The Journal of Bone and Joint Surgery (American) 80:1220-33 (1998)
© 1998 The Journal of Bone and Joint Surgery, Inc.
Instructional Course Lecture |
Instructional Course Lectures, The American Academy of Orthopaedic Surgeons - Running Injuries: A Biomechanical Approach*
TOM F. NOVACHECK, M.D. , ST. PAUL, MINNESOTA
An Instructional Course Lecture, American Academy of Orthopaedic Surgeons
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Introduction
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Approximately thirty million Americans run for recreation or competition. A marathon runner takes an average of 25,000 steps during a race. At each step, his or her body is subjected to a ground-reaction force that is several times body weight. An individual who runs fifty miles (eighty kilometers) a week may take as many as three million strides each year. Often, it is the number of repetitions that is responsible for the development of an injury. Each year, between one-quarter and one-half of all runners sustain an injury that is severe enough to cause a change in practice or performance12. The injury may lead the runner to seek consultation, to alter training, or to use medication. A variety of intrinsic and extrinsic factors have been blamed for such injuries14,16,28.
In addition, particular patterns of injury have been noted. James and Jones, in a series of 180 patients, found that injury to the anterior aspect of the knee, the iliotibial band, the plantar aspect of the foot, the Achilles tendon, or the posterior tibial muscle accounted for approximately two-thirds of all complaints (Fig. 1)14. Interestingly, although one might assume intuitively that particular anatomical abnormalities lead to specific patterns of injuryfor example, that hyperpronation predisposes to posterior tibial syndrome (pain along the posteromedial aspect of the tibia in the region of the origin of the posterior tibial muscle) or that genu varum leads to iliotibial-band syndromefew such relationships have been found.
The challenge during the last ten to fifteen years has been to make more sense of why and how these injuries occur. Greater understanding, which will lead to improvements in diagnosis and counseling, will come from new biomechanical information collected at gait-analysis laboratories31,34. In the last two decades, gait analysis has been used primarily for research and for the clinical evaluation of walking-gait abnormalities of children and of patients who have had an amputation. Investigators at gait-analysis laboratories can now measure three-dimensional motion with use of computerized motion-analysis systems and can calculate net joint moments by combining motion analysis with force-plate data. Newer systems that can obtain data at rates greater than 200 hertz have made it possible to evaluate the biomechanical aspects of walking and running associated with various sports activities.
This new dynamic biomechanical information, combined with an understanding of the physiology and pathophysiology of the musculoskeletal system, will shed light on the genesis of overuse injuries that are associated with running. This Instructional Course Lecture includes information on the biomechanics of human locomotion; the biomechanics, physiology, and pathophysiology of tendon function; and the soft-tissue stresses applied to some of the musculotendinous structures that are frequently injured in long-distance runners, including the tendons that make up the extensor mechanism of the knee, the iliotibial band, the Achilles tendon, and the plantar fascia.
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Biomechanics of Forward Human Locomotion
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The demarcation between walking and running (Fig. 2, point A) occurs when the two periods of the gait cycle that are known as double support (when both feet are simultaneously in contact with the ground) are eliminated in favor of two periods that are referred to as double float (when neither foot is touching the ground). Generally, as speed increases further, the point of initial contact changes from the hindfoot to the forefoot (Fig. 2, point B). This change typically represents the distinction between running and sprinting. For practical purposes, the difference between running and sprinting is related to the goal to be achieved. Running is performed over longer distances, with an emphasis on endurance and the conservation of aerobic energy; jogging, road racing, and marathon running are examples. Not all distance runners, however, make initial contact with the hindfoot. Sprinting activities are done over shorter distances and at faster speeds; the goal is to cover a relatively short distance as rapidly as possible without attempting to maintain aerobic metabolism. Elite sprinters make initial contact with the forefoot; in fact, the hindfoot may never contact the ground.

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Fig. 2 Diagram depicting forward locomotion in humans. Point A is the demarcation between walking and running, and point B is where the initial contact changes from the hindfoot to the forefoot.
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Gait Cycle
The basic unit of measurement in gait analysis is the gait cycle10. The gait cycle begins when one foot comes into contact with the ground (initial contact) and ends when the same foot makes contact with the ground again (subsequent initial contact). For the purpose of this discussion, the stance phase will be plotted before the swing phase (although not all authors follow this convention). The stance phase occurs when the foot first makes contact with the ground (initial contact) and ends when the foot leaves the ground (toe-off). The swing phase begins with toe-off and lasts until the foot contacts the ground again. Both of these phases are subdivided further (Figs. 3-A, 3-B, 3-C through 3-D). During walking, the stance phase accounts for more than 50 per cent of the gait cycle, which means that there are two periods of double support: one at the beginning and one at the end of the stance phase (Fig. 4). During running, toe-off occurs before 50 per cent of the gait cycle is completed; therefore, there are no periods when both feet are in contact with the ground. Instead, both feet are simultaneously airborne twice during the gait cycle: once at the beginning and once at the end of the swing phase27. As mentioned previously, the periods when both feet are airborne are referred to as double float. The timing of toe-off depends on speed. Less time is spent in the stance phase as the athlete moves faster. In a previous study, I found that toe-off occurred at 39 and 36 per cent of the gait cycle during running and sprinting, respectively23. Faster runners and elite sprinters spend even less time in the stance phase; in world-class sprinters, toe-off occurs at as early as 22 per cent of the gait cycle20.

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Figs. 3-A through 3-D: Diagrams depicting the gait cycle. (Fig. 3-A is reprinted from: Gage, J. R.: An overview of normal walking. In Instructional Course Lectures, American Academy of Orthopaedic Surgeons. Vol. 39, p. 291. Park Ridge, Illinois, American Academy of Orthopaedic Surgeons, 1990. Figs. 3-B and 3-D are reproduced, with modification, from: Novacheck, T. F.: Walking, running, and sprinting: a three-dimensional analysis of kinematics and kinetics. In Instructional Course Lectures, American Academy of Orthopaedic Surgeons. Vol. 44, p. 498. Rosemont, Illinois, American Academy of Orthopaedic Surgeons, 1995.)
Figs. 3-A and 3-B: Diagrams depicting a walking figure and the phases of
the walking-gait cycle. IC = initial contact (the point in time when the
foot first contacts the ground, marking the onset of the stance phase); LR
= loading response (the first period of double support, during which body
weight is accepted onto the forward limb [this period corresponds to the
pre-swing period for the contralateral limb]); MST = mid-stance (the period
of single support before the trailing limb has passed the limb that is in
the stance phase); TST = terminal stance (the period of single support
after the swinging limb has passed the limb that is in the stance phase);
PS = pre-swing (the second period of double support, during which body
weight is transferred to the contralateral limb in its period of loading
response); TO = toe-off (the point in time when the foot leaves the ground,
marking the end of the stance phase and the onset of the swing phase); and
ISW, MSW, and TSW = initial swing, midswing, and terminal swing (three
subdivisions of the swing phase that are not pertinent to the present
discussion).
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Figs. 3-A and 3-B: Diagrams depicting a walking figure and the phases of the walking-gait cycle. IC = initial contact (the point in time when the foot first contacts the ground, marking the onset of the stance phase); LR = loading response (the first period of double support, during which body weight is accepted onto the forward limb [this period corresponds to the pre-swing period for the contralateral limb]); MST = mid-stance (the period of single support before the trailing limb has passed the limb that is in the stance phase); TST = terminal stance (the period of single support after the swinging limb has passed the limb that is in the stance phase); PS = pre-swing (the second period of double support, during which body weight is transferred to the contralateral limb in its period of loading response); TO = toe-off (the point in time when the foot leaves the ground, marking the end of the stance phase and the onset of the swing phase); and ISW, MSW, and TSW = initial swing, midswing, and terminal swing (three subdivisions of the swing phase that are not pertinent to the present discussion).
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Figs. 3-C and 3-D: Diagrams depicting a running figure and the phases of the running-gait cycle. IC = initial contact; TO = toe-off; StR = stance-phase reversal (the point in time during the stance phase when the muscles stop decelerating the motion of the runner and start to generate power); SwR = swing-phase reversal (the point in time during the swing phase when the muscles stop accelerating the motion of the runner and start to decelerate the forward momentum of the lower limbs); absorption = the period beginning at swing-phase reversal, continuing through inital contact, and ending at stance-phase reversal; generation = the period beginning at stance-phase reversal, continuing through toe-off, and ending at swing-phase reversal; stance-phase absorption = the continuation of the absorption period during the stance phase, beginning at the time of initial contact and ending at the time of stance-phase reversal; stance-phase generation = the portion of the generation period that begins during the stance phase at the time of stance-phase reversal and ends at toe-off; swing-phase generation = the continuation of the generation period during the swing phase, beginning at toe-off and ending at the time of swing-phase reversal; and swing-phase absorption = the portion of the absorption period that begins during the swing phase at the time of swing-phase reversal and ends at the time of initial contact. (The musculoskeletal animation in Fig. 3-C was produced with use of SIMM [Software for Musculoskeletal Modelling; Musculographics, Chicago, Illinois].)
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Figs. 3-C and 3-D: Diagrams depicting a running figure and the phases of the running-gait cycle. IC = initial contact; TO = toe-off; StR = stance-phase reversal (the point in time during the stance phase when the muscles stop decelerating the motion of the runner and start to generate power); SwR = swing-phase reversal (the point in time during the swing phase when the muscles stop accelerating the motion of the runner and start to decelerate the forward momentum of the lower limbs); absorption = the period beginning at swing-phase reversal, continuing through inital contact, and ending at stance-phase reversal; generation = the period beginning at stance-phase reversal, continuing through toe-off, and ending at swing-phase reversal; stance-phase absorption = the continuation of the absorption period during the stance phase, beginning at the time of initial contact and ending at the time of stance-phase reversal; stance-phase generation = the portion of the generation period that begins during the stance phase at the time of stance-phase reversal and ends at toe-off; swing-phase generation = the continuation of the generation period during the swing phase, beginning at toe-off and ending at the time of swing-phase reversal; and swing-phase absorption = the portion of the absorption period that begins during the swing phase at the time of swing-phase reversal and ends at the time of initial contact. (The musculoskeletal animation in Fig. 3-C was produced with use of SIMM [Software for Musculoskeletal Modelling; Musculographics, Chicago, Illinois].)
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Fig. 4 Diagrams depicting the periods of double support (DS) and double
float (DF) during walking, running, and sprinting. (Reprinted from:
Novacheck, T. F.: Walking, running, and sprinting: a three-dimensional
analysis of kinematics and kinetics. In Instructional Course Lectures,
American Academy of Orthopaedic Surgeons. Vol. 44, p. 497. Rosemont,
Illinois, American Academy of Orthopaedic Surgeons,
1995.)
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Potential and Kinetic Energy
The relationship between potential and kinetic energy during walking differs critically from that during running (Fig. 5). During walking, the two types of energy are out of phase: in other words, when potential energy is high, kinetic energy is low, and vice versa. During running, the two types of energy are in phase. An appreciation of this difference makes it possible to understand why walking has been referred to as controlled falling (with the center of mass falling from its zenith during mid-stance to its nadir during double support) while running has been likened to the motion of an individual on a pogo stick1 (with the individual propelling himself or herself from a low point during mid-stance [stance-phase reversal] to a peak during double float).

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Fig. 5 Graphs showing the interactions between potential and kinetic
energy during walking and running. The figures above the curves depict an
individual on a pogo stick, indicating alternating periods of low and high
energy. (Reprinted, with permission, from: Alexander, R. M.: The Human
Machine, p. 75. New York, Columbia University Press,
1992.)
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As a result of this difference between walking and running, the body completely alters the methods that it uses to maintain energy efficiency. Large fluctuations in total energy going into and out of the system would be disadvantageous regardless of the pace of movement. During walking, efficiency is maintained by the effective interchange between potential and kinetic energy, which are out of phase. During running, in which the two forms of energy are in phase, this effective interchange is not possible. Instead, efficiency is maintained primarily in two ways23,24,31: (1) the storage and later return of elastic potential energy through the stretch of elastic structures (especially tendons) and (2) the transfer of energy from one body segment to another by muscles (such as the rectus femoris and the hamstrings) that cross two joints. I will elaborate later on the importance of the first of these two points, in the sections on the physiology of tendons and the pathophysiology of chronic running injuries.
Kinematics
Kinematics is the description of movement without consideration of the forces causing that movement. This type of analysis can be done in different ways. In the laboratory at Gillette Children's Specialty Healthcare, retroreflective markers are placed over particular landmarks on the trunk and the lower extremities (Figs. 6-A and 6-B). These markers, which reflect infrared light from emitters in the corners of the room, are tracked with use of a video-camera system. The specific locations of the markers in space are identified with use of a computer-software system. These marker locations are then used to determine specific body-segment positions and joint movements (Fig. 7). Clinicians have a qualitative understanding of what constitutes normal motion of the knee. Kinematic analysis provides an objective way to quantify the position of various joints at different points in the gait cycle as well as the degree of movement of each joint. The illustration of a running figure (Fig. 3-C) provides a visual reference for the quantitative measurement of movement (Fig. 7).

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Fig. 6-A Photographs showing a runner being tested with use of markers and force-plates. The retroreflective markers are placed in specific locations over key osseous landmarks, and the force-plates are located in the running surface.
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Fig. 6-B Photographs showing a runner being tested with use of markers and force-plates. The retroreflective markers are placed in specific locations over key osseous landmarks, and the force-plates are located in the running surface.
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Fig. 7 Kinematic graph. The gait cycle is plotted along the x axis as the time of one initial contact to that of the next. The cycle is depicted in percentages, but it also could have been shown as a function of time. The vertical line in the mid-portion of the graph (in this case, at 39 per cent) represents toe-off, with stance phase to the left of the line and swing phase to the right. The degrees of movement of the joint being considered (in this case, the knee) are depicted along the y axis. This type of graph provides answers to questions such as "What is the position of the knee at the time that the foot makes contact with the ground?", "What is the total range of motion of the knee during running?", and "What is the maximum degree of extension of the knee that occurs during running?" Flx = flexion and Ext = extension.
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Kinetics
Kinetics is the study of the forces that are responsible for movement. This information is gathered by measuring ground-reaction forces with use of force-plates in the running surface. The ground-reaction force is the force that the ground exerts on the foot during each instant of the stance phase. During running, the ground-reaction force is characterized by an initial spike of short duration followed by a broader wave that peaks in mid-stance (Fig. 8)1,31,34.

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Fig. 8 Graph depicting ground-reaction forces during running. These forces can be measured only during the stance-phase portion of the gait cycle, when the foot is in contact with the ground. Therefore, the graph depicts only the stance phase of gait.
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Inverse dynamics is a mathematical method used to calculate net moments about the hip, knee, and ankle joints. Body-segment positions (determined with use of the motion-analysis measurement system), the size and direction of the ground-reaction force vector (determined with use of force-plates), and the mass and location of the center of mass of each body segment (estimated with use of anthropometric data) are incorporated into a series of mathematical equations to calculate the net joint moments about the major joints of the lower extremity.
A moment, also known as a force couple, is expressed in newton-meters. This force acts at a distance from an axis of rotation to cause an angular acceleration about that axis (Figs. 9 and 10). External moments include the ground-reaction forces and inertial forces mentioned previously. Internal moments are those produced within the body; they may be generated by a muscle, ligament, or joint capsule. These moments are calculated with use of the mathematical equations that define inverse dynamics. Current modeling techniques do not allow for the calculation of individual tissue forces; however, an understanding of the magnitude and timing of net joint moments provides insight into which tissues are subjected to the highest stresses.

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Fig. 9 Diagram depicting moments about the ankle in the sagittal plane. MF = muscle force, M = moment, d = length of moment arm (the perpendicular distance from the point of application of a force to the center of the joint), and GRF = ground-reaction force. (Reproduced, with modification, from: Gage, J. R.: An overview of normal walking. In Instructional Course Lectures, American Academy of Orthopaedic Surgeons. Vol. 39, p. 293. Park Ridge, Illinois, American Academy of Orthopaedic Surgeons, 1990.)
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Fig. 10 Graph depicting moments about the ankle in the sagittal plane. As in the kinematic graph (Fig. 7), the gait cycle is depicted along the x axis in percentages. Internal moments are depicted along the y axis. The moments are measured in newton-meters; for standardization, they are commonly divided by body weight and expressed in newton-meters per kilogram. Deflections above the zero line (in this example) represent net moments of plantar flexion (Pla), during which the plantar flexors of the ankle are dominant. Deflections below the line represent predominance of the ankle dorsiflexors (Dor), which is not observed at any point during the running-gait cycle. This type of graph provides answers to questions such as "Which group of muscles is predominant at the time of stance-phase reversal?" and "What is the maximum moment that the plantar flexors of the ankle of a given individual are able to produce?"
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Joint power is the product of the net joint moment and the joint angular velocity (power = force x distance x ) and is expressed in watts per kilogram (Fig. 11). This type of analysis provides insight into which musculotendinous structures are responsible for deceleration and also makes it possible to identify the timing and location of the sources of power for forward movement. This information has been presented in detail previously24,27. In summary, the main sources of power are the gastrocnemius-soleus complex, at push-off; the quadriceps, during the first half of the generation phase (just after stance-phase reversal); the hip extensors, during the late swing and early stance phases; the hip flexors, at push-off and during the early swing phase; and the hip abductors, during the first half of the generation phase (just after stance-phase reversal). Interestingly, each of these musculotendinous units absorbs power by stretching (eccentric contraction) just before it generates power by shortening (concentric contraction).

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Fig. 11 Graph depicting the generation and absorption of ankle power in the sagittal plane. Again, the gait cycle is plotted along the x axis. Power, measured in watts per kilogram of body weight, is plotted on the y axis. Positive values indicate that power is being generated (Gen) by concentric contraction of the muscle group that is predominant at the joint at that time. Negative values indicate that power is being absorbed (Abs) by eccentric muscle activity. This type of graph provides answers to questions such as "Do the plantar flexors of the ankle function eccentrically and, if so, when?", "When do the plantar flexors of the ankle function concentrically?", and "How much power do the plantar flexors of the ankle generate just before push-off?"
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Recent animal studies have indicated that the changes in the length of the muscle belly itself are relatively slight29. Instead, the muscles function as tensioners of the musculotendinous springs (the tendons). Most of the change in length results from the stretch and recoil of the tendons; therefore, most of the work is done by the tendons. Tendons are, in fact, excellent biological springs (Fig. 12). Accordingly, we should begin to think of tendons as springs and of muscles as the tensioners of the springs19. This concept makes the analogy of a runner to a person on a pogo stick even more comprehensible. If we consider the Achilles tendon, for example, we can visualize the way that it stretches during the first portion of the stance phase of the gait cycle and then recoils to return the energy back to the system at the time of push-off. Its function is similar to that of the spring of the pogo stick (except that the tendon stretches under tension whereas the spring of the pogo stick compresses under pressure). I will elaborate on these concepts in the next section, on the physiology and pathophysiology of tendons.

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Fig. 12 Hysteresis curve for a tendon. If subjected to stretch (stress), the tendon elongates (strain), as shown by the arrow directed upward and to the right. The energy is stored as elastic potential energy. If the amount of deformation is within the physiological range, the tendon recoils, returning most of the energy that is absorbed during stretching, as shown by the arrow directed downward and to the left. In general, 90 to 95 per cent of the absorbed energy is returned to the system in the form of kinetic energy. The rest of the energy is dissipated as heat.
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We can begin to draw some conclusions on the basis of biomechanical analysis. Alexander found that the total energy turnover during each stance phase is approximately 100 joules when a seventy-kilogram man is running at 4.5 meters per second1. He calculated that thirty-five joules is stored as strain energy in the heel cord and that seventeen joules is stored in the arch of the foot. Additional energy is stored in the quadriceps tendon and the patellar ligament. As a result, less than half of this energy has to be removed by the muscles when they are acting as brakes and returned by the muscles when they are doing work. The muscles must still exert tension, but they shorten and lengthen less.
Until this type of biomechanical analysis was available, the forces that created the tissue trauma responsible for chronic injuries in runners were not known. This lack of knowledge led to inaccurate assumptions, the greatest of which was that most injuries are caused by the high impact forces that occur at the time of heel-strike. As a result, much research has been focused on footwear and the running surface as well as on how these two factors alter the impact of heel-strike3,4,7,8,21,22,33. It is easy to see that the passive forces associated with heel-strike are smaller in magnitude and shorter in duration than the active forces that occur during the latter three-quarters of the stance phase (Fig. 8)34. While attenuation of the shock of ground contact is still important, one must understand that absorption does not occur instantaneously, as it does when a bowling ball lands on a cement sidewalk. Instead, several different tissues dissipate this force over time during the first half of stance phase, thereby minimizing the shock to the body25. These tissues include the Achilles tendon, the plantar fascia, the quadriceps mechanism, and the hip abductors.
The fact that this list includes many of the sites most commonly injured in distance runners indicates the extent to which inverse dynamics has advanced the art of biomechanical evaluation. Winter was one of the first authors to point out that forces are highest during mid-stance and late stance and that most chronic injuries associated with jogging are more likely to be related to these forces than to those that occur at the time of heel-strike33. On the basis of these calculations, he recommended training with eccentric knee exercises (contracting the quadriceps and the hamstrings against forces that are greater than those generated by the muscles) and concentric plantar-flexion exercises (contracting the gastrocnemius-soleus complex against a force that is less than that generated by the muscles) to help to avoid injury. We now have knowledge that can provide insight into the biomechanical stresses that cause some of the most common patterns of injury. These biomechanical data will be presented in the last section of this Instructional Course Lecture. Before that discussion, however, it will be helpful to review the anatomy, physiology, and biomechanical behavior of tendons.
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Biomechanics, Physiology, and Pathophysiology of Tendons: Insights into Mechanisms of Injury
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Tendons are relatively avascular. They consist of 30 per cent collagen, 2 per cent elastin, and 68 per cent water. The cells that are incorporated in the tendon are called tenocytes. Tendons have a breaking point similar to that of steel. When collagenous tissues are first formed, there are no cross-links between the tropocollagen molecules. Cross-links develop during the growth of a collagen fibril, between the sixth and fourteenth days of formation. Fibrils, oriented randomly at first, later come to lie parallel to the tensile forces of the tissue. Thus, when a tendon is first formed, it is not as strong. In addition, if it is immobilized for too long after an injury, it can lose 20 to 40 per cent of its ground substance. Early motion helps to align the collagen fibers, thereby improving tensile strength and gliding ability. Training also increases the tensile and maximum static strength of the tendon. Exercise increases collagen synthesis, the number and size of the fibrils, and the concentration of metabolic enzymes26.
With aging, the production of enzymes that are essential for collagen formation decreases. The repair of soft tissue is delayed in older individuals. The collagen becomes less elastic, the tensile strength is reduced, the fibers shrink, and the tendon stiffens and is more likely to tear18,26.
Tendons are subjected to large tensile forces. As discussed earlier, if the forces are in the physiological range, the tendon deforms and then returns to its original state (Fig. 13). Tendons are stronger than muscles and can withstand larger forces. Longer fibers elongate more than shorter ones. The greater the cross-sectional area, the larger the load that can be withstood without deformation5. Tendons that go around corners are subjected to greater strain and are more likely to have interference with their blood supply. Because tendons are viscoelastic, their response to stress is rate and size-dependent; that is, the ability of a tendon to respond to stress depends on the rate of application of the stress and the size of the tendon6. Maximum load capacity and resistance to tears peak in the third decade and decrease with age thereafter26.

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Fig. 13 Stress-strain curve for a tendon. The first region (the toe
region) constitutes 0 to 2 per cent strain (stretch). The wavy
configuration of the tendon disappears in this region as the normally
crimped collagen fibers straighten. The second region is a physiological
zone in which the collagen fibers deform and respond linearly to load. If
the strain is less than 4 per cent, the tendon returns to its original
length. The size and number of fibers determine the force that the tendon
can withstand. The third region (also referred to as the region of
microscopic failure) constitutes 4 to 8 per cent strain. In this region,
the collagen fibers begin to slide past one another as the cross-links
start to fail. Macroscopic failure occurs in the fourth region, at strains
of more than 8 per cent. In this region, there is tensile failure of the
fibers and sheer failure between them. There is a threefold to fourfold
difference between the loads that are well tolerated in the physiological
range (the second region) and those that cause failure. (Reprinted, with
permission, from: Curwin, S., and Stanish, W. D. [editors]: Tendinitis: Its
Etiology and Treatment, p. 11. Lexington, Massachusetts, D. C. Heath,
1984.)
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Musculoskeletal tissues respond to stress either physiologically (by means of an anabolic or regenerative response) or pathologically (by means of a catabolic or degenerative response). Leadbetter described in detail the catabolic cell-matrix response to injury18. In a catabolic response, the cells are overwhelmed by the injury process and are not able to regenerate or repair the extracellular matrix. Sports-related injuries occur in association with the loss of cells or extracellular matrix resulting from sports-induced trauma (Fig. 14). This failure of cells and matrix to adapt to load exposure can be caused either by sudden overload or by cumulative overload secondary to cyclical overuse; injuries caused by cyclical overuse have been variously referred to as cumulative trauma disorders or cumulative cell-matrix adaptive responses18. An acute injury occurs when a sudden crisis causes failure either through aberrant tissue or as a result of high strain rates17. In contrast, a chronic injury is characterized by a slow, insidious onset that implies an antecedent subthreshold spectrum of structural damage. This damage eventually leads to a crisis episode, often heralded by pain or signs of inflammation, or both. Chronic injuries are characterized by persistent symptoms that do not resolve. It is worthwhile to note that pain has been emphasized disproportionately in the definition of inflammation, to the extent that any painful structure is immediately presumed to be inflamed.

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Fig. 14 Schematic of the pathogenic pathway that leads to the
detrimental responses of increased matrix degradation (left) and inadequate
matrix synthesis (right). These responses contribute to the onset of the
detrimental, positive feedback loop known as the tendinosis cycle.
(Reproduced, with modification, from: Leadbetter, W. B.: Cell-matrix
response in tendon injury. Clin. Sports Med., 11: 571, 1992. Reprinted with
permission.)
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The new tissue that is produced during a regenerative response is structurally and functionally identical to normal tissue. In contrast, the new tissue that is produced during a degenerative response is of a lower or less functional form. This tissue, which is more vulnerable to both cyclical and sudden overloading leading to mechanical fatigue and failure, represents a profound imbalance in cell-matrix homeostasis. Heat generated within the tendon may cause tenocyte necrosis, which in turn promotes degeneration32.
The four pathological conditions that make up the spectrum of tendinopathy are paratenonitis (inflammation of only the paratenon due to friction); tendinosis (intratendinous degeneration due to atrophy); paratenonitis with tendinosis (inflammation of the paratenon associated with intratendinous degeneration); and tendinitis (symptomatic degeneration of the tendon with vascular disruption and an inflammatory repair response)18. Overload or overuse of a tendon leads to an initial adaptive cell-matrix response. Continued abusive sports activity has two detrimental microscopic consequences: increased matrix degradation and inadequate matrix synthesis (Fig. 14). Factors that influence this process include hypoxia, poor nutrition, hypovascularity, hormonal changes, chronic inflammation, and aging. The combination of increased matrix degradation and inadequate matrix synthesis generates a feedback loop (the tendinosis cycle), during which degeneration of the tendon and microtears occur alternately (Fig. 14). Ultimately, there is structural deterioration, partial tissue failure, and the potential for a complete tear.
Periodization (the practice of alternating low and high-intensity workouts) in athletic training is currently recommended and is based on the principle of transition17,18. A sports-related injury is most likely to occur when the athlete experiences any change in use of the involved structure. This is a rate-dependent process. If training is within the physiological range, there is cellular homeostasis with an overall anabolic response. Insufficient training is associated with disuse and deconditioning, which can cause a catabolic response that ultimately leads to injury. Overtraining also can cause a catabolic response that leads to injury. Transitional risks (aspects of altered training that have the potential to cause injury) include an increased level of performance; improper training; changes in equipment; environmental changes, such as new surfaces or different altitudes; alterations in the frequency, intensity, or duration of training; attempts to master new techniques; a return to sports activity too soon after an injury; and body growth.
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Soft-Tissue Stresses for Specific Musculotendinous Units
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As discussed previously, the state of the art has indeed advanced beyond the evaluation of kinematic variables and the ground-reaction force under the supporting foot. We can gain a better understanding of the etiology of some of the most common injuries by evaluating the forces to which the soft tissues are subjected. Inverse dynamics allows for the evaluation of the net joint moments about the hip, knee, and ankle and provides insight into the location and timing of these soft-tissue stresses23,24,34. It should be remembered, however, that actual stress levels within specific musculotendinous structures cannot currently be calculated. The development of improved models will allow for the accurate calculation of stress levels within individual tissues. Four of the most common clinical entities are anterior knee pain, iliotibial-band syndrome, Achilles tendinopathy, and plantar fasciitis.
Anterior Knee Pain
The extensor mechanism of the knee is the most common site of chronic running injuries. Different anatomical sites within this structure can be involved13. Pain may be caused by periarticular soft-tissue degeneration and inflammation or by excessive stress on the articular cartilage of the patellofemoral joint. A thorough examination of the extensor mechanism includes an assessment of quadriceps strength, contracture, and the position of the vastus medialis obliquus as well as the position, tracking, stability, and mobility of the patella. The examiner also looks for a painful arc and areas of point tenderness. The extensor mechanism is a common site of chronic injury because it functions eccentrically to absorb 42 per cent of the actively absorbed energy associated with ground contact23.
The net knee-extensor moment in the stance phase of the gait cycle is as much as five times greater during running than it is during walking (Fig. 15). Moreover, at the time that the knee-extensor moment is greatest, the knee is flexed more during running than it is during walking (approximately 45 degrees compared with 22 degrees) (Fig. 16). This increased flexion places a much greater amount of stress on the quadriceps muscles, the quadriceps tendon, and the patellar ligament2. It also increases the compression force on the articular cartilage of the patellofemoral joint. In the skeletally immature or growing athlete, the growth centers about the patella and at the tibial tubercle are subjected to these stresses. Therefore, Osgood-Schlatter disease and jumper's knee are common15. Typically, these forces do not exceed the single-event injury threshold, but the cumulative effects of subthreshold stresses over time may be sufficient to damage the soft-tissue structures about the knee.

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Fig. 15 Graph depicting the flexor (Flx) and extensor (Ext) moments about the knee in the sagittal plane. The peak net extensor moment in the stance phase (at approximately 15 per cent of the gait cycle) is five times greater during running than during walking. (These data were derived from one running-gait cycle and one walking-gait cycle for a typical adult who has moderate experience in distance running.) The vertical lines indicate the time of toe-off during running (solid line) and walking (dotted line).
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Fig. 16 Graph depicting motion of the knee in the sagittal plane. Throughout the gait cycle, the knee is flexed more during running than during walking. (These data were derived from one running-gait cycle and one walking-gait cycle for a typical adult who has moderate experience in distance running.) The vertical lines indicate the time of toe-off during running (solid line) and walking (dotted line). Flx = flexion and Ext = extension.
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Iliotibial-Band Syndrome
Friction between the iliotibial band and the lateral femoral condyle is thought to cause iliotibial-band syndrome. The presenting symptom is tenderness in the region of the distal end of the iliotibial band along the outside of the knee34. The ground-reaction force normally occurs medial to the knee joint during single-limb support in any activity. This ground-reaction force produces an external varus moment. The iliotibial band stabilizes the knee against this external force by generating an internal valgus moment to help to maintain an upright position. The peak valgus moment (calculated in the coronal plane) is two and one-half times greater during running than it is during walking (Fig. 17).

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Fig. 17 Graph depicting the valgus moments (Val) about the knee in the coronal plane. The peak internal moment occurs in mid-stance and is 2.5 times higher during running than during walking. (These data were derived from one running-gait cycle and one walking-gait cycle for a typical adult who has moderate experience in distance running.) The vertical lines indicate the time of toe-off during running (solid line) and walking (dotted line). Var = varus moments.
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At the time that this peak internal moment occurs, the knee is at the point of maximum stance-phase flexion (approximately 45 degrees) (Fig. 16). Therefore, there is a high valgus moment at the time that the knee is flexed. This degree of flexion places the iliotibial band directly over the lateral femoral condyle, where it is most susceptible to a friction injury. It often has been reported that iliotibial-band syndrome is more common in runners who have a neutral or varus alignment of the knee16. This anatomical variation causes the ground-reaction force to occur in a more medial position. The external varus moment is therefore larger and the iliotibial band must generate a larger valgus moment to balance it, resulting in an increase in the amount of friction. This is an excellent example of how one can begin to understand the way in which a common pattern of chronic injury occurs. The combination of kinematic and kinetic data provides insight into both the position of the joint and the joint forces that create the tissue stress responsible for injury.
Achilles Tendinopathy
The Achilles tendon and its insertion are frequent sites of chronic injury in athletes. Pain along the course of the tendon is the most frequent presenting symptom. Tenderness along the course of the tendon, with or without swelling, also is common. Acute tears are almost always preceded by a prodromal period of low-grade pain9,11,34.
The Achilles tendon is another anatomical structure that stretches during the first half of stance phase and recoils later in a spring-like fashion. It stores energy as it is stretched and efficiently returns 90 per cent of this energy at the time of push-off1. If initial contact is with the forefoot, the eccentric function of the gastrocnemius-soleus-Achilles tendon complex is exaggerated as the heel is slowly lowered to the ground. The gastrocnemius-soleus complex generates greater plantar-flexion moments about the ankle during running than it does during walking (Fig. 18).

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Fig. 18 Graph depicting the moments about the ankle in the sagittal plane. The peak moment occurs in the second half of the stance phase during both walking and running and is approximately two times greater during running than during walking. (These data were derived from one running-gait cycle and one walking-gait cycle for a typical adult who has moderate experience in distance running.) The vertical lines indicate the time of toe-off during running (solid line) and walking (dotted line). Pla = plantar and Dor = dorsal.
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Because few other structures are involved, peak forces in the Achilles tendon can be estimated; these forces range from six to eight times body weight1. Peak moments occur not at the time of initial contact but during mid-stance. They are generated by the powerful contraction of the gastrocnemius-soleus complex rather than by the shock of initial contact with the ground. Injuries of the Achilles tendon are caused by the active muscle forces that occur during mid-stance rather than the passive impact forces that occur at the time of initial contact. Shoewear and the type of running surface are much less important factors in the genesis of these injuries than is commonly believed. Shoewear may play a role in decreasing locally increased stress in an individual who runs on an uneven surface or in one who runs with hyperpronation of the foot. If the shoe can control the position of the hindfoot, it may decrease localized stresses both along the medial aspect of the Achilles tendon and further up the kinetic chain9,14,30.
Plantar Fasciitis
The plantar fascia functions in much the same way as the Achilles tendon. It stores elastic potential energy when it stretches and efficiently returns most of it later in the cycle. Pain, especially on rising in the morning, is the most common presenting symptom. Tenderness, either along the course of the plantar fascia or at its origin on the medial aspect of the calcaneal tuberosity, is a typical finding on examination34. Stress in the plantar fascia can be as high as three times body weight1. Peak stress occurs around the time of mid-stance, when most of the weight-bearing forces have been transferred from the hindfoot to the ball of the foot. Excessive pronation increases the traction along the medial part of the plantar fascia, predisposing it to excessive stress and injury.
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Summary
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An understanding of the biomechanics of running activities and the physiology of the musculoskeletal system sheds light on the pathophysiology of overuse injuries associated with running. The list of factors that may contribute to chronic running injuries can be overwhelming. The goal of this Instructional Course Lecture has been to help the reader to better understand these concepts by presenting new information regarding the biomechanics of normal running together with previously available data on the response of musculoskeletal tissue to mechanical stress. Because a recent change in the training program is frequently an inciting factor, the concept of a safe, healthful transitional training window is a key component of treatment and prevention. The three-dimensional kinematic and kinetic data that have been presented briefly here to explain potential areas of injury have been described in much greater detail elsewhere23,24. This information is essential for an understanding of the intricacies of running gait. A knowledge of what is normal is a prerequisite to an understanding of what can go wrong. Only in this way can an insightful treatment plan addressing shoewear, orthotic devices, exercise, and modifications of training be developed.
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Footnotes
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*Printed with permission of the American Academy of Orthopaedic Surgeons. This article will appear in Instructional Course Lectures, Volume 48, American Academy of Orthopaedic Surgeons, Rosemont, Illinois, March 1999.
Although the author has not received and will not receive benefits for personal or professional use from a commercial party related directly or indirectly to the subject of this article, benefits have been or will be received but are directed solely to a research fund, foundation, educational institution, or other non-profit organization with which the author is associated. No funds were received in support of this study.
Gillette Children's Specialty Healthcare, 200 East University Avenue, St. Paul, Minnesota 55101. E-mail address for Dr. Novacheck: novac001@tc.umn.edu.
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