (2) the control by ligaments, and (3) the force-couple action of muscular synergists.⁷³

With normal or ideal movement of joints, the question arises, “What is the cause of deviations in joint movement when a pathologic condition or specific injury is not the problem?” Suggested causes of deviations in joint movement patterns are repeated movements and sustained postures associated with daily activities of work and recreation. For example, baseball pitchers and swimmers perform repeated motions and commonly experience shoulder pain.16,31 Prolonged sitting has been cited as a factor in the development of back pain.⁵² Cyclists who spend 3 hours riding their bicycles in a position of lumbar flexion have a reduced lumbar curve when compared with control subjects who do not ride bicycles.¹⁰

Therapists and other clinicians involved in exercise prescription believe that repeated movements can be used therapeutically to produce desired increases in joint flexibility, muscle length, and muscle strength, as well as to train specific patterns of movement. All individuals who participate in exercise accept the fact that repeated movements affect muscle and movement performance. Thus these individuals should also accept the idea that repeated motions of daily activities, as well as those activities of fitness and sports, may also induce undesirable changes in the movement components. Stretching and strengthening exercises performed for shorter than 1 hour are believed to produce changes in muscular and connective tissues. However, repeated movements and sustained postures associated with everyday activities that are performed for many hours each day may eventually induce changes in the components of the movement system. The inevitable result is the development of movement impairments, tissue stress, microtrauma, and eventually macrotrauma. In accordance with this proposed theory, the effects of repeated movements and sustained postures modify the kinesiologic model so that it becomes a kinesiopathologic model (Figure 2-7), that is, a study of disorders of the movement system.

Figure 2-7 The kinesiopathologic model.

Clinical Relevance of the Model

The kinesiopathologic model serves as a general guide for identifying the components that have been altered by movement. Identifying the alterations or suboptimal functions of components provides a guide to prevention, diagnosis, and intervention. If there is suboptimal function of any component of an element, operationally defined as an impairment, it may be considered a problem and corrected before the client develops musculoskeletal pain. Identifying impairments and correcting them before they become associated with symptoms is using the information incorporated in the model as a guide to prevention. If the impairment is not corrected and the repeated movements continue, the sequence of movement impairment leading to microtrauma and macrotrauma progresses with the consequence of pain and, eventually, identifiable tissue abnormalities.

If pain is present, the kinesiopathologic model can be used to identify all the contributing factors that must be addressed in a therapeutic exercise program. Reversal of the deleterious sequence requires the identification and correction of the movement and component impairments. More important than developing a therapeutic exercise program, the performance of functional activities that cause pain must be identified and corrected.

Based on clinical examinations, muscular, skeletal, and neurologic component impairments have contributed to musculoskeletal pain syndromes. (Each of these impairments is individually discussed in this chapter.) The key to diagnosis and effective intervention is the identification of all impairments contributing to a specific movement impairment syndrome. (Syndromes and their multiple associated impairments are discussed in the relevant chapter on diagnostic categories.)

How do repeated movements and sustained postures cause changes in the component systems? The prevailing characteristic of the muscular system is its dramatic and rapid adaptation to the demands placed on it. Most often, adaptations such as changes in strength are considered advantageous; however, changes in strength can also be detrimental and may contribute to movement impairments. Muscles become longer or shorter as the number of sarcomeres in series increases or decreases. Everyday activities can change the strength and length of muscles that alter the relative participation of synergists and antagonists and, eventually, the movement pattern.

Identifying the types of changes that occur in muscle and the causative factors for these changes is the key to maintaining or restoring optimal musculoskeletal health. Changes in muscle occur even when an individual lives a sedentary lifestyle; muscular changes are not limited to those who perform physically demanding work. The most sedentary occupation or lifestyle is associated with some form of repeated movement or sustained posture. For example, individuals who sit at a desk during most of the day perform many rotational or side-bending movements of their spine when they move from a writing surface to the computer or when they reach for the telephone or into a file drawer.

Movements repeated at the extremes of frequency (either high or low) and movements that require the extremes of tension development (either high or low) can cause changes in muscle strength, length, and stiffness. Similarly, sustained postures and particularly those postures that are maintained in faulty alignments can induce changes in the muscles and supporting tissues that can be injurious, especially when the joint is at the end of its range.⁷⁰

One of the most surprising characteristics of muscle performance evident to those who perform specific manual muscle testing is the presence of weakness, even in those individuals who regularly participate in physical activities. A frequently held assumption is that participation in daily activities or participation in sports places adequate demands on all muscles, ensuring normal performance. However, careful and specific muscle testing demonstrates that several muscles commonly test weak. For example, muscles frequently found to be weak are the lower trapezius, external oblique abdominal, gluteus maximus, and posterior gluteus medius. Even individuals who are active in sports demonstrate differences in the strength of synergistic muscles; one muscle can be notably weaker than its synergist.

The following example illustrates how repeated movements can alter muscle performance and lead to movement impairments. When the gluteus maximus and piriformis muscles are the dominant muscles producing hip extension, their proximal attachments provide more optimal control of the femur in the acetabulum than do the hamstring muscles. The attachments of the piriformis and gluteus maximus muscles onto the greater trochanter and intertrochanteric line of the femur provide control of the proximal femur during hip extension. The gluteus maximus through the iliotibial band also attaches on the tibia distally. Therefore this muscle is producing movement of both the proximal and distal aspects of the thigh, which reinforces the maintenance of a relatively constant position of the femoral head in the acetabulum during hip extension (Figure 2-8).

Figure 2-8 Hip extension in prone. A, Normal hip extension with constant position of femur in acetabulum; B, Abnormal hip extension because of anterior glide of femoral head.

The normal pattern can become altered, particularly in distance runners who develop weakness of the iliopsoas and gluteus maximus muscles. In contrast, the tensor fascia lata (TFL), rectus femoris, and hamstring muscles often become stronger and more dominant in distance runners than in nonrunners. The lack of balance in the strength and pattern of activity among all the hip flexor and extensor muscles can contribute to movement impairments, because each muscle has a slightly different action on the joint to which it attaches. When one in the group becomes dominant, it alters the precision of the joint motion. In the scenario where the activity of the hamstring muscles is dominant and the gluteus maximus muscle is weak, the result can be hamstring strain and a variety of hip problems that are painful. One plausible reason hip joint motion becomes altered is that the hamstring muscles, with one exception, originate from the ischial tuberosity and insert into the tibia. (The exception is the short head of the biceps femoris muscle, which attaches distally on the femur.) Because the hamstring muscles, with the exception of the short head, do not attach into the femur, they cannot provide precise control of the movement of the proximal end of the femur during hip extension. When the hamstring muscular activity is dominant during hip extension, the proximal femur creates stress on the anterior joint capsule by anteriorly gliding during hip extension rather than maintaining a constant position in the acetabulum (see Figure 2-8). This situation can be exaggerated if the iliopsoas is stretched or weak and is not providing the normal restraint on the femoral head.

These changes in dominance are not presumed; they are confirmed through manual muscle testing and careful monitoring of joint movement. Manual muscle testing ³² is used to assess the relative strength of synergists and the identification of muscle imbalances. Carefully monitoring the precision of joint motion as indicated by the PICR is also necessary when the muscle imbalance has produced a movement impairment. For example, monitoring the greater trochanter during hip extension will identify which muscles are exerting the dominant effect. The greater trochanter will move anteriorly when the hamstrings are the dominant muscles. In contrast, the greater trochanter will either maintain a constant position or move slightly posteriorly when the gluteus maximus and piriformis muscles are the prime movers for hip extension.

Muscle testing identifies the muscles that demonstrate performance deficits as a result of weakness, length changes, or altered recruitment patterns. In addition to reduced contractile capacity of muscle, other factors such as length and strain can be responsible for altered muscle performance, and the muscle can score a less than normal grade in a manual muscle test. The different mechanisms that contribute to these factors can be identified by performance variations during manual muscle testing and are discussed in this chapter.

Base Element Impairments of the Muscular System

Muscle Strength

To design an appropriate intervention program, it is necessary to identify the specific factors that are causing the impairments of the muscular system and contributing to movement impairment. Factors affecting the contractile capacity of the muscle are the number of muscle fibers, the number of contractile elements in each fiber (atrophy or hypertrophy), the arrangement (series or parallel), the fundamental length of the fibers, and the configuration (disruption, over-lengthened, or overlapped) of the contractile elements.

Muscular force is in proportion to the physiologic cross-sectional area.³⁶ The physiologic cross-sectional area is a function of the number of contractile elements in the muscle (Figure 2-9). Muscle will atrophy, or lose contractile elements, when it is not routinely required to develop other than minimal tension. Conversely, the muscle cells hypertrophy when routinely required to develop large amounts of tension, as long as the tension demands are within the physiologic limit of its adaptive response. The change in size (circumference) of a muscle occurs either by a decrease in sarcomeres (atrophy) (Figure 2-10) or an increase in sarcomeres (hypertrophy) (Figure 2-11). In hypertrophy the addition of sarcomeres in parallel is accompanied by the addition of sarcomeres in series, though to a lesser extent than those added in parallel.

Figure 2-10 Atrophy of muscle. Micrographs from normal muscles (top panel). Micrographs from immobilized muscles illustrating atrophied muscles where the sarcomeres have decreased in diameter (bottom panel). (From Leiber RL et al: Differential response of the dog quadriceps muscle to external skeletal fixation of the knee, Muscle Nerve 11:193, 1988.)

Figure 2-9 Structure of skeletal muscle. A, Skeletal muscle organ, composed of bundles of contractile muscle fibers held together by connective tissue. B, Greater magnification of single fiber showing small fibers, myofibrils in the sarcoplasm. C, Myofibril magnified further to show sarcomere between successive Z lines. Cross striae are visible. D, Molecular structure of myofibril showing thick myofilaments and thin myofilaments. (From Thibodeau GA, Patton KT: Anatomy & physiology, 3e, St Louis, 1996, Mosby.)

Figure 2-11 Hypertrophy of muscle. Cross-section of control rat soleus muscle (left). Cross-section of hypertrophied rat soleus muscle (right). (From Goldberg AL et al: Mechanism of work-induced hypertrophy of skeletal muscle, Med Sci Sports 3:185, 1975.)

Decreased Muscle Strength Caused by Atrophy

One cause of muscle weakness is a deficiency in the number of contractile elements (actin and myosin filaments) that make up the sarcomere structure of the muscle. Atrophy of a muscle is not typically associated with pain during either contraction or palpation. A lack of resistive load on muscle can cause atrophy, not only by reducing the numbers of sarcomeres in parallel and, to a lesser extent, in series, but also by decreasing the amount of connective tissue.

The decreased number of sarcomeres and the decreased amount of connective tissue can affect both the active ³⁶ and passive⁹ tension of a muscle, which affects the dynamic and static support exerted on each joint it crosses. The effect is diminished capacity for the development of active torque and less stability of the joint controlled by the muscle. For example, if the peroneal muscles of the leg are weak, the motion of eversion will be weak and the passive stability that helps restrain inversion will be diminished.

The passive tension of muscles also affects joint alignment. When the elbow flexor muscles are weak or have minimal passive tension, the elbow remains extended when the shoulder is in neutral. When the elbow flexors are hypertrophied from weight training, the resting position of the elbow joint is often one of flexion. Because atrophy means a deficiency of contractile elements, the size of a muscle (cross-sectional area) and its firmness can be used as guides to assess strength. For example, poor definition of the gluteal muscles is usually a good indication that these muscles are weak, particularly when the definition of the hamstring muscles suggests hypertrophy. Examiners should not rely solely on observation, but they should perform a manual muscle test to confirm or refute the hypothesis.

As mentioned, when muscle in the normal individual is tested, it is not uncommon to find deficient performances, even in those who exercise regularly. These deficiencies develop because subtle differences in an individual’s physical structure and manner of performing activities can have a major effect on the participation of different muscles. When an individual shorter than 5 feet, 2 inches in height stands from sitting in a standard chair, the demands placed on his or her hip and knee extensor muscles are not the same as those in the individual who is 6 feet, 2 inches in height or who has long tibias that cause the knees to be higher than the hips when sitting. A greater demand is placed on the extensor musculature when the knees are higher than the hips while sitting and the individual stands from a sitting position. These differences become apparent when standing from a low chair or sofa. When individuals use their hands to push up from a chair, they also contribute to the weakness of the hip and knee extensor muscles by decreasing their participation.

Another example of altering the use of specific muscles is seen in the individual who returns to an upright position from a forward flexed position by swaying the hips forward rather than maintaining a relatively fixed position of the hips. The individual with the relatively fixed position of the hips lifts the length of the pelvis and trunk by extending the hips and back (Figure 2-12). Typically, individuals who sway their pelvis forward have weak gluteus maximus muscles. There are numerous ways in which slight subtleties in movement patterns contribute to specific muscle weaknesses. The relationship between altered movement patterns and specific muscle weaknesses requires that remediation addresses the changes to the movement pattern; the performance of strengthening exercises alone will not likely affect the timing and manner of recruitment during functional performance.

Figure 2-12 Return from forward bending using three different strategies. Optotrak depiction of movement of markers placed at the head of the fifth metatarsal, ankle joint, lateral epicondyle of the knee, greater trochanter, iliac crest, and tip of shoulder. A, The motion is initiated by hip extension, followed by immediate and continuous lumbar extension, and is accompanying the rest of the hip motion. B, The motion is initiated by lumbar extension and followed by hip extension. C, In the forward-bending position, the subject is swayed backward with the ankles in plantar flexion. The return motion is a combination of ankle dorsiflexion and hip extension by forward sway of the pelvis. (Courtesy of Amy Bastian, PhD, PT.)

Clinical Relevance of Muscle Atrophy

Identifying specific muscle weakness requires manual testing. When a muscle is atrophied, it is unable to hold the limb in the manual test position or at any point in the range when resistance is applied. The muscle is not painful when palpated or when contracting against resistance. When a muscle tests weak, the therapist carefully examines movement patterns for subtleties of substitution. Correction of these movement patterns in addition to a specific muscle-strengthening program is required for an optimal outcome. Another factor that must be corrected is the habitual use of any position or posture that subjects the muscle to stretching, particularly when the patient is inactive (e.g., sleeping). Sleeping postures can place the muscles of the hip and shoulder in stretched positions. (This type of stretch weakness is discussed in the section on lengthened muscle in this chapter.)

To initiate the reversal of muscle atrophy, the patient’s ability to activate the muscle volitionally is augmented. Studies indicate that after 2 weeks of training, 20% of the change in muscle tension development can be attributed to muscular factors (contractile capacity) and 80% from enhanced neural activation.⁴³ Training specific muscles is particularly important when the problem is an imbalance of synergists rather than generalized atrophy.

Exercises that emphasize major muscle group contraction can contribute to the imbalance, rather than correct it. When the patient performs hip abduction with the hip flexed or medially rotated, the activities of the TFL, anterior gluteus medius, and gluteus minimus muscles are enhanced to a greater extent than the activity of the posterior gluteus medius muscle, even though all these muscles are hip abductors. The end result is hip abduction with hip flexion and medial rotation rather than pure abduction. Resistance exercises performed on machines can contribute to imbalances unless proper precautions are observed.

Approximately 4 weeks of strengthening exercises are required to verify the morphologic increase in muscle cross-sectional area.⁴³ Studies at the cellular level suggest that change may be occurring earlier than 4 weeks, which is consistent with the metabolic properties of other proteins. Because 4 weeks is required for changes in the number of contractile elements, early improvements in muscle performance are attributed to neuromotor recruitment. The rate of recruitment and the absolute frequency of activation of muscles are important factors in the performance of producing, improving, and maintaining the tension-generating properties of muscles.

Decreased Muscle Strength Secondary to Strain

Strain can result from excessive stretching for short duration or excessive physiologic loading usually associated with eccentric contraction.³⁵ (Additional discussion of the cellular manifestation of strain is found in the section on increased muscle length in this chapter.) Unless there is an actual tear of muscle fibers and obvious signs of hemorrhage, strain is not readily recognized as a source of muscle weakness. The intervention is different than when the muscle is strained and not merely atrophied.

Muscles that are strained are usually painful when palpated or when contracting. As with atrophy, a strained muscle is weak and unable to hold the limb in any position when resistance is applied throughout the range of motion. The presence of pain is usually an indicator of weakness from strain rather than from atrophy. When the length of the strained muscle is not constrained by its joint attachments, it is elongated in the resting position, such as a dropped or forward shoulder with a strain of the trapezius muscle. Strained muscles need to be rested at the ideal resting length to decrease the elongation of the muscle cells. The strained muscle can be supported by external support such as tape, preferably a type that has a strong adhesive and lacks elasticity. Exercises and active motions should be pain free or cause only mild discomfort.

The same principles used to manage atrophied muscles are applied to strained muscles, once the muscle is no longer painful.

Increased Muscle Strength Caused by Hypertrophy

Studies have shown that when a muscle is subjected to overload conditions, the response is the addition of contractile and connective tissue proteins. The value of hypertrophy in increasing the tension-generating capability of muscle is well known and frequently used by those involved in rehabilitation and athletics. Less appreciated is the effect of hypertrophy on the passive-tension properties of muscle and other connective tissue. Many tissues respond to stress by adapting (see Figure 2-11), which for muscle is hypertrophy. The quantity of connective tissue proteins of ligaments, tendons, and muscle also increases with hypertrophy. Tendons and ligaments become stronger and stiffer when subjected to stress, but they grow weaker when they are not subjected to stress.^64,67,72 The result is an increase in the passive tension of these tissues, not just the active tension that is generated by muscle during contraction. (The cellular factors are described in the section on muscle stiffness in this chapter.)

The use of strengthening exercises that are based on requiring muscle to lift maximal loads is well known to physical therapists. Strengthening exercises not only increase the tension-generating capacity of the muscle, but they also increase the stiffness of the muscle and the stability of the joints. Hypertrophy is important in improving muscle control under both active and passive conditions.

Strain is a minor form of a tear in which the filaments of the muscle have been stretched or stressed beyond their physiologic limit resulting in disruption of the Z-lines to which the actin filaments attach (Figure 2-13). Disruptions that alter the alignment of the myofilaments interfere with the tension-generating ability of these contractile elements.³⁵ The consequence is muscular weakness and, in many cases, pain when the muscle is palpated or when resistance is applied during contraction of the muscle.

Figure 2-13 Micrograph showing normal striation pattern and Z-disks perpendicular to the long myofibrillar axis (A) and various disrupted regions (B). Streaming and smearing of the X-disk material (arrowheads) and extension of the Z-disks into adjacent A-bands (circled areas) are shown. (From Lieber RL, Friden JO, McKee-Woodbum TG: Muscle damage induced by eccentric contractions of twenty-five percent strain, J Appl Physiol 70:2498, 1991.)

If a muscle is strained, the reparative process occurs more readily when the muscle is not subjected to strong resistance or to constant tension. For most muscles the anatomic limits imposed by joints to which the muscles attach help maintain the fibers at their appropriate resting length. Postural muscles of the shoulder and hip can become excessively stretched. For example, if the upper trapezius muscle is strained, weight of the shoulder girdle is excessive for the muscle, the shoulder’s pull on the muscle causes it to elongate, and the muscle is unable to heal. Frequently, strained muscles are painful because they are actually under continuous tension, even when they appear to be at rest. The discomfort is often reduced when the muscle is supported at its normal resting length, the passive tension is reduced, and the patient is instructed to relax the muscle, thereby eliminating any voluntary or involuntary contractile activity. As long as the patient avoids excessive loads on the muscle, it should heal within 3 to 4 weeks.

The typical findings with manual muscle testing of a strained muscle is its inability to support the tested extremity against gravity when positioned at the end of its range. Further, the muscle is unable to maintain its tension at any point in the range when resistance is applied throughout the range, and pain is elicited. Clearly the tension-generating capacity of the muscle is impaired. If the strain is severe, the motion of the joint upon which the muscle is acting will also show quality of movement and range-of-motion impairment.

Case Presentation 2

History.: A 32-year-old woman, whose job requires her to load food trays on a conveyor belt at shoulder height, has a sudden and severe onset of pain between the vertebral border of the right scapula and thoracic spine. The pain began after she attempted to lift a filing cabinet at work. She is seen immediately by a physician who refers her to a physical therapist, prescribing heat to the affected area and shoulder exercises three times a week. After 1 week, the patient returns to light duty at work, but 6 weeks later she still complains of severe pain and she is unable to return to her normal job. A magnetic resonance image of her thoracic spine does not indicate an abnormality.

Symptoms.: She is referred to a second physical therapy clinic. During her initial visit the patient is observed to be approximately 60 pounds overweight, with large arms and breasts and deep indentations on the tops of her shoulders from the pressure of her bra straps. Her facial expression and the manner in which she holds her right arm close to her body with her elbow flexed indicate that she is still in pain. She rates her pain as 6 to 8 on a scale of 10 when attempting any type of shoulder motion and 4 to 5 out of 10 with her arm at rest. (The 10 rating is the most severe.)

Muscle Length and Strength.: An examination indicates that the right scapula is greatly abducted and tilted anteriorly (Figure 2-14, A). Her scapula is manually positioned in the correct alignment, and her arm and forearm are supported by the physical therapist. After she is instructed to relax the musculature of her right shoulder girdle, she reports her pain has subsided (Figure 2-14, B). A manual muscle test indicates the strength of all components of her trapezius muscle as weak, graded 3—/5. Weakness and pain limit her ability to move through the normal range of motion even in a gravity-lessened position.

Tape (Leukotape P with cover roll underwrap) is applied to the posterior aspect of the right shoulder girdle to support and maintain the scapula in a neutral position and to reduce some of the strain on the trapezius muscle by decreasing the abduction and depression of the scapula. The case report written by Host demonstrates that scapular position can be altered by the application of tape to the posterior shoulder girdle.²⁸

Her bra straps are taped together, bringing them closer to her neck to reduce the downward pull on the lateral aspect of her shoulders. She is also instructed to support her arms on pillows whenever she sits and to support her right arm with her left arm to reduce the downward pull on her shoulder girdle whenever she stands. All shoulder exercises are eliminated for the next 5 days (Figure 2-14, C).