Tissue Adaptation to Physical Stress: A Proposed ''Physical Stress Theory'' to Guide Physical Therapist Practice, Education, and Research

Michael J Mueller and Katrina S Maluf PHYS THER. 2002; 82:383-403.

The online version of this article, along with updated information and services, can be found online at: http://ptjournal.apta.org/content/82/4/383 Collections This article, along with others on similar topics, appears in the following collection(s): Anatomy and Physiology: Musculoskeletal System Disability Models Kinesiology/Biomechanics Perspectives To submit an e-Letter on this article, click here or click on "Submit a response" in the right-hand menu under "Responses" in the online version of this article. Sign up here to receive free e-mail alerts

e-Letters

E-mail alerts

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

Perspective

Tissue Adaptation to Physical Stress: A Proposed Physical Stress Theory to Guide Physical Therapist Practice, Education, and Research
The purpose of this perspective is to present a general theorythe Physical Stress Theory (PST). The basic premise of the PST is that changes in the relative level of physical stress cause a predictable adaptive response in all biological tissue. Specific thresholds define the upper and lower stress levels for each characteristic tissue response. Qualitatively, the 5 tissue responses to physical stress are decreased stress tolerance (eg, atrophy), maintenance, increased stress tolerance (eg, hypertrophy), injury, and death. Fundamental principles of tissue adaptation to physical stress are described that, in the authors opinion, can be used to help guide physical therapy practice, education, and research. The description of fundamental principles is followed by a review of selected literature describing adaptation to physical stress for each of the 4 main organ systems described in the Guide to Physical Therapist Practice (ie, cardiovascular/pulmonary, integumentary, musculoskeletal, neuromuscular). Limitations and implications of the PST for practice, research, and education are presented. [Mueller MJ, Maluf KS. Tissue adaptation to physical stress: a proposed physical stress theory to guide physical therapist practice, education, and research. Phys Ther. 2002;82:383 403.]

Key Words: Adaptation, Biomechanics, Force, Stress. Michael J Mueller, Katrina S Maluf

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

383

Many different theories and

hysical therapists have expertise in the application of interventionssuch as exercise, postural instruction, orthotic devices, and modalitiesthat allow them to modify the physical stresses applied to tissues of the body.15 Physical stress is defined as the force applied to a given area of biological tissue.6 Exercise interventions that modify physical stress have been shown to decrease impairments, functional limitations, disability, and pain in a variety of patient populations.79 These same interventions can help people with and without disease increase muscle performance,10 bone mineral density,11 and fitness levels.9 An increasing amount of evidence indicates that exercise can have positive effects on disease processes such as diabetes,12 arthritis,79 and coronary artery disease.13 We believe that the many different theories and approaches currently used in physical therapy share fundamental principles that can be organized into a general theory to guide prevention and treatment of a broad range of patient problems. The general theory we present is based on fundamental principles that appear to govern the adaptive response of biological tissues to physical stress. Therefore, we refer to this theory as the Physical Stress Theory (PST). The PST integrates existing knowledge into a deliberately broad theory with potential application to physical therapist practice, education, and research. Physical therapists have emphasized the evaluation and treatment of movement dysfunction.14 16 Movement can be defined by the basic physical components (mass acceleration) of a segment or body. The mass acceleration of a body segment is defined as force (force mass acceleration, Newtons second law of motion). The application of force over a given area of tissue during movement results in stress to the tissue (stress force/area, where force may be applied in any direction [tension, shear, compression]).6 Although movement is a major source of physical stress on tissues, other forces generated both inside the body (eg, isometric muscle contractions) and outside of the body (eg, gravity) also may

approaches currently used in physical therapy share fundamental principles that can be organized into a general theory to guide prevention and treatment of a broad range of patient problems.
contribute to tissue stress. The PST was developed to address how tissues, organs, and organ systems adapt to varying levels of physical stress (Tab. 1). In addition, this theory describes how other factors (Tab. 2) can modify both the level of physical stress and the response of biological tissues to a given stress level. The PST focuses on the physical stresses that influence all biological tissues. Tissues are formed from groups of similarly specialized cells that cooperate to perform one or more functions within the body.17,18 The 4 fundamental types of tissue are: (1) epithelial tissue, which covers internal and external surfaces of the body and forms glands, (2) connective tissue, which provides structural and functional support to other tissues of the body, (3) muscular tissue, which has specialized contractile properties for producing movement, and (4) nervous tissue, which collects, transmits, and integrates stimuli to control the functions of the body.17,18 These 4 basic tissues combine to form organs. Groups of anatomically or functionally related organs are referred to as organ systems.17,18 Our discussion of the PST will be limited to tissues that form the organ systems identified as most relevant to physical therapists in the Guide to Physical Therapist Practice (ie, cardiovascular/pulmonary, integumentary, musculoskeletal, and neuromuscular systems).14 The PST does not address molecular or cellular mechanisms of adaptation. Rather, the PST identifies common principles from the literature that we suggest may be used to predict adaptive tissue changes that occur in response to physical stress.

MJ Mueller, PT, PhD, is Associate Professor and Director of the Movement Science Laboratory, Program in Physical Therapy, Washington University School of Medicine, 4444 Forest Park Blvd, Campus Box 8502, St Louis, MO 63110-2212 (USA) (muellermi@msnotes.wustl.edu). Address all correspondence to Dr Mueller. KS Maluf, PT, MSPT, is a graduate student in the Movement Science Program, Program in Physical Therapy, Washington University School of Medicine. Both authors provided concept/project design, writing, and fund procurement. Dr Mueller provided project management. The authors acknowledge Amy J Bastian, Marybeth Brown, David Brown, Scott D Minor, Barbara J Norton, Shirley A Sahrmann, and Linda VanDillen for discussions and their review of a previous draft of the manuscript. This work was supported by grants RO1 HD36802 and RO1 HD36895 to Dr Mueller from the National Center for Medical Rehabilitation Research, National Institutes of Health, and a Promotion of Doctoral Studies Award from the Foundation for Physical Therapy to Ms Maluf.

384 . Mueller and Maluf

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

Table 1.
Summary of Fundamental Principles for Physical Stress Theory Basic Premise: Changes in the relative level of physical stress cause a predictable adaptive response in all biological tissue. Fundamental Principles: A. Changes in the relative level of physical stress cause a predictable response in all biological tissues. B. Biological tissues exhibit 5 characteristic responses to physical stress (Fig. 1). Each response is predicted to occur within a defined range along a continuum of stress levels. Specific thresholds define the upper and lower stress levels for each characteristic tissue response. Qualitatively, the 5 tissue responses to physical stress are decreased stress tolerance (eg, atrophy), maintenance, increased stress tolerance (eg, hypertrophy), injury, and death. C. Physical stress levels that are lower than the maintenance range result in decreased tolerance of tissues to subsequent stresses (eg, atrophy). D. Physical stress levels that are in the maintenance range result in no apparent tissue change. E. Physical stress levels that exceed the maintenance range (ie, overload) result in increased tolerance of tissues to subsequent stresses (eg, hypertrophy). F. Excessively high levels of physical stress result in tissue injury. G. Extreme deviations from the maintenance stress range that exceed the adaptive capacity of tissues result in tissue death. H. The level of exposure to physical stress is a composite value, defined by the magnitude, time, and direction of stress application. I. Individual stresses combine in complex ways to contribute to the overall level of stress exposure. Tissues are affected by the history of recent stresses. J. Excessive physical stress that causes injury can occur from 1 or more of the following 3 mechanisms: (1) a high-magnitude stress applied for a brief period, (2) a low-magnitude stress applied for a long duration, and (3) a moderate-magnitude stress applied to the tissue many times. K. Inflammation occurs immediately following tissue injury and renders the injured tissue less tolerant of stress than it was prior to injury. Injured and inflamed tissues must be protected from subsequent excessive stress until acute inflammation subsides. L. The stress thresholds required to achieve a given tissue response may vary among individuals depending on the presence or absence of several modulating variables. Factors that can influence thresholds for tissue adaptation and injury are summarized in Table 2 and include movement and alignment, extrinsic, behavioral, and physiological factors.

Table 2.
Factors Affecting the Level of Physical Stress on Tissues or the Adaptive Response of Tissues to Physical Stress Movement and Alignment Factors Muscle performance (force generation, length) Motor control Posture and alignment Physical activity Occupational, leisure, and self-care activities Extrinsic Factors Orthotic devices, taping, assistive devices Footwear Ergonomic environment Modalities Gravity Psychosocial Factors Physiological Factors Medication Age Systemic pathology Obesity

describe the fundamental principles of the PST, followed by a review of selected literature describing adaptation to physical stress for each of the 4 main organ systems described in the Guide to Physical Therapist Practice.14 The fundamental principles are based on an analysis of the literature and our clinical experiences. Because the principles are general and represent what we contend are the common denominators of a variety of research findings and clinical approaches, references are not provided in the description of the theory or in the listing of Fundamental Principles in Table 1. Supporting literature is provided in the subsequent section and is summarized in Table 3. The literature review also will address how we believe the PST relates to other physical therapy theories and approaches. Limitations and implications of the PST for practice, research, and education will then be discussed. Description of Physical Stress Theory The basic premise of the PST is that changes in the relative level of physical stress cause a predictable adaptive response in all biological tissue (Tab. 1). Figure 1 illustrates primary adaptive responses and thresholds for tissue adaptation in response to physical stress. Factors that may influence either the level of physical stress on tissues or the adaptive response of tissues to a given stress level are outlined in Table 2. The fundamental principles of the PST are summarized in Table 1 and are described in further detail below. Fundamental Principle AChanges in the relative level of physical stress cause a predictable response in all biological tissues. Physical stress is the force, or load, acting on a given area of tissue.6 In the PST, we propose that tissues accommodate to physical stresses by altering
Mueller and Maluf . 385

In its present form, we believe the PST can be applied most easily to the care of patients with primary problems involving the musculoskeletal and integumentary systems. However, we believe this theory also has potential applications for patients with primary problems involving the cardiovascular/pulmonary and neuromuscular systems.14 We contend that the PST relates to a continuum of care and, therefore, also has direct applications for issues related to wellness and the prevention of physical disabilities. The purpose of this perspective is to present a general theory, based on principles of adaptation to physical stress, that we believe can be used to help guide physical therapy practice, education, and research. First, we will

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

386 . Mueller and Maluf Stress/Activity Level Low 2BMD 2strength Fracture Strain 2contractile protein 2fiber diameter 2peak tension 2peak power 2CSA 2stiffness 2strength 2CSA 2stiffness 2strength 2proteoglycan content 2cartilage thickness 2stiffness 2collagen content 2collagen fiber diameter 2skin thickness 2strength 2cardiac muscle mass 2capillary density 2stroke volume No change 1proteoglycan content 1cartilage thickness 1stiffness No change 1collagen content 1collagen fiber diameter 1skin thickness 1strength No change 1CSA 1stiffness 1strength No change 1CSA 1stiffness 1strength Strain No change 1contractile protein 1fiber diameter 1peak tension 1peak power No change 1BMD 1strength Normal High Excessive Sprain Degeneration or tear Abrasion or wound Fibrosis Aneurysm Ventricular hypertrophy Fibrosis Aneurysm No change 1maximum discharge rate Axonal demyelination and degeneration 2recruitment threshold 1activation during MVC neurogenesis (hippocampus) 1motor unit synchronization 1dendritic arborization 1serotonergic neural activity 1synaptic transmission No change 1cardiac muscle mass 1capillary density 1stroke volume 1metabolic capacity No change 1vascular diameter 1arterial compliance 2maximum discharge rate 1recruitment threshold 2activation during MVC neuron loss

Table 3.

Effect of Physical Stress and Activity on Tissues of the 4 Major Organ Systems Listed in the Guide to Physical Therapist Practicea

Organ System

Tissue/Organ

Musculoskeletal

Bone75,88,131135

Muscle52,136 140

Tendon126,141

Ligament126,141,142

Cartilage143148

Integumentary

Skin95

Cardiopulmonary/vascular Heart13,101105

Blood vessels101,102,149 151 2vascular diameter 2arterial compliance

Neuromuscular

Neurons106,108,115118

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

Strength is defined as maximum stress, strain, and/or energy density prior to failure. 1 increase, 2 decrease, BMD bone mineral density, CSA cross-sectional area, MVC maximum voluntary contraction.

Figure 1.
Effect of physical stress on tissue adaptation. Biological tissues exhibit 5 adaptive responses to physical stress. Each response is predicted to occur within a defined range along a continuum of stress levels. Specific thresholds define the upper and lower stress levels for each characteristic tissue response. The relative relationship between these thresholds is fairly consistent between people, whereas the absolute values for thresholds vary greatly.

Figure 2.
Effect of prolonged low stress lowers thresholds for subsequent adaptation and injury. Prolonged physical stress levels that are lower than the maintenance range result in decreased tolerance of tissues to subsequent stresses (eg, atrophy). Although relative thresholds remain the same, the absolute magnitude of physical stress is lower for each threshold. Injury (and all other adaptations) occurs at a lower level of physical stress than required previously.

their structure and composition to best meet the mechanical demands of routine loading. Deviations from routine or steady-state loading provide a stimulus for tissue adaptation that allows tissues to meet the mechanical demands of a novel environment. Fundamental Principle BBiological tissues exhibit 5 characteristic responses to physical stress. Each response is predicted to occur within a defined range along a continuum of stress levels. Specific thresholds define the upper and lower stress levels for each characteristic tissue response. These thresholds can be viewed as boundaries for the effective dose-response to physical stress. The 5 qualitative responses to physical stress are decreased stress tolerance (eg, atrophy), maintenance, increased stress tolerance (eg, hypertrophy), injury, and death. Fundamental Principle CPhysical stress levels that are lower than the maintenance range result in decreased tolerance of tissues to subsequent stresses. Atrophy is one common mechanism by which tissues become less tolerant of subsequent physical stresses (Fig. 2). Atrophy occurs when tissue degeneration exceeds tissue production and has been observed in all 4 major organ systems in response to reduced stress levels (Tab. 3). Other examples of adaptations that may reduce stress tolerance include hormonal changes, altered cell membrane excitability, and changes in the material properties of tissues (Tab. 3). Fundamental Principle DPhysical stress levels that are in the maintenance range result in no apparent tissue

change. Tissue homeostasis occurs when tissue degeneration is equal to tissue production, resulting in tissue turnover without net gain or loss. The range of stress levels that promote tissue homeostasis is defined as the maintenance stress range and may be different for different people. This steady-state or equilibrium response occurs when tissues are exposed to the same levels of stress to which they have become accustomed. Fundamental Principle EPhysical stress levels that exceed the maintenance range (ie, overload) result in increased tolerance of tissues to subsequent stresses. Hypertrophy is one common mechanism by which tissues become more tolerant of subsequent physical stresses (Fig. 3). Hypertrophy occurs when tissue production exceeds tissue degeneration, and can be defined as a general increase in bulk of a tissue.19 In general, biological tissues adapt to increased levels of stress by increasing cross-sectional area, density, or volume (Tab. 3). Other examples of adaptations that may increase tissue stress tolerance include hormonal changes, altered cell membrane excitability, and changes in the material properties of tissues (Tab. 3). Although stress overload can promote tissue hypertrophy and improve stress tolerance, adequate recovery between bouts of increased stress is needed for this adaptive response to occur (see below).20 Fundamental Principle FExcessively high levels of physical stress result in tissue injury. For the purposes of this theory, injury is defined as tissue damage caused by excessive stress resulting in pain or discomfort, impaired function of the tissue, or both. Damages that are not felt
Mueller and Maluf . 387

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

Figure 3.
Effect of overload stress raises thresholds for subsequent adaptation and injury. Prolonged physical stress levels that are higher than the maintenance range result in increased tolerance of tissues to subsequent stresses (eg, hypertrophy). Although relative thresholds remain the same, the absolute magnitude of physical stress is higher for each threshold. Injury (and all other adaptations) occurs at a higher level of physical stress than required previously.

Figure 4.
Physical stress level is a composite value. Stress magnitude refers to the amount of stress (force per unit area) on a tissue. Time factors include the duration, number of repetitions, and the rate at which stress is applied to tissues of the body. Stress will have a different effect depending on whether it is applied in tension, compression, shear, or torsion.

or are not causing noticeable dysfunction are not considered clinically significant injuries. The maximum stress threshold is defined as the amount of stress the tissue can bear just before it fails, if the tissue is fully rested and recovered from previous stresses. Stress levels that exceed the maximum stress threshold are considered excessive and result in tissue injury. Fundamental Principle GExtreme deviations from the maintenance stress range that exceed the adaptive capacity of tissue result in tissue death. The PST represents the potential range of responses of viable tissues to a given level of physical stress. To the extent that the stress level can be altered, viable tissues exhibit a variable stress response. For example, healthy tissues that are injured as a result of exposure to high stress levels may return to the maintenance range if stress levels are appropriately reduced. In cases where stress levels deviate substantially from maintenance conditions, tissues may no longer be viable and tissue death can result. Thus, tissue death can occur when tissues are exposed to either extremely high or extremely low stress levels and are unable to adapt or recover. Fundamental Principle HThe level of exposure to physical stress is a composite value, defined by the magnitude, time, and direction of stress application (Fig. 4). Stress magnitude refers to the amount of stress (force per unit area) on a tissue at any given moment in time. Time factors include the duration, the number of repetitions, and the rate at which stress is applied to tissues of the body. Each of these factors has a direct relationship with the level of stress exposure. For example, a longer
388 . Mueller and Maluf

duration of stress application results in a greater level of stress on the tissue. The direction of stress application also influences tissue adaptation. Stress will have a different effect depending on whether it is applied in tension, compression, shear, or torsion. Use of a composite measure to quantify the level of stress exposure implies that stress levels may be altered by changing one or more of the stress-related variables that comprise this measure. Fundamental Principle IIndividual stresses combine in complex ways to contribute to the overall level of stress exposure. Tissues are affected by the history of recent stresses. In the PST, the effect of any given stress will depend on the previous stress experience of the tissue. For example, 1 repetition of a biceps muscle curl against a resistance of 13.6 kg (30 lb) may have little effect on subsequent muscle performance. However, 3 sets of 10 repetitions, 3 times a week, for 2 weeks can lead to muscle hypertrophy and increase the muscles ability to generate force. One consequence of the cumulative effect of repeated stresses is that tissues require periods of rest in which the level of stress exposure is substantially reduced so that they can adapt and recover from previous stresses. Fundamental Principle JExcessive physical stress that causes injury can occur through 1 or more of the following 3 mechanisms: (1) a high-magnitude stress applied for a brief duration, (2) a low-magnitude stress applied for a long duration, and (3) a moderatemagnitude stress applied to the tissue many times. This

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

principle is closely related to Fundamental Principle H (Tab. 1), which identifies stress magnitude and time factors (eg, duration and number of repetitions of stress application) as important variables used to determine the composite level of stress to which tissues are exposed. Fundamental Principle KRegardless of the mechanism of injury, inflammation occurs immediately following tissue injury and renders the injured tissue less tolerant of stress than it was prior to injury. In the context of the PST, the threshold for subsequent tissue injury is lowered as a result of previous injury and the presence of inflammation. Stress levels that did not cause pain before the tissue was injured would then have the potential to cause pain and further tissue damage. Injured and inflamed tissues must be protected from subsequent excessive stress until acute inflammation subsides. Continued stress, even at a level considered normal for uninjured tissue, can prevent tissue regeneration following injury. Fundamental Principle LThe stress thresholds required to achieve a given tissue response may vary among individuals depending on the presence or absence of several modulating variables. In developing the PST, we identified 4 categories of variables (Tab. 2) that can modulate either: (1) the level of stress on tissues, or (2) the response of tissues to a given level of physical stress (ie, threshold values for tissue adaptation and injury). Because of the complex interaction among variables, it is not yet possible to determine the absolute value of the thresholds for tissue adaptation proposed within this theory. However, we propose that the PST can be used to construct models that predict the relative influence of both stress-related and nonmechanical variables on tissue adaptation and injury. With additional research, it should be possible to estimate the relative threshold value, based on a percentage of maximum stress tolerance, that is required to promote a desired tissue response given the individual circumstances of each patient. Rehabilitation programs then could be tailored to enhance factors contributing to tissue repair and to minimize factors contributing to tissue failure. Factors that can change the level of stress on tissues or the threshold values for tissue adaptation and injury are summarized in Table 2 and include movement and alignment, extrinsic, psychosocial, and physiological factors. Each of these factors is described below, and those factors that can be modified with physical therapy interventions are emphasized. Movement and Alignment Factors According to the PST, movement is the most important factor that physical therapists can use to influence tissue adaptation. As noted, movement occurs because of

forces. Forces are applied to tissues over a given area that result in stresses, which contribute to tissue adaptation as outlined in this theory. Physical therapists often focus on the treatment of movement dysfunction,15,16,21,22 and one theory has designated movement as its core principle.15 By comparison, the core principle of the PST is tissue adaptation in response to physical stress. As summarized in Table 3, movement can have beneficial effects (eg, exercise-related tissue hypertrophy) as well as detrimental effects (eg, overuse injury) on tissues of the body. According to the PST, movement and alignment factors are considered primarily for their ability to place stress on biological tissue. The components of movement and alignment considered by this theory are muscle performance, motor control, posture and alignment, and physical activity. Muscle Performance Muscle performance (force generation, muscle length) is a critical aspect of movement that can influence tissue stress. Muscles are highly adaptable. They generate movement and, hence, forces that place stress on tissues. Muscle also is an important shock absorber, and muscle contraction is well recognized for its ability to protect bones, cartilage, and ligaments from excessive stress.23 As a general theory, the PST can be used in combination with other theories and approaches that provide a more detailed analysis of the mechanisms by which muscle performance contributes to stress on tissues of the body.24 30 Motor Control Motor control has been defined as the study of the nature and cause of movement,31 and it, therefore, represents a major component of physical therapists expertise.21 Evaluation of the ways in which people control their movements to accomplish tasks provides physical therapists with insight into how stresses are applied to tissues of the body during movement. For example, Maluf et al32 have proposed that the daily repetition of similar movements and postures may result in excessive stress on tissues of the low back. These authors suggest that physical therapists can identify and modify motor recruitment patterns which potentially contribute to patients low back pain during the performance of daily activities. Maluf et al32 contend that an important role of physical therapists is to identify patterns of movement that contribute to excessive tissue stress and to teach patient-appropriate movement strategies to prevent tissue injury and pain. Posture and Alignment Kendall et al25 have emphasized the relationship between posture, impairments, and pain. The Kendalls basic premise, based on their clinical observations, is that there is a standard or ideal posture and that

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

Mueller and Maluf . 389

deviations from this ideal posture lead to characteristic patterns of musculoskeletal impairments and pain.25(p5) For example, the Kendalls predict that a person with excessive lumbar lordosis would have weak abdominal and hamstring muscles, with short, strong low-back and hip flexor muscles.25(p126) Some studies3337 have questioned, and even refuted, a large relationship between these variables in people with and without back pain. Rather than emphasizing an ideal standard of posture and hypothesizing that there is a large relationship among specific postures, impairments, and pain patterns, the PST proposes that pain is caused by excessive tissue stress and that postural deviations are one of many potential variables that contribute to the excessive stress levels that result in pain. We commonly observe people with poor posture who are pain-free and other people with good posture who have pain. The types of activities performed by people varies widely, resulting in different stress demands on tissues of the body. The PST predicts that no one ideal posture exists for all people because tissues will adapt to meet the unique stress demands of each person. Injury occurs when tissues are unable to adapt to meet the demands of a given posture or task. Therefore, rather than comparing a persons posture to an ideal standard, the therapists examination should focus on the postures or movements that cause pain.26,32,38,39 Within this context, postural deviations become one of many potential factors that may place stress on injured tissues. In some people, the postural deviation may be the primary factor contributing to excessive tissue stress (see Implications for Physical Therapist Practice and Implications for Research sections). In our view, the PST expands upon the Kendalls theory by proposing that postural deviations are one important component of musculoskeletal pain; however, pain patterns should be evaluated in a broader context that considers other potential sources of tissue stress. Physical Activity Physical activity is another component of movement that results in tissue stress. The US Department of Health and Human Services and the American College of Sports Medicine have adopted the definition of physical activity as bodily movement that is produced by the contraction of skeletal muscle and that substantially increases energy expenditure.40(p4) Physical activity may be divided into the specific subcategories of occupational, leisure, and self-care activities. The PST predicts that physical activity improves health because it increases stress on a broad range of tissues, making the tissues more tolerant of subsequent physical activity. Because the tissues are more tolerant of physical stress, they are less likely to be

injured. This reduction in the likelihood of injury occurs regardless of whether the tissue is part of the cardiovascular/pulmonary, integumentary, musculoskeletal, or neuromuscular system. Increased physical activity has been linked to many positive health benefits, including lower risk for noninsulin-dependent diabetes mellitus,41 stroke,42 and obesity.43 The federal government, in Healthy People 2010, has set a number of goals to increase physical activity (Objective 22; Physical Activity and Fitness) in people who are otherwise healthy. We believe that physical therapists should use their expertise to provide instruction on how people can increase overall physical activity without injuring specific structures (ie, back or knee). Extrinsic Factors Extrinsic factors are factors outside of the body that can influence either the level of stress on tissues or the thresholds for tissue adaptation and injury. For the purpose of this perspective, those extrinsic factors that can be modified or utilized by physical therapists are emphasized. Orthotic devices can be used to modify physical stress on biological tissues and can be used as an adjunct to other interventions in several phases of tissue adaptation. An orthotic device can be used to relieve stress from injured tissue (eg, a resting hand splint for patients with carpal tunnel syndrome, a lumbosacral corset for a person with low back pain). An orthotic device also can be used to apply stress to tissue to cause a change in the tissue (eg, orthotic devices that apply low loads for prolonged periods to increase muscle length and joint range of motion at the elbow).44 According to the PST, orthotic devices are an appropriate adjunct to treatment when other means of movement can not adequately control stress on the tissue to meet desired guidelines. We contend that components of the orthotic device should be chosen for their ability to achieve a desired stress level on the tissue. Likewise, taping45,46 and assistive devices (eg, crutches, walkers, canes) may be effective adjuncts to help modify stress on injured tissues. Footwear is another extrinsic factor that can influence stresses applied to the foot. Narrow toe boxes are thought to apply damaging stresses to the forefoot that lead to the formation of bunions and hammer-toe deformities.47 However, footwear also can be used for therapeutic purposes such as helping to decrease stress on the foot and ankle at heel strike (ie, shock absorption) or helping to control excessive movement of the rear foot.48 The ergonomic environment is another extrinsic factor that can be modified to influence tissue stress. Changes in the ergonomic environment can be achieved by

390 . Mueller and Maluf

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

redesigning the job site or work tools to reduce the demands of jobs that require high force, high repetition, and awkward postures.49 Primary principles of ergonomic design include reduction of extreme joint motion, excessive force magnitudes, and highly repetitive movements. Appropriate size and placement of a workstation can reduce extreme joint motion. Tools or machines can be designed to reduce excessive forces or repetitive motions (eg, using an electric drill rather than a manual one).49 Modalities (eg, heat, cold, electrical stimulation) are extrinsic factors that can be used to modify the level of tissue stress or the response of biological tissues to stress application. As described in the PST, modalities have a secondary role in treatment but may be indicated to augment the bodys own adaptive capabilities. For instance, electrical stimulation can be used to augment short- and long-term muscle force production, especially in the presence of pathology that limits the normal force generating capacity of muscle (eg, after ligament injury50 or spinal cord injury51). Heat is an example of a modality that can be used to modify the response of tissues to physical stress. For example, elevation of muscle temperature is thought to help prevent strain injuries (ie, raise the threshold for muscle injury) by allowing muscles to stretch more and tolerate higher loads before failure.52 Gravity is an extrinsic factor that physical therapists can use to modify the external load on the body. By modifying the orientation of the body or limbs with respect to the ground, physical therapists can increase or decrease forces exerted on the body during movement and, consequently, alter the forces that must be generated internally to produce movement.53 Modalities or devices, such as aquatic therapy54 or weight-supported walking devices,55 also may be used to modify tissue stress by altering the effects of gravity. Psychosocial Factors Psychosocial factors represent those factors that are unique to the lifestyle of each person and that potentially can be modified. Psychosocial factors can have a profound influence on tissue adaptation, especially as related to tissue injury.56 We believe psychosocial factors primarily influence individual threshold values for tissue adaptation and injury. For example, researchers investigated the role of mechanical and psychosocial factors in the onset of forearm pain in a 2-year-long prospective study (N 1,953).56 Besides linking injury to repetitive movements of the arm or wrist (relative risk of 4.1 and 3.4, respectively), the investigators reported that people who were only occasionally or never satisfied with support from supervisors and colleagues had a relative risk of 4.7 (95% confidence interval 2.2, 10) for forearm injury. These data indicate that, in some circum-

stances, psychosocial factors can be as important as mechanical factors for tissue injury. Although we recognize that psychosocial factors can play an important role in a persons response to physical stress, this role is not developed extensively in this perspective. We encourage others to develop the psychosocial component of the PST. Physiological Factors Physiological factors influence the ability of tissue to respond to physical stress, but these factors often are difficult, if not impossible, to modify. Physiological factors assume a less important role in physical therapy treatment compared with the factors described previously because physical therapists usually can not modify or treat physiological factors directly. Physical therapists should be aware of the influence of physiological factors, however, because these factors will affect the prognosis of tissue adaptation and recovery from injury. Medications can influence tissue physiology and, consequently, the ability of tissues to adapt to physical stress. For example, corticosteroid use has a complex effect on tissue. Corticosteroids can simultaneously cause a decrease in inflammation in one tissue (positive effect on stress tolerance) and cause atrophy in other tissues such as skin, bone, and muscle (negative effect on stress tolerance).57 Physical therapists do not prescribe medications. However, the impact of medications on the adaptive capacity of tissue is important, and physical therapists should be aware of these effects on their patients. In addition, exercise may help to offset muscle atrophy from medications such as glucocorticoids.58 Age is another important physiological factor. Although it is beyond the scope of this perspective to discuss the effects of age on tissue adaptation, it is important to discuss several general points. Aging has a negative effect on tissue adaptation. The magnitude of this negative effect in humans, however, is not clear. Kohrt59 believes that a considerable portion of the negative effects that have been attributed to aging may be due to ageassociated decreases in activity. Two predictions regarding the effects of age can be derived from the PST. The first prediction is that aging lowers the ability of tissues to tolerate stress and has a general tendency to lower the threshold for injury, similar to the effect illustrated in Figure 2. The level of stress required to promote tissue hypertrophy and increase stress tolerance generally is greater for young subjects who are healthy compared with older subjects. Young people, therefore, can exercise and stress their tissues more aggressively with less fear of injury than older people. The second prediction is that the negative effects of aging can be modified through increased stress on the tissue. Increased stress, applied through progressive increases in activity or exer-

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

Mueller and Maluf . 391

cise, theoretically can help prevent or reverse some of the negative effects of aging (Fig. 3). Increasing evidence suggests that tissues remain responsive to physical stress well into old age and that positive adaptations to increased activity and exercise can result in decreases in functional limitations and disability.7,8,10 Systemic pathology includes the many diseases that can affect the ability of tissues to adapt to physical stress. Examples of systemic pathology that physical therapists often encounter are diabetes mellitus and rheumatoid arthritis. Similar to the effects of aging, many forms of systemic pathology lower the ability of tissue to tolerate stress, and they have a general tendency to lower the threshold for injury. One example of this principle is the effect of peripheral neuropathy on cortical bone mass in the feet and hands of patients with diabetes. Patients with diabetes and peripheral neuropathy have been shown to have lower cortical bone mass, with a higher incidence of metatarsal fractures, compared with a matched group of patients with diabetes alone.60 As interpreted by the PST, pathology associated with peripheral neuropathy reduces the injury threshold for bone to a level experienced during normal walking. Although the PST recognizes the negative impact of systemic pathology on tissue adaptation, it also proposes that carefully applied physical stresses can have positive effects for people with chronic disease. Growing evidence supports this prediction.9,13,61 63 Traditionally, people with rheumatoid arthritis have been excluded from vigorous activities that might exacerbate joint inflammation.9 However, studies have shown that progressive resistive exercises and aerobic exercise programs can increase muscle performance, fitness levels, and bone mineral density with no exacerbation of disease activity in patients with rheumatoid arthritis.9,61,62 The positive effects of aerobic exercise for patients with cardiovascular disease have been well documented.13 Likewise, evidence indicates that increased activity, even in small increments, can have positive effects on reducing the burden of hyperinsulinemia and diabetes.63 William H Herman, an associate editor for Clinical Diabetes, summarized the effect of exercise on diabetes: An ideal treatment for type 2 diabetes would lower blood glucose concentrations acutely, improve longterm glycemic control, and enhance insulin sensitivity. It would improve mild to moderate hypertension, reduce low-density lipoprotein cholesterol and triglycerides, increase high-density lipoprotein cholesterol, and serve as an adjunct to caloric restriction for weight reduction. Finally, it would increase patients sense of well-being and improve their quality of life. As a drug, such an agent would be a blockbuster, with greater than $1 billion per year sales potential. Yet

such a treatment exists and has been recognized for centuries. It is regular physical activitythat is exercise.12 Although systemic pathology may lower the threshold for tissue injury, many people with systemic pathology respond positively to exercise, both in terms of increased stress tolerance and reduction of disease complications. We also consider obesity a physiological factor within the context of the PST that can be modified, but not easily. Obesity is defined as an increase in body weight beyond the limitation of skeletal and physical requirements, as the result of an excessive accumulation of fat.64 Body weight provides an indication of the stresses that must be borne by tissues of the body during physical activity. The PST predicts that obesity is a risk factor for certain types of injury and a negative factor for recovery from injury. In addition, obesity has been linked with low activity levels.43 People who are obese, therefore, may be at greater risk of injury than people who are not obese because high-stress, low-repetition activities are thought to be more damaging than low-stress, high-repetition activities.49,65 68 Evidence exists to support this prediction. For example, a population-based (n 350, 95 men and 255 women, 55 years of age or older) longitudinal study (mean follow-up duration 5.1 years) reported that the risk of incident radiographic knee osteoarthritis was significantly increased among subjects with higher baseline body mass index (odds ratio 18.3, 95% confidence interval 5.1 65.1).69 Literature Review The PST focuses on how biological tissues respond to physical stress. Existing evidence and approaches that share common principles with the PST will be described next for each of the 4 major systems described in the Guide to Physical Therapist Practice.14 Because physical therapists often work with patients with injuries, each section will begin by discussing how physical stress can contribute to injury. Discussion of the effects of physical stress on injury will then be followed by a discussion of the effects of physical stress on tissue atrophy, maintenance, and hypertrophy. These effects are summarized in Table 3. Musculoskeletal System Some authors29,70 have described mechanical principles involved in the management of patients with low back pain. McGill70 proposed that injury, or failure of a tissue, occurs when the applied load exceeds the failure tolerance of the tissue. In addition, McGill70 contended that the structures of the back are influenced by the history of recent physical stresses, so that the accumulation of individual stresses can cause injury. He argued that the characteristics of the load (load rate, mode of

392 . Mueller and Maluf

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

load compression, bending, torsion, shear) and the properties of the tissue determine the type and extent of tissue damage. McGill70 described the same 3 mechanisms of injury to low back tissues that are proposed within the PST (Principles H, I, and J, Tab. 1). One mechanism of injury to low back tissues is a single application of a relatively high load or stress. McGill provided the example of a person riding a snowmobile who is thrown from the machine and lands on a flexed spine and experiences a sudden posterior disk herniation. A second mechanism of injury to low back tissues is multiple moderate loads or stresses applied to the structures of the low back. In this case, injury is the result of accumulated trauma. McGill provided the example of a worker lifting boxes in which tissues of the low back are loaded repeatedly, causing a slow degradation of the tissue tolerance. A third mechanism of injury is low loads sustained by the low back over a long period of time. An example of this mechanism of injury is construction workers who install rods in the floors of a new building and remain in a flexed posture for prolonged periods of time. Injury to other types of tissue can result from the same mechanisms as those described above for the low back. Bones can fracture from one bout of high-magnitude force (eg, sudden impact fracture of the femur bone from a motor vehicle accident) or from bouts of moderate-magnitude force that occur many thousands of times (eg, stress fracture of the tibia or metatarsal bones from running,71 prolonged marching72). Similar to bones, ligaments can tear with one bout of a highmagnitude force (eg, injury of the medial collateral ligament from a tackle to the lateral knee). Increasing evidence, however, suggests that ligaments also can fail from repeated bouts of moderate-magnitude stress.73 For example, women have a much higher incidence of anterior cruciate ligament injury from noncontact sporting events compared with men.73 Huston et al73 speculated that this finding may be related to anatomical differences, such as a wider pelvis and greater Q angle in women, that result in greater cumulative stress on the anterior cruciate ligament during typical activities such as walking or running. Radin and colleagues65 68 have described similar mechanisms of injury (Principle J, Tab. 1) involved in degeneration of articular cartilage and joints. McPoil and Hunt27 also have recognized the importance of mechanical stress in the management of foot and ankle injuries. These authors have described a treatment approach based on a Tissue Stress Model. This approach proposes that clinicians focus on reducing excessive mechanical stress from injured tissues in the foot and ankle rather than attempting to place the foot

in an ideal posture, or subtalar joint neutral position, as advocated by the Root Theory.74 The authors use a case study to illustrate application of their model.27 Stress levels that are higher than the maintenance stress range, yet are lower than the threshold value for injury, can have positive effects on tissue adaptation. Based on Principle E of the PST, musculoskeletal tissues subjected to levels of stress that are higher than normal become more tolerant to subsequent physical stresses and are more resistant to injury (ie, tissues become stronger). Principle I suggests that this type of adaptation occurs only when tissues are able to recover and adapt to previous bouts of physical stress. Controlled increases in physical stress through progressive resistive exercise cause muscle fibers to hypertrophy and become capable of generating greater force. Likewise, higher-thannormal levels of physical stress can promote remodeling in bone.75 Wolffs Law provides an excellent example of how one specific biological tissue, bone, responds to physical stress by remodeling. Wolffs Law states that the thickness, number, and orientation of trabeculae will correspond to the distribution of mechanical stresses on bone.75 A consequence of stress-induced bone remodeling is that the strength of bone is greatest in the direction in which loads are most commonly imposed.76 For example, the maximum stress tolerated by bone just prior to failure has been found to be higher for compressive loads than for tensile or shear loads, reflecting the predominantly compressive loads experienced by bone during weight bearing.77 Runners with a documented increase in bone mineral density (BMD) in the leg, but not arm, compared with nonathletes provide one example of mechanically induced adaptations in bone.51 Similarly, contralateral differences in arm BMD have been observed in volleyball, basketball, and tennis players, but not in swimmers.78,79 Similar to bone, models of tendon and ligament adaptation predict that deviations from a typical range of strain (change in length relative to original length) stimulus values promote adaptive responses in these tissues. According to these models, strain values of 1.5% to 3.0% are required to maintain tissue homeostasis.80 Strain values above this range will lead to increases in the cross-sectional area and stiffness of tendon and ligament, whereas strain values below this range predict decreases in these parameters. The models further predict that the more the strain stimulus deviates from steady-state values, the faster adaptive responses occur in tissue. Modelbased simulations of tissue adaptation are consistent with histology data for tendon and ligament in animals and humans.80 Other research has demonstrated that both tendon and ligament respond to exercise-induced stress with increases in cross-sectional area, stiffness, and tensile strength.81 84

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

Mueller and Maluf . 393

Evidence also supports the idea that tissues within the musculoskeletal system atrophy and become less tolerant of physical stress if stress on the tissue diminishes below a baseline level.59,85 88 Unfortunately, tissues typically atrophy at a faster rate than they hypertrophy.59,85 Muscle can lose 6% to 40% of its ability to generate force over a 4- to 6-week period of bed rest or immobilization.86 Bone mineral density also is lost in response to diminished physical stress. Leblanc et al87 found that BMD is reduced 3% to 4% at the femoral neck and lumbar spine after 17 weeks of bed rest in young men who are healthy. Holick88 summarized the current literature by indicating that unloading of the skeleton, either due to strict bed rest or in zero gravity, leads, on average, to a 1% to 2% reduction in BMD at selected skeletal sites each month. Likewise, ligaments respond to reduced mechanical stress. Woo and colleagues85,89 have documented a decline in the mechanical properties of the rabbit medial collateral ligament in response to 9 weeks of immobilization. These researchers reported that the stiffness, the ultimate load before failure, and the energy-absorbing capacity of the immobilized medial collateral ligament-bone complex were approximately one third of those variables in the contralateral, nonimmobilized control limb.89 Integumentary System Tissues in the integumentary system also demonstrate patterns of response to physical stress similar to those described for the musculoskeletal system. Mechanisms of excessive stress resulting in injury to the skin have been described by Brand24 regarding his work with patients with Hansen disease and foot ulcers. Brand24 proposed the same 3 basic mechanisms of injury to skin that we describe for musculoskeletal tissues and that are outlined in this theory (Principle J, Tab. 1). According to Brand,24 direct mechanical damage to the skin can occur with high levels of pressure (100 kg/cm2 or 1,300 psi) applied for a brief duration, such as when a person steps on a tack. Ischemic skin lesions can occur when a relatively low magnitude of pressure (15 psi) is applied to the skin for a long duration, such as when people wear tight shoes or are confined to bed for prolonged periods of time. Inflammatory autolysis, similar in concept to cumulative trauma injury, can occur when pressures of a moderate magnitude (20 psi) are applied to the skin hundreds or thousands of times each day, such as stresses applied to plantar tissues during normal walking.24 Integument failure due to repetitive stress was shown when repetitive stress (10,000 repetitions per day) was applied to denervated rat footpads in an attempt to simulate stress on the foot during walking. Footpad ulcers occurred within 7 to 10 days of commencing the simulated walking procedures.90 Brand24 and others91,92

subsequently documented similar relationships among time, pressure, and skin breakdown in patients with diabetes and peripheral neuropathy. Skin also exhibits positive adaptations to controlled increases in physical stress. Clinicians have observed that skin adapts to progressive loading with improved stress tolerance. A common practice for treating patients with a new orthotic or prosthetic device is to slowly progress the magnitude and duration of weight-bearing to allow skin and underlying tissues to adapt to new weightbearing forces.93 In addition, the incidence of blisters in the feet of runners has been found to be highest in the early stages of training, and it is much lower in people who consistently run relatively long distances (eg, 48 km [30 miles] per week) as compared with people who are just beginning to run.94 Sanders et al95 have provided a review of the growing body of literature that suggests that skin exhibits an adaptive response to stress similar to the response of other biological tissues. Skin under tension shows changes similar to ligaments and tendons under tension. Increases in collagen fibril diameter, collagen crosslinking, and sulfated proteoglycan content render skin more resistant to tensile forces. Skin adapts to increases in shear stress with an increase in the size and density of cells at the basement membrane and an increase in the thickness of the stratum corneum (the outermost cell layer on the surface of the skin). Increased thickness of the stratum corneum results in a greater volume of skin through which shear loads can be distributed. Distribution of shear loads causes a reduction in the shear gradient and, consequently, decreases the potential for skin breakdown. Cardiovasuclar/Pulmonary System Similar to what can occur to tissues in the musculoskeletal and integumentary systems, excessive physical stress can injure tissues in the cardiovascular/pulmonary system. Mechanical stretch induced by high blood pressure is thought to be an initial event that leads to cardiac hypertrophy and eventual cardiac failure.96 High blood pressure is an established risk factor for conditions such as stroke,97 myocardial infarction,98 and atherosclerotic disease.99 In addition, vigorous and unaccustomed physical activity has been associated with a higher incidence of cardiovascular events.100 The positive effects of physical stress in the form of exercise also are well documented for tissues in the cardiovascular/pulmonary system. McArdle et al13 outlined fundamental principles of exercise training for the cardiopulmonary system. The overload principle states that exercise overload specific to an activity must be applied to enhance physiologic improvement and bring

394 . Mueller and Maluf

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

about a training effect. As described for other systems, achieving overload without tissue injury requires an appropriate balance among training intensity (or magnitude), frequency, and duration (time factors). When developing training programs, physical therapists also must consider whether stress levels designed to improve cardiovascular performance have the potential to cause injury to tissues in the musculoskeletal system. Training can enhance cardiovascular function in athletes, people who are sedentary, people with disabilities, and people with previous cardiac impairments.13 Training causes adaptations in tissues within the cardiovascular and pulmonary systems, including an increase in the weight and volume of the heart, an increase in the size of the left ventricular cavity and the thickening of its walls, an increase in plasma volume, an increase in maximum cardiac output, and an increase in lung volumes. Intensive training can increase aerobic capacity 15% to 30% during the first 3 months, with as much as a 50% increase over a 2-year period (Tab. 3).101105 Similar to other systems described, the positive effects of physical stress (ie, aerobic exercise training) are quickly reversible for tissues in the cardiopulmonary system.13 Reductions in metabolic and exercise capacity can occur after only 1 to 2 weeks of detraining, and many other improvements are lost within several months of detraining.13 McArdle et al,13 for instance, reported a 25% reduction in maximum oxygen consumption in 5 subjects who remained bedridden for 20 consecutive days. Maximal stroke volume and cardiac output also decreased, resulting in a loss of aerobic capacity by an average of 1% per day.13(p396) Neuromuscular System In our opinion, adaptation of the nervous system in response to physical stress has not been studied as extensively as the adaptive response of tissues in the musculoskeletal, integumentary, and cardiovascular/ pulmonary systems. Increasing evidence, however, suggests that physical stress and activity affect the peripheral and central nervous systems in a manner similar to that of other tissues in the body.106 108 Excessive stress can cause injury to tissues within the nervous system via the 3 mechanisms discussed for other systems. Examples of nerve injuries caused by high-magnitude stress applied over a brief duration include spinal cord injuries resulting from gunshot wounds or motor vehicle accidents. Nerve injury also may be caused by lower-magnitude stresses applied repetitively or over a long duration. Examples of these mechanisms of nerve injury include carpal tunnel syndrome, tarsal tunnel syndrome, thoracic outlet syndrome, ulnar nerve palsy, spinal stenosis, and lumbar root lesions.

Novak and Mackinnon28,109,110 described excessive physical stress from various postural alignments and repetitive motions that can contribute to nerve injury and pain. The incidence of cumulative trauma disorders has risen dramatically over the last 15 years and has been linked to jobs that require high-force and highrepetition activities, especially when performed in awkward postures.49(pp37) The odds ratio for developing carpal tunnel syndrome has been reported to be greater than 15 for high-force, high-repetition jobs compared with jobs requiring low-force, low-repetition activities.111 Pressures within the carpal tunnel have been shown to be higher when the wrist is in extreme flexion or extension compared with a neutral position.112 Furthermore, jobs requiring excessive wrist deviations are considered a risk factor for injury to the median nerve.109 Lumbar spinal stenosis is another condition that can place excessive physical stress on neural tissues.113 Movements and postures of lumbar extension can further reduce the diameter of the spinal canal and vertebral foramen in people with spinal stenosis, causing compression of lumbar nerves and resulting in lower-extremity pain and parathesias.113 People with lumbar stenosis generally have reduced lower-extremity symptoms when their spine is flexed because this posture allows the vertebral foramen to widen, thereby reducing compressive and shear forces on neural tissues.114 Mechanical injury of nerve tissue can occur with lowmagnitude stresses applied for a long duration (compression injury) or from repetitive bouts of moderatemagnitude stresses (cumulative trauma disorders). Although some nerve injuries may require surgical correction, we believe one role of the physical therapist is to determine how excessive stress on the nerve can be relieved in a conservative fashion to facilitate healing of the nervous tissue. We have limited our discussion of the neuromuscular system to nerve injuries caused by mechanical stress on the nerve and surrounding structures. Although beyond the scope of this perspective, a growing body of literature suggests that neurons adapt to high and low levels of physical activity by altering their electrical activity106,108,115118 (Tab. 3; eg, rate of discharge, threshold of recruitment). The observation that physical activity can stimulate neural adaptation has important implications for the rehabilitation of patients with primary neurological disorders (eg, stroke, traumatic brain injury). We predict that the fundamental principles outlined in the PST can be used to describe neural adaptations following central or peripheral nervous system injury, and we encourage others to investigate this prediction.

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

Mueller and Maluf . 395

Limitations of the Physical Stress Theory The PST represents an effort to integrate common principles from the approaches and evidence described above. We also expand existing theories to place the role of tissue injury within a continuum of tissue viability so that the theory encompasses pathological conditions and principles of wellness and prevention. Like any theory, the PST has limitations. These limitations will be discussed next, followed by a discussion of the implications of the theory for physical therapist practice, education, and research. In the PST, we assume that tissue exposure to physical stress can be quantified, and we assume that knowledge of the level of stress exposure and factors that influence the adaptive capacity of tissues (eg, age, disease) can be used to predict tissue adaptation and injury. In its current form, however, the PST does not define absolute threshold values for tissue adaptation and injury. For example, we do not know whether a tissue is about to be injured until it begins to show signs of inflammation (ie, pain, heat, swelling, or redness). Although attempts are being made to identify biological markers that may identify thresholds of adaptation or injury (ie, integrins in the muscle119 and serum keratan sulfate in intervertebral disks120), much more research is needed to define these thresholds in multiple tissue types. We believe the PST provides an appropriate framework for investigating the influence of multiple factors on the level of physical stress required for tissue adaptation and injury avoidance. Despite the absence of specific values for thresholds of change, the PST currently provides an overall framework that outlines relative relationships along a continuum of tissue responses to physical stress. Elaboration and refinement of this preliminary framework should eventually allow for a quantitative understanding of the thresholds that indicate when atrophy, maintenance, hypertrophy, injury, and death of various tissues begin. Another limitation of this theory is that it describes changes at the tissue level and does not indicate how tissue change is related to functional limitations or disability. Therefore, we believe the PST must be used in combination with other theories or models of disablement121 to address the entire spectrum of physical disability. We believe that physical disablement models are critical for understanding the overall relationship between disease or pathophysiology and resulting impairments, functional limitations, and disability.121 We further believe that the PST can be used to complement the physical disablement models by helping us to understand the mechanisms of injuries and repair at a tissue level.

Certain areas within physical therapy are not well developed in the PST in its current form. For example, the PST does not address issues of adaptation in the central nervous system. In addition, the PST does not identify the specific psychosocial factors that most influence tissue adaptation and injury. We believe the current theory, however, does provide a useful framework a wide range of physical therapy issues and has implications for practice, research, and education. Implications for Physical Therapist Practice We believe the PST provides a useful framework to approach patient care. It emphasizes the role of physical stress by addressing factors known to influence the level of physical stress and the response of tissues to stress application. According to this theory, the primary role of the physical therapist is to modify physical stresses to achieve a desired goal. Two broad goals will be discussed. The first goal is to reduce pain and subsequent impairments, functional limitations, and disabilities that result from injury. The second goal is to increase activity tolerance. Each of these goals will be discussed further in subsequent sections. Implications for Treating Patients With Tissue Injury The PST provides a general model for evaluating and treating people with injury. Chronic tissue injury, defined as injury that results in pain lasting greater than 8 weeks, often is caused by stresses of moderate magnitude that are repeated hundreds or even thousands of times a day.24,49,63 Examples of injuries resulting from this mechanism include many forms of back and cervical pain,70 patellofemoral pain,122 tendinitis injuries (eg, Achilles tendon, posterior tibial tendon), impingement syndrome of the shoulder, stress fractures,71,72 neuropathic plantar ulcers,24 and carpal tunnel syndrome.49 The primary questions asked in the evaluation and treatment of these and other forms of tissue injury are: (1) What factors appear to be contributing to excessive stress on the injured tissue? and (2) How can these contributing factors be modified to reduce stress on the tissue and allow the tissue to heal? We believe proper identification of the injured tissue usually can help determine the factors contributing to excessive stress on the tissue. For example, suspected tendinitis might lead the clinician to investigate sources of stress caused by movements that are controlled by the muscle and tendon. In many cases, however, physical therapists are not able to confirm injury of a specific tissue using the tools currently available to them. The PST describes general principles of tissue adaptation and injury, applicable to all types of biological tissue, that can be used to guide treatment regardless of whether the injury can be localized to a specific structure. In our view, appropriate treatment, therefore, does not always

396 . Mueller and Maluf

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

require accurate identification of the injured structure. For instance, if low back pain can be eliminated by teaching the patient to move at the hips rather than moving at the lumbar spine when movements of the lumbar spine cause pain, identifying the specific injured tissue is of little benefit. We believe general principles that govern the response of all biological tissues to stress can be used to guide physical therapy intervention, even when pathology of a specific structure cannot be determined. In this context, we contend that the most important question to guide treatment becomes: What factors appear to be contributing to excessive stress on the injured tissue? This question relates to Fundamental Principles F, I, J, and K in Table 1. In our opinion, the factors in Table 2 should be systematically evaluated for their potential to contribute to excessive tissue stress or for their potential to modify the response of tissues to stress application. In our experience, various types of injury tend to be associated with a similar set of contributing factors. For example, we have observed that factors contributing to overuse injuries of the foot and ankle often include movement and alignment factors (ie, excessive pronation or supination,123 changes in activity) and extrinsic factors (ie, footwear). Factors that contribute to excessive tissue stress or modify the tissue response can be added to or subtracted from the model depending on individual characteristics of the patient and the therapists current working set of hypotheses. We suggest that a physical therapist develop a hypothesis regarding the factors that are contributing to excessive tissue stress and causing injury. The next logical question is: How can I modify these contributing factors to reduce stress on the tissues and allow the tissues to heal? Successful outcomes, in our opinion, help to confirm the initial hypothesis, whereas poor outcomes direct the clinician to investigate other potential sources of stress not identified by the initial hypothesis. This approach is consistent with the hypothesis-oriented algorithm for clinicians.124 The basic principles discussed can be illustrated with several examples. Maluf et al32 described evaluation and treatment of a patient with chronic low back pain. The authors speculated that repetition of rotation and extension movements of the lumbar spine contributed to excessive stress and injury to structures within the low back region. Low back symptoms improved following instructions designed to restrict lumbar rotation and extension movements during the performance of daily activities.32 McPoil and Hunt27 described a similar approach in the treatment of a patient with heel pain. The authors speculated that a recent change in activity level, poor footwear, and excessive pronation at the

subtalar joint contributed to excessive stress on the plantar fascia and resultant heel pain. The treatment plan, therefore, was designed to modify these factors to decrease stress on the plantar fascia (eg, modifying the patients work schedule to limit weight-bearing time, purchasing shoes with cushioned midsoles, obtaining temporary orthotic devices to control excessive pronation).27 Similar principles can be applied to the evaluation and treatment of many types of wounds. Mueller and Diamond125 described an approach emphasizing reduction of stress on plantar tissues in a patient with diabetes, peripheral neuropathy, and a chronic plantar ulcer (21 months). They speculated that a fixed equinus and rear-foot varus deformity contributed to excessive pressure on tissues in the forefoot during walking and prevented the chronic ulcer from healing. The wound healed after a total contact cast, followed by protective footwear, was applied to reduce excessive stress at the site of the wound.125 An approach based on principles of stress reduction also has been described for the treatment of peripheral nerve injuries such as carpal tunnel syndrome and brachial plexus injuries.109 Novak and Mackinnon109 have described how postures, movements, impairments, and physical activities can contribute to stress on peripheral nerve tissue. Furthermore, these authors have described how factors contributing to excessive stress on peripheral nerves can be modified to allow the nerve tissue to heal and, consequently, reduce the symptoms associated with nerve injury.109 Even after sources of excessive stress have been identified and removed, we contend that injured tissues will be less tolerant of stress than they were prior to injury due to pain, inflammation, and disuse associated with the injury (Principles C and K, Tab. 1). Therefore, after pain and inflammation have subsided, previously injured tissues, in our opinion, should be exposed to progressively higher levels of physical stress to gradually restore the tissues ability to tolerate greater levels of stress (Principle E, Tab. 1). Stress, we contend, should be applied progressively, with attention paid to the bodys need for rest and recovery. Implications for Improving Activity Tolerance Our examples were designed to illustrate how to promote healing and progressive strengthening of injured tissues. The goal of helping patients to improve activity tolerance will now be considered. Examples of this goal include increasing muscle peak force production, achieving independence in transfers, and improving walking tolerance. Activity can be considered a form of physical stress.40 Therefore, a systematic approach for evaluating and treating individuals with the goal of improving activity tolerance can be derived from the

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

Mueller and Maluf . 397

PST. We propose that the following questions are relevant to the goal of increasing activity tolerance: (1) What is the activity goal? (2) What are the current modifiable factors limiting the activity goal? and (3) How should these factors be modified to meet the activity goal? For example, the activity goal of an elderly person may be to stand independently from a sitting position. A physical therapist may hypothesize that the primary modifiable factors limiting this goal are: (1) lower-extremity muscle atrophy resulting in poor force production, (2) decreased dorsiflexion range of motion, (3) poor motor control (movement and alignment factors), and (4) a low seat surface (extrinsic factor). The persons age is an important physiological factor that may limit the potential for tissue adaptation and lower the threshold for tissue injury. A treatment plan designed to modify these factors based on the PST might include: (1) a progressive resistive exercise program for lower-extremity extensor muscles with at least 70% of maximum effort, 2 to 3 times a week, for several weeks to increase muscle force production, (2) stretching exercises to increase dorsiflexion range of motion, (3) practice standing from a seated position using appropriate movement strategies, and (4) advising the patient to obtain a higher chair so that lower muscle force production is needed to achieve the activity. The overload principle (Principle E, Tab. 1),13,40 in which maintenance stress levels are raised to the range of stress that promotes tissue hypertrophy, has tremendous implications for physical therapy and forms the basis for progressive resistance exercises to increase muscle performance and activity tolerance. Physical stress must be of sufficient magnitude and repetition to cause the desired change in performance. The role of the physical therapist, in our view, is to instruct people in the appropriate magnitude and repetition of exercise or activity to provide an adequate stimulus for hypertrophy of intended tissues without injuring other tissues. Although clinicians are accustomed to using the overload principle to achieve hypertrophy of muscle, these same principles can be applied to other tissues such as ligament, tendon,126 and skin95 (Tab. 3). Implications for Physical Therapist Education In a time when scientific and medical knowledge is expanding at an exponential rate, we believe the PST can help educators focus on appropriate content for a substantial portion of the physical therapy curriculum. According to the PST, key elements of the curriculum should include a clear understanding of how the body adapts to physical stress and how physical therapists can apply or modify stress on the body to achieve desired outcomes (Tabs. 1 and 3).

In the PST, we propose that several key content areas should be emphasized. Kinesiology, we argue, should be taught with an emphasis on tissue mechanics and how different types of movement contribute to stress on specific tissues. Classes related to exercise physiology, in our view, should present guidelines for exercise and activity prescription that are designed to fall within the range of stress that promotes tissue hypertrophy while avoiding injury. We contend that instruction about orthotic devices or modalities should focus on their use in modifying either the level of stress applied to the body or the bodys response to stress. The content of classes related to medicine and pathology should focus on providing an understanding of how particular diseases or pathologies modify the bodys response to various forms of physical stress including exercise and activity. Classes related to clinical diagnosis and management could be organized using the approach described in the section titled Implications for Physical Therapist Practice. We contend that the list of factors in Table 2 could form the focus of factors to consider for evaluation and intervention. Although there are other content areas that must be addressed in a curriculum (eg, administration), we contend that the factors listed above are the most important and could serve as the focus of content unique to a physical therapy curriculum. Students should be trained to develop a clinical hypothesis that identifies the most important factors contributing to a patients problem, to address each modifiable factor, and to revise the initial hypothesis based on evaluation of treatment outcomes. Implications for Research The PST provides a framework for generating research hypotheses that focus attention on what we believe to be the most important and basic treatment technique used by physical therapists: modifying physical stresses to facilitate tissue adaptation and prevent injury. Although emphasizing the role of physical stress (Tab. 1), the PST also recognizes the multifactorial nature of tissue adaptation and injury (Tab. 2). We believe this theory helps to clarify and expand on documented theoretical approaches currently used in physical therapy. Disablement models have provided an excellent theoretical framework for studying the relationship among impairments, functional limitations, and disability. We agree that a limitation of these models, however, is that they often do not address the underlying cause of the patients symptoms.127 For example, disablement models postulate that back pain leads to certain functional limitations, such as difficulty performing household chores. However, we believe these models do not encourage identification of the specific mechanisms that cause the pathology leading to low back pain. The PST helps to fill this theoretical void by proposing that

398 . Mueller and Maluf

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

excessive physical stress causes the pathology, resulting in pain and subsequent disability. We believe the PST also can be used to complement the American Physical Therapy Associations current Clinical Research Agenda for Physical Therapy.128 The agenda was designed to support, explain, and enhance physical therapy clinical practice by facilitating research that is useful primarily to clinicians.128(p499) The Clinical Research Agenda consists of 72 questions, organized according to the elements of the physical therapist patient/client management model. In addition to generating new research questions, we believe the PST provides a theoretical framework to help direct research for questions in the research agenda. For example, question 1.4.9. of the agenda asks, Do measures of postural alignment in people with spinal disorders influence clinical decision making, and, if so, how?128(p505) The PST directs the investigator to consider posture and alignment factors in the context of how these factors might contribute to excessive physical stress on the spine. Based on the PST, an investigator might hypothesize that, in the general population, posture and alignment contribute a small but meaningful effect size to spinal dysfunction. The PST suggests that other factors such as movement patterns, age, ergonomic environment, and psychosocial factors also must be considered in clinical decision making when examining and managing patients with spinal dysfunction. Furthermore, we believe the PST provides an organized framework for identifying and studying the relative contribution of each of these factors to the development, persistence, and recurrence of spinal disorders. This is one example of the many multifactorial problems encountered by physical therapists. In the PST, we suggest that contributing factors should not be investigated in isolation when studying the etiology of any given disorder. Another example of how the theory could be used to generate and test hypotheses put forth in the agenda is in the management of skin breakdown on the plantar surface of the foot in patients with diabetes and peripheral neuropathy. Question 2.2.1. asks, What are the modifiable risk factors for cumulative trauma syndrome?128(p505) Neuropathic plantar ulcers are one of many conditions that can be considered cumulative trauma syndrome.24 Investigators91,129 have determined that the location of plantar ulcers corresponds with areas of high physical stress, identified by peak plantar pressure. Identifying the magnitude of pressure that predicts injury of plantar tissues, however, has been elusive.130 The PST predicts that there is no single threshold of peak pressure that predicts injury for all patients. Rather, the theory suggests that a combination of stress-related variables (eg, magnitude, duration, repetition, and direction of pressures) must be considered when assess-

ing a patients risk for skin breakdown (Fundamental Principles H and J, Tab. 1).24 Furthermore, the threshold for injury is influenced by individual movement and alignment factors (eg, activity level, foot deformities), extrinsic factors (eg, type of shoes), psychosocial factors (eg, adherence), and physiological factors (eg, severity of peripheral vascular disease and peripheral neuropathy) (Tab. 1). Researchers who are attempting to investigate the complex issue of skin breakdown would need to account for these many factors. The PST provides a framework for connecting the factors that can be used to guide research questions for a broad range of problems encountered by physical therapists. Conclusion The PST emphasizes the application and modification of physical stress on tissues of the human body to elicit positive adaptations and avoid injury. Many of the thoughts presented in this article are not new. The summary and integration of these thoughts into a defined theory, however, does offer a comprehensive approach that we believe can help to direct physical therapist practice and research for a wide range of people with and without impairments. We assert that there is considerable evidence to support current physical therapist interventions directed at modifying physical stress. We challenge readers to test, modify, and develop this theory through practice and published research. Our hope is that readers will see common elements described in this perspective in their own areas of practice and that physical therapy can continue to move forward in a more systematic and evidence-based manner.
References
1 Mueller G, Morlock MM, Vollmer M, et al. Intramuscular pressure in the erector spinae and intra-abdominal pressure related to posture and load. Spine. 1998;23:2580 2590. 2 Milgrom C, Finestone A, Simkin A, et al. In-vivo strain measurements to evaluate the strengthening potential of exercises on the tibial bone. J Bone Joint Surg Br. 2000;82:591594. 3 Child RB, Brown SJ, Day SH, et al. Manipulation of knee extensor force using percutaneous electrical myostimulation during eccentric actions: effects on indices of muscle damage in humans. Int J Sports Med. 1998;19:468 473. 4 Adams MA, May S, Freeman BJ, et al. Effects of backward bending on lumbar intervertebral discs: relevance to physical therapy treatments for low back pain. Spine. 2000;25:431 437. 5 Mueller MJ. Therapeutic footwear helps protect the diabetic foot. J Am Podiatr Med Assoc. 1997;87:360 364. 6 Tipler PA. Physics. 2nd ed. New York, NY: Worth Publishers Inc; 1982. 7 Brown M, Holloszy JO. Effects of a low intensity exercise program on selected physical performance characteristics of 60- to 71-year olds. Aging (Milano). 1991;3:129 139. 8 Fiatarone MA, ONeill EF, Ryan ND, et al. Exercise training and nutritional supplementation for physical frailty in very elderly people. N Engl J Med. 1994;330:1769 1775.

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

Mueller and Maluf . 399

9 Minor MA, Hewett JE, Webel RR, et al. Efficacy of physical conditioning exercise in patients with rheumatoid arthritis and osteoarthritis. Arthritis Rheum. 1989;32:1396 1405. 10 Frontera WR, Meredith CN, OReilly KP, et al. Strength conditioning in older men: skeletal muscle hypertrophy and improved function. J Appl Physiol. 1988;64:1038 1044. 11 Kohrt WM, Ehsani AA, Birge SJ Jr. Effects of exercise involving predominantly either joint-reaction or ground-reaction forces on bone mineral density in older women. J Bone Miner Res. 1997;12:12531261. 12 Herman WH. Diabetes and exercise [commentary]. Clin Diabetes. 1999;17:156. 13 McArdle WM, Katch FI, Katch VL. Exercise Physiology: Energy, Nutrition, and Human Performance. 4th ed. Baltimore, Md: Williams & Wilkins Co; 1996. 14 Guide to Physical Therapist Practice. 2nd ed. Alexandria, Va: American Physical Therapy Association; 2001. 15 Cott CA, Finch E, Gasner D, et al. The movement continuum theory of physical therapy. Physiotherapy Canada. 1995;47:8795. 16 Sahrmann SA. Diagnosis by the physical therapista prerequisite for treatment: a special communication. Phys Ther. 1988;68:17031706. 17 Leeson TS, Leeson CR. Histology. 4th ed. Philadelphia, Pa: WB Saunders Co; 1981. 18 Ross MH, Reith EJ. Histology: A Text and Atlas. 3rd ed. New York, NY: Harper & Row; 1985. 19 Stedmans Medical Dictionary. 23rd ed. Baltimore, Md: Williams & Wilkins Co; 1976. 20 Clarkson PM, Sayers SP. Etiology of exercise-induced muscle damage. Can J Appl Physiol. 1999;24:234 248. 21 Philosophical Statement on Physical Therapy. HOD 06-83-03-05, 17. Alexandria, Va: American Physical Therapy Association; 1987. Applicable House of Delegates Policies. 22 Hislop HJ. Tenth Mary McMillan Lecture: The not-so-impossible dream. Phys Ther. 1975;55:1069 1080. 23 Radin EL, Paul IL, Rose RM. Mechanical factors in the aetiology of osteoarthritis. Ann Rheum Dis. 1975;34:132133. 24 Brand PW. The diabetic foot. In: Ellenberg M, Rifkin H, eds. Diabetes Mellitus: Theory and Practice. 3rd ed. New Hyde Park, NY: Medical Examination Publishing Co Inc; 1983:829 849. 25 Kendall HO, Kendall FP, Boynton DA. Posture and Pain. Malabar, Fla: Robert E Krieger Publishing Co Inc; 1985. 26 Delitto A, Erhard RE, Bowling RW. A treatment-based classification approach to low back syndrome: identifying and staging patients for conservative treatment. Phys Ther. 1995;75:470 485. 27 McPoil TG, Hunt GC. Evaluation and management of foot and ankle disorders: present problems and future directions. J Orthop Sports Phys Ther. 1995;21:381388. 28 Novak CB, Mackinnon SE. Nerve injury in repetitive motion disorders. Clin Orthop. 1998;10 20. 29 Porterfield JA, DeRosa C. Mechanical Low Back Pain: Perspectives in Functional Anatomy. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1998. 30 Sahrmann SA. Diagnosis and Treatment of Movement Impairment Syndromes. St Louis, Mo: Mosby; 2002. 31 Shumway-Cook A, Woollacott MH. Motor Control: Theory and Practical Applications. Baltimore, Md: Williams & Wilkins Co; 1995.

32 Maluf KS, Sahrmann SA, Van Dillen LR. Use of a classification system to guide nonsurgical management of a patient with chronic low back pain. Phys Ther. 2000;80:10971111. 33 Christie HJ, Kumar S, Warren SA. Postural aberrations in low back pain. Arch Phys Med Rehabil. 1995;76:218 224. 34 Hansson T, Bigos S, Beecher P, Wortley M. The lumbar lordosis in acute and chronic low-back pain. Spine. 1985;10:154 155. 35 Walker ML, Rothstein JM, Finucane SD, Lamb RL. Relationships between lumbar lordosis, pelvic tilt, and abdominal muscle performance. Phys Ther. 1987;67:512516. 36 Youdas JW, Garrett TR, Egan KS, Therneau TM. Lumbar lordosis and pelvic inclination in adults with chronic low back pain. Phys Ther. 2000;80:261275. 37 Youdas JW, Garrett TR, Harmsen S, et al. Lumbar lordosis and pelvic inclination of asymptomatic adults. Phys Ther. 1996;76: 1066 1081. 38 McKenzie R. The Lumbar Spine: Mechanical Diagnosis and Therapy. Waikanae, New Zealand: Spinal Publication Ltd; 1989. 39 Van Dillen LR, Sahrmann SA, Norton BJ, et al. Reliability of physical examination items used for classification of patients with low back pain. Phys Ther. 1998;78:979 988. 40 ACSMs Guidelines for Exercise Testing and Prescription. Franklin BA, Whaley MH, Howley ET, eds. 6th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2000. 41 Helmrich SP, Ragland DR, Leung RW, Pattenbarger RS Jr. Physical activity and reduced occurrence of non-insulin-dependent diabetes mellitus. N Engl J Med. 1991;325:147152. 42 Hu FB, Stampfer MJ, Colditz GA, et al. Physical activity and risk of stroke in women. JAMA. 2000;283:29612967. 43 Schrauwen P, Westerterp KR. The role of high-fat diets and physical activity in the regulation of body weight. Br J Nutr. 2000;84:417 427. 44 Bonutti PM, Windau JE, Ables BA, Miller BG. Static progressive stretch to reestablish elbow range of motion. Clin Orthop. 1994;303: 128 134. 45 Host HH. Scapular taping in the treatment of anterior shoulder impingement. Phys Ther. 1995;75:803 812. 46 Larsen B, Andreasen E, Urfer A, et al. Patellar taping: a radiographic examination of the medial glide technique. Am J Sports Med. 1995;23:465 471. 47 Rudicel SA. The shod foot and its implications for American women. J South Orthop Assoc. 1994;3:268 272. 48 McPoil TG. Athletic footwear: design, performance and selection issues. J Sci Med Sport. 2000;3:260 267. 49 Cumulative Trauma Disorders: A Manual for Musculoskeletal Diseases of the Upper Limbs. Putz-Anderson V, ed. New York, NY: Taylor and Francis; 1988. 50 Snyder-Mackler L, Delitto A, Bailey SL, Stralka SW. Strength of the quadriceps femoris muscle and functional recovery after reconstruction of the anterior cruciate ligament: a prospective, randomized clinical trial of electrical stimulation. J Bone Joint Surg Am. 1995;77: 1166 1173. 51 Belanger M, Stein RB, Wheeler GD, et al. Electrical stimulation: can it increase muscle strength and reverse osteopenia in spinal cord injured individuals? Arch Phys Med Rehabil. 2000;81:1090 1098. 52 Garrett WE Jr. Muscle strain injuries. Am J Sports Med. 1996;24(suppl 6):S2S8.

400 . Mueller and Maluf

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

53 Kendall FP, McCreary EK. Muscles: Testing and Function. 3rd ed. Baltimore, Md: Williams & Wilkins Co; 1983. 54 Prins J, Cutner D. Aquatic therapy in the rehabilitation of athletic injuries. Clin Sports Med. 1901;18:447 461. 55 Wernig A, Muller S. Laufband locomotion with body weight support improved walking in persons with severe spinal cord injuries. Paraplegia. 1992;30:229 238. 56 Macfarlane GJ, Hunt IM, Silman AJ. Role of mechanical and psychosocial factors in the onset of forearm pain: prospective population based study. BMJ. 2000;321:676 679. 57 Craig CR, Stitzel RE. Modern Pharmacology. 4th ed. Boston, Mass: Little Brown & Co; 1994. 58 Czerwinski SM, Kurowski TG, ONeil TM, Hickson RC. Initiating regular exercise protects against muscle atrophy from glucocorticoids. J Appl Physiol. 1987;63:1504 1510. 59 Kohrt W. Physical activity plays a leading role in skeletal health. Biomech. April 1999:57 64. 60 Cundy TF, Edmonds ME, Watkins PJ. Osteopenia and metatarsal fractures in diabetic neuropathy. Diabet Med. 1985;2:461 464. 61 van de Ende CH, Breedveld FC, le Cessie S, et al. Effect of intensive exercise on patients with active rheumatoid arthritis: a randomized clinical trial. Ann Rheum Dis. 2000;59:615 621. 62 Westby MD, Wade JP, Rangno KK, Berkowitz J. A randomized controlled trial to evaluate the effectiveness of an exercise program in women with rheumatoid arthritis taking low dose prednisone. J Rheumatol. 2000;27:1674 1680. 63 Irwin ML, Mayer-Davis EJ, Addy CL, et al. Moderate-intensity physical activity and fasting insulin levels in women: the Cross-Cultural Activity Participation Study. Diabetes Care. 2000;23:449 454. 64 Anderson DM, Patwell JM, Plaut K, McCullough K, eds. Dorlands Medical Dictionary. 27th ed. Philadelphia, Pa: WB Saunders Co; 1988. 65 Radin EL. Osteoarthrosis: what is known about prevention. Clin Orthop. 1987;222:60 65. 66 Radin EL, Parker HG, Pugh JW, et al. Response of joints to impact loading, III: relationship between trabecular microfractures and cartilage degeneration. J Biomech. 1973;6:5157. 67 Radin EL, Paul IL. Response of joints to impact loading, I: in vitro wear. Arthritis Rheum. 1971;14:356 362. 68 Simon SR, Radin EL, Paul IL, Rose RM. The response of joints to impact loading, II: in vivo behavior of subchondral bone. J Biomech. 1972;5:267272. 69 Cooper C, Snow S, McAlindon TE, et al. Risk factors for the incidence and progression of radiographic knee osteoarthritis. Arthritis Rheum. 2000;43:9951000. 70 McGill SM. The biomechanics of low back injury: implications on current practice in industry and the clinic. J Biomech. 1997;30:465 475. 71 Marshall P. The rehabilitation of overuse foot injuries in athletes and dancers. Clin Sports Med. 1988;7:175191. 72 Milgrom C, Giladi M, Stein M, et al. Stress fractures in military recruits: a prospective study showing an unusually high incidence. J Bone Joint Surg Br. 1985;67:732735. 73 Huston LJ, Greenfield ML, Wojtys EM. Anterior cruciate ligament injuries in the female athlete: potential risk factors. Clin Orthop. 2000;372:50 63. 74 Root ML, Orien WP, Weed JH. Normal and Abnormal Function of the Foot. 2nd ed. Los Angeles, Calif: Clinical Biomechanics Corp; 1977.

75 Turner CH. Three rules for bone adaptation to mechanical stimuli. Bone. 1998;23:399 407. 76 Frankel VH, Nordin M. Basic Biomechanics of the Skeletal System. Philadelphia, Pa: Lea and Febiger; 1980. 77 Weiner S, Traub W, Wagner HD. Lamellar bone: structure-function relations. J Structural Biol. 1999;126:241255. 78 Calbet JA, Moysi JS, Dorado C, Rodriguez LP. Bone mineral content and density in professional tennis players. Calcif Tissue Int. 1998;62: 491 496. 79 Lee EJ, Long KA, Risser WL, et al. Variations in bone status of contralateral and regional sites in young athletic women. Med Sci Sports Exerc. 1995;27:1354 1361. 80 Wren TA, Beaupre GS, Carter DR. A model for loading-dependent growth, development, and adaptation of tendons and ligaments. J Biomech. 1998;31:107114. 81 Cabaud HE, Chatty A, Gildengorin V, Feltman RJ. Exercise effects on the strength of the rat anterior cruciate ligament. Am J Sports Med. 1980;8:79 86. 82 Tipton CM, Matthes RD, Vailas AC, et al. The response of the galago senegalensis to physical training. Comp Biochem Physiol A. 1979;63:29 36. 83 Woo SL, Gomez MA, Sites TJ, et al. The biomechanical and morphological changes in the medial collateral ligament of the rabbit after immobilization and remobilization. J Bone Joint Surg Am. 1987;69: 1200 1211. 84 Woo SL, Ritter MA, Amiel D, et al. The biomechanical and biochemical properties of swine tendons: long term effects of exercise on the digital extensors. Connect Tissue Res. 1980;7:177183. 85 Woo SL, Gomez MA, Akeson WH. Mechanical behaviors of soft tissues: measurements, modifications, injuries, and treatments. In: Nahum AM, Melvin J, eds. The Biomechanics of Trauma. East Norwalk, Conn: Appleton Century Croft; 1985:109 133. 86 Bloomfield SA. Changes in musculoskeletal structure and function with prolonged bed rest. Med Sci Sports Exerc. 1997;29:197206. 87 Leblanc AD, Schneider VS, Evans HJ, et al. Bone mineral loss and recovery after 17 weeks of bed rest. J Bone Miner Res. 1990;5:843 850. 88 Holick MF. Perspective on the impact of weightlessness on calcium and bone metabolism. Bone. 1998;22(suppl 5):105S111S. 89 Woo SL, Gomez MA, Woo YK, Akeson WH. Mechanical properties of tendons and ligaments, II: the relationships of immobilization and exercise on tissue remodeling. Biorheology. 1982;19:397 408. 90 Manley MT, Darby T. Repetitive mechanical stress and denervation in plantar ulcer pathogenesis in rats. Arch Phys Med Rehabil. 1980;61: 171177. 91 Boulton AJ, Betts RP, Franks CI, et al. The natural history of foot pressure abnormalities in neuropathic diabetic subjects. Diabetes Res. 1987;5:7377. 92 Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation: basis for prevention. Diabetes Care. 1990;13:513521. 93 Shur DG, Cook TM. Prosthetics and Orthotics. Englewood Cliffs, NJ: Appleton & Lange, Prentice Hall; 1990:76 80. 94 Jagoda A, Madden H, Hinson C. A friction blister prevention study in a population of marines. Mil Med. 1981;146:42 44. 95 Sanders JE, Goldstein BS, Leotta DF. Skin response to mechanical stress: adaptation rather than breakdowna review of the literature. J Rehabil Res Dev. 1995;32:214 226.

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

Mueller and Maluf . 401

96 Yamazaki T, Komuro I, Shiojima I, Yazaki Y. The molecular mechanism of cardiac hypertrophy and failure. Ann NY Acad Sci. 1999;874: 38 48. 97 Ringelstein EB, Nabavi D. Long-term prevention of ischaemic stroke and stroke recurrence. Thromb Res. 2000;98:8396. 98 Mehta RH, Bossone E, Eagle KA. Current concepts in secondary prevention after acute myocardial infarction. Herz. 2000;25:47 60. 99 Taylor WR. Mechanical deformation of the arterial wall in hypertension: a mechanism for vascular pathology. Am J Med Sci. 1998;316: 156 161. 100 Shephard RJ. Exercise in coronary heart disease. Sports Med. 1986;3:26 49. 101 Bishop JE. Regulation of cardiovascular collagen deposition by mechanical forces. Molecular Medicine Today. 1998;4:69 75. 102 Kingwell BA, Arnold PJ, Jennings GL, et al. The effects of voluntary running on cardiac mass and aortic compliance in Wistar-Kyoto and spontaneously hypertensive rats. J Hypertension. 1998;16:181185. 103 Levine BD, Zuckerman JH, Pawelczyk JA. Cardiac atrophy after bed-rest deconditioning: a nonneural mechanism for orthostatic intolerance. Circulation. 1997;96:517525. 104 McCole SD, Brown MD, Moore GE, et al. Enhanced cardiovascular hemodynamics in endurance-trained postmenopausal women athletes. Med Sci Sports Exerc. 2000;32:10731079. 105 Wyatt HL, Mitchell J. Influences of physical conditioning and deconditioning on coronary vasculature of dogs. J Appl Physiol. 1978; 45:619 625. 106 Enoka RM. Neural adaptations with chronic physical activity. J Biomech. 1997;30:447 455. 107 McEwen BS. The neurobiology of stress: from serendipity to clinical relevance. Brain Res. 2000;886:172189. 108 Kempermann G, van Praag H, Gage FH. Activity-dependent regulation of neuronal plasticity and self repair. Prog Brain Res. 2000;127: 35 48. 109 Novak CB, Mackinnon SE. Repetitive use and static postures: a source of nerve compression and pain. J Hand Ther. 1997;10:151159. 110 Novak CB, Mackinnon SE. Thoracic outlet syndrome. Orthop Clin. 1996;27:747762. 111 Silverstein BA, Fine LJ, Armstrong TJ. Occupational factors and carpal tunnel syndrome. Am J Ind Med. 1987;11:343358. 112 Lundborg G, Gelberman RH, Minteer-Convery M, et al. Median nerve compression in the carpal tunnelfunctional response to experimentally induced controlled pressure. J Hand Surg Am. 1982;7: 252259. 113 Nowakowski P, Delitto A, Erhard RE. Lumbar spinal stenosis. Phys Ther. 1996;76:187190. 114 Penning L, Wilmink JT. Posture-dependent bilateral compression of L4 or L5 nerve roots in facet hypertrophy: a dynamic CT-myelographic study. Spine. 1987;12:488 500. 115 Carlstedt T, Cullheim S. Spinal cord motoneuron maintenance, injury and repair. Prog Brain Res. 2000;127:501514. 116 Sale DG. Neural adaptation to resistance training. Med Sci Sports Exerc. 1988;20(suppl 5):S135S145. 117 Rydevik B, Nordborg C. Changes in nerve function and nerve fibre structure induced by acute, graded compression. J Neurol Neurosurg Psychiatry. 1980;43:1070 1082.

118 Ochoa J, Fowler TJ, Gilliatt RW. Anatomical changes in peripheral nerves compressed by a pneumatic tourniquet. J Anat. 1972;113: 433 455. 119 Carson JA, Wei L. Integrin signalings potential for mediating gene expression in hypertrophying skeletal muscle. J Appl Physiol. 2000;88: 237343. 120 Kuiper JI, Verbeek JH, Frings-Dresen MHW, Kuiper S. Assessment of short-term physical loading of the back: Is serum keratan sulfate an appropriate biomarker? J Orthop Sports Phys Ther. 2001;31:472 480. 121 Jette AM. Physical disablement concepts for physical therapy research and practice. Phys Ther. 1994;74:380 386. 122 Dye SF. The knee as a biologic transmission with an envelope of function: a theory. Clin Orthop. 1996;325:10 18. 123 Dahle LK, Mueller MJ, Delitto A, et al. Visual assessment of foot type and relationship of foot type to lower extremity injury. J Orthop Sports Phys Ther. 1991;14:70 74. 124 Rothstein JM, Echternach JL. Hypothesis-oriented algorithm for clinicians: a method for evaluation and treatment planning. Phys Ther. 1986;66:1388 1394. 125 Mueller MJ, Diamond JE. Biomechanical treatment approach to diabetic plantar ulcers: a case report. Phys Ther. 1988;68:19171920. 126 Wren TA, Beaupre GS, Carter DR. A model for loading-dependent growth, development, and adaptation of tendons and ligaments. J Biomech. 1998;31:107114. 127 Di Fabio RP. Disablement: the patients problem no longer matters. J Orthop Sports Phys Ther. 2000;30:304 305. 128 Clinical Research Agenda for Physical Therapy. Phys Ther. 2000; 80:499 513. 129 Boulton AJ, Hardisty CA, Betts RP, et al. Dynamic foot pressure and other studies as diagnostic and management aids in diabetic neuropathy. Diabetes Care. 1983;6:26 33. 130 Armstrong DG, Peters EJ, Athanasiou KA, Lavary LA. Is there a critical level of plantar foot pressure to identify patients at risk for neuropathic foot ulceration? J Foot Ankle Surg. 1998;37:303307. 131 Rubin CT, Lanyon LE. Regulation of bone formation by applied dynamic loads. J Bone Joint Surg Am. 1984;66:397 402. 132 Rubin CT, Lanyon LE. Regulation of bone mass by mechanical strain magnitude. Calcif Tissue Int. 1985;37:411 417. 133 Notomi T, Lee SJ, Okimoto N, et al. Effects of resistance exercise training on mass, strength, and turnover of bone in growing rats. Eur J Appl Physiol. 2000;82:268 274. 134 Black DM, Cooper C. Epidemiology of fractures and assessment of fracture risk. Clin Lab Med. 2000;20:439 453. 135 American College of Sports Medicine position stand: osteoporosis and exercise. Med Sci Sports Exerc. 1995;27:ivii. 136 Fitts RH, McDonald KS, Schluter JM. The determinants of skeletal muscle force and power: their adaptability with changes in activity pattern. J Biomech. 1991;24(suppl 1):111122. 137 Yarasheski KE, Pak-Loduca J, Hasten DL, et al. Resistance exercise training increases mixed muscle protein synthesis rate in frail women and men 76 yr old. Am J Phys. 1999;277(1 pt 1):E118 E125. 138 Fitts RH, Riley DR, Widrick JJ. Physiology of a microgravity environment invited review: microgravity and skeletal muscle. J Appl Physiol. 2000;89:823 839. 139 Trappe S, Williamson D, Godard M, et al. Effect of resistance training on single muscle fiber contractile function in older men. J Appl Physiol. 2000;89:143152.

402 . Mueller and Maluf

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012 Physical Therapy . Volume 82 . Number 4 . April 2002

140 Tamaki T, Uchiyama S. Absolute and relative growth of rat skeletal muscle. Physiol Behav. 1995;57:913919. 141 Hayashi K. Biomechanical studies of the remodeling of knee joint tendons and ligaments. J Biomech. 1996;29:707716. 142 Noyes FR. Functional properties of knee ligaments and alterations induced by immobilization: a correlative biomechanical and histological study in primates. Clin Orthop. 1977;123:210 242. 143 Cohen NP, Foster RJ, Mow VC. Composition and dynamics of articular cartilage: structure, function, and maintaining healthy state. J Orthop Sports Phys Ther. 1998;28:203215. 144 Palmoski M, Perricone E, Brandt KD. Development and reversal of a proteoglycan aggregation defect in normal canine knee cartilage after immobilization. Arthritis Rheum. 1979;22:508 517. 145 Kiviranta I, Jurvelin J, Tammi M, et al. Weight bearing controls glycosaminoglycan concentration and articular cartilage thickness in the knee joints of young beagle dogs. Arthritis Rheum. 1987;30:801 809. 146 Saamanen AM, Tammi M, Kiviranta I, et al. Maturation of proteoglycan matrix in articular cartilage under increased and decreased joint loading: a study in young rabbits. Connect Tissue Res. 1987;16: 163175.

147 Jurvelin J, Kiviranta I, Saamanen AM, et al. Partial restoration of immobilization-induced softening of canine articular cartilage after remobilization of the knee (stifle) joint. J Orthop Res. 1989;7:352358. 148 Jurvelin J, Kiviranta I, Tammi M, Helminen HJ. Softening of canine articular cartilage after immobilization of the knee joint. Clin Orthop. 1986;207:246 252. 149 Benetos A, Laurent S, Asmar RG, et al. Large artery stiffness in hypertension. J Hypertension. 1997;15:S89 S97. 150 Huonker M, Halle M, Keul J. Structural and functional adaptations of the cardiovascular system by training. Int J Sports Med. 1996; 17(suppl 3):S164 S172. 151 Tanaka H, Dinenno FA, Monahan KD, et al. Aging, habitual exercise, and dynamic arterial compliance. Circulation. 2000;102: 1270 1275.

Physical Therapy . Volume 82 . Number 4 . April 2002 Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012

Mueller and Maluf . 403

Tissue Adaptation to Physical Stress: A Proposed ''Physical Stress Theory'' to Guide Physical Therapist Practice, Education, and Research Michael J Mueller and Katrina S Maluf PHYS THER. 2002; 82:383-403.

References

This article cites 127 articles, 30 of which you can access for free at: http://ptjournal.apta.org/content/82/4/383#BIBL This article has been cited by 19 HighWire-hosted articles: http://ptjournal.apta.org/content/82/4/383#otherarticles http://ptjournal.apta.org/subscriptions/

Cited by

Subscription Information

Permissions and Reprints http://ptjournal.apta.org/site/misc/terms.xhtml Information for Authors http://ptjournal.apta.org/site/misc/ifora.xhtml

Downloaded from http://ptjournal.apta.org/ by guest on February 25, 2012