Extracellular connective tissues within muscle are divided into three sets: epimysium, perimysium, and endomysium. Figure 3-1 shows these tissues as they surround the various components of muscle—from the muscle belly to the very small active proteins. The epimysium is a tough structure that surrounds the entire surface of the muscle belly and separates it from other muscles. In essence, the epimysium gives form to the muscle belly. The epimysium contains tightly woven bundles of collagen fibers that are resistive to stretch. The perimysium lies beneath the epimysium and divides muscle into fascicles (i.e., groups of fibers) that provide a conduit for blood vessels and nerves. This connective tissue, like epimysium, is tough and relatively thick and resistive to stretch. The endomysium surrounds individual muscle fibers, immediately external to the sarcolemma (cell membrane). The endomysium marks the location of the metabolic exchange between muscle fibers and capillaries.⁹⁵ This delicate tissue is composed of a relatively dense meshwork of collagen fibers that are partly connected to the perimysium. Through lateral connections from the muscle fiber, the endomysium conveys part of the muscle’s contractile force to the tendon.

Muscle fibers within a muscle may be of varying length, with some extending from tendon to tendon and others only a fraction of this distance. Extracellular connective tissues help interconnect individual muscle fibers and therefore help transmit contractile forces throughout the entire length of the muscle.⁶⁵ Although the three sets of connective tissues are described as separate entities, they are interwoven as a continuous sheet of tissue. This arrangement confers strength, support, and elasticity to the whole muscle. Box 3-2 provides a summary of the functions of extracellular connective tissues within muscle.

BOX 3-2. Summary of the Functions of Extracellular Connective Tissues within Muscle

• Provides gross structure to muscle

• Serves as a conduit for blood vessels and nerves

• Generates passive tension, most notably when the muscle is stretched to its near-maximal length

• Assists muscle to regain shape after it is stretched

• Conveys contractile force to the tendon and ultimately across the joint

Muscle Morphology

Muscle morphology describes the basic shape of a whole muscle. Muscles have many shapes, which influence their ultimate function (Figure 3-2). Two of the most common shapes are fusiform and pennate (from the Latin penna, meaning feather). Fusiform muscles, such as the biceps brachii, have fibers running parallel to one another and to the central tendon. Pennate muscles, in contrast, possess fibers that approach their central tendon obliquely. For reasons described in the next section, pennate muscles contain a larger number of fibers and therefore generate relatively large forces. Most muscles in the body are considered pennate and may be further classified as unipennate, bipennate, or multipennate, depending on the number of similarly angled sets of fibers that attach into the central tendon.

FIGURE 3-2. Different shapes of muscle are shown. The varying shapes are based on dissimilar fiber orientations relative to the tendon and the direction of pull. (Modified from Standring S: Gray’s anatomy: the anatomical basis of clinical practice, ed 39, New York, 2005, Churchill Livingstone.)

Muscle Architecture

This section describes two important architectural features of a muscle: physiologic cross-sectional area and pennation angle. These features significantly affect the amount of force that is transmitted through the muscle and its tendon, and ultimately to the skeleton.

The physiologic cross-sectional area of a whole muscle reflects the amount of active proteins available to generate a contraction force. The physiologic cross-sectional area of a fusiform muscle is determined by cutting through its muscle belly or by dividing the muscle’s volume by its length. This value, expressed in square centimeters, represents the sum of the cross-sectional areas of all muscle fibers within the muscle. Assuming full activation, the maximal force potential of a muscle is proportional to the sum of the cross-sectional area of all its fibers. In normal conditions, therefore, a thicker muscle generates greater force than a thinner muscle of similar morphology. Measuring the physiologic cross-sectional area of a fusiform muscle is relatively simple because all fibers run essentially parallel. Caution needs to be used, however, when measuring the physiologic cross-section of pennate muscles, because fibers run at different angles to one another. For physiologic cross-sectional area to be measured accurately, the cross-section must be made perpendicular to each of the muscle fibers.

Pennation angle refers to the angle of orientation between the muscle fibers and tendon (Figure 3-3). If muscle fibers attach parallel to the tendon, the pennation angle is defined as 0 degrees. In this case essentially all of the force generated by the muscle fibers is transmitted to the tendon and across a joint. If, however, the pennation angle is greater than 0 degrees (i.e., oblique to the tendon), then less of the force produced by the muscle fiber is transmitted longitudinally through the tendon. Theoretically, a muscle with a pennation angle of 0 degrees transmits 100% of its contractile force through the tendon, whereas the same muscle with a pennation angle of 30 degrees transmits 86% of its force through the tendon. (The cosine of 30 degrees is 0.86.) Most human muscles have pennation angles that range from 0 to 30 degrees.⁶⁵

FIGURE 3-3. Unipennate muscle is shown with its muscle fibers oriented at a 30-degree pennation angle (θ).

In general, pennate muscles produce greater maximal force than fusiform muscles of similar volume. By orienting fibers obliquely to the central tendon, a pennate muscle can fit more fibers into a given length of muscle. This space-saving strategy provides pennate muscles with a relatively large physiologic cross-sectional area and hence a relatively large capability for generating high force. Consider, for example, the multipennate gastrocnemius muscle, which must generate very large forces during jumping. The reduced transfer of force from the pennate fiber to the tendon, because of the greater pennation angle, is small compared with the large force potential gained in physiologic cross-sectional area. As shown in Figure 3-3, a pennation angle of 30 degrees still enables the fibers to transfer 86% of their force through to the long axis of the tendon.

SPECIAL FOCUS 3-1 Method for Estimating the Maximal Force Potential of Muscle

Specific force of skeletal muscle is defined as the maximum amount of active force produced per unit physiologic cross-sectional area. This value is typically expressed in units such as newtons per square meter (N/m²) or pounds per square inch (lb/in²). The specific force of human muscle is difficult to estimate, but studies indicate values between 15 and 60 N/cm² or, on average, 30 N/cm² (about 45 lb/in²).²⁶ This large variability likely reflects the technical difficulty in measuring a person’s true physiologic cross-sectional area, in addition to differences in fiber type composition across persons and muscles.³⁹ Generally, a muscle with a higher proportion of fast twitch fibers can have a slightly higher specific force than a muscle with a higher proportion of slow twitch fibers.

The fact that the maximal force generated by a healthy muscle is highly correlated with its cross-sectional area is a simple but very informative concept. Consider, for example, a quadriceps muscle in a healthy, average-sized man, with a physiologic cross-sectional area of 180 cm². Assuming a specific force of 30 N/cm², the muscle would be expected to exert a maximal force of about 5400 N (180 cm² × 30 N/cm²), or about 1214 lb. Consider, in contrast, the much smaller adductor pollicis muscle in the hand—a muscle that has a similar specific force rating as the quadriceps. Because an average-sized adductor pollicis has a physiologic cross-sectional area of only about 2.5 cm², this muscle is capable of producing only about 75 N (17 lb) of contractile force.

The striking difference in maximal force potential in the two aforementioned muscles is not surprising considering their very different functional roles. Normally the demands on the quadriceps are large—this muscle is used routinely to lift much of the weight of the body against gravity. The architecture of the quadriceps significantly affects the amount of force that is transmitted through its tendon and ultimately to the skeleton across the knee. Assuming the quadriceps has an average angle of pennation of about 30 degrees, the maximal force expected to be transmitted through the tendon and across the knee would be about 4676 N (cosine 30 degrees × 5400 N), or 1051 lb. Although the magnitude of this force may seem implausible, it is actually within reason. Expressing this force in terms of torque may be more meaningful for the clinician who regularly works with strength-testing devices that measure knee extension strength. Assuming the quadriceps has a knee extensor moment arm of 4 cm,⁶¹ the best estimate of the maximal knee extensor torque would be about 187 Nm (0.04 m × 4676 N)—a value that certainly falls within the range reported in the literature for an adult healthy male.^36,109

Muscle and Tendon: Generation of Force

PASSIVE LENGTH-TENSION CURVE

On stimulation from the nervous system, the contractile (active) proteins within the sarcomeres cause a contraction or shortening of the entire muscle. These proteins—most notably actin and myosin—are physically supported by structural proteins, plus a network of other noncontractile extracellular connective tissues, namely, the epimysium, perimysium, endomysium. For functional rather than anatomic purposes, these noncontractile tissues have been described as parallel and series elastic components of muscle (Figure 3-4). Series elastic components are tissues that lie in series with the active proteins. Examples of these tissues are the tendon and large structural proteins, such as titin. The parallel elastic components, in contrast, are tissues that surround or lie in parallel with the active proteins. These noncontractile tissues include the extracellular connective tissues (such as the perimysium) and a family of other structural proteins that surround and support the muscle fiber.

FIGURE 3-4. A highly diagrammatic model of a whole muscle attaching between two bones, depicting noncontractile elements (such as extracellular connective tissues and the protein titin) and contractile elements (such as actin and myosin). The model differentiates the noncontractile elements (as coiled springs) as either series or parallel elastic components. Series elastic components (aligned in series with the contractile components) are illustrated by the tendon and the structural protein titin, shown within the sarcomere. The parallel elastic components (aligned in parallel with the contractile components) are represented by extracellular connective tissues (such as perimysium) and other structural proteins located throughout the muscle.

Stretching a whole muscle by extending a joint elongates both the parallel and series elastic components, generating a springlike resistance, or stiffness, within the muscle. The resistance is referred to as passive tension because it is does not depend on active or volitional contraction. The concept of parallel and serial elastic components is a simplified description of the anatomy; however, it is useful to explain the levels of resistance generated by a stretched muscle.

When the parallel and series elastic components are stretched within a muscle, a generalized passive length-tension curve is generated (Figure 3-5). The curve is similar to that obtained by stretching a rubber band. Approximating the shape of an exponential mathematic function, the passive elements within the muscle begin generating passive tension after a critical length at which all of the relaxed (i.e., slack) tissue has been brought to an initial level of tension. After this critical length has been reached, tension progressively increases until the muscle reaches levels of very high stiffness. At even higher tension, the tissue eventually ruptures, or fails.

FIGURE 3-5. A generalized passive length-tension curve is shown. As a muscle is progressively stretched, the tissue is slack during the muscle’s initial shortened length until it reaches a critical length at which it begins to generate passive tension. Beyond this critical length, the tension builds as an exponential function.

The passive tension in a stretched healthy muscle is attributed to the elastic forces produced by noncontractile elements, such as extracellular connective tissues, the tendon, and structural proteins. These tissues demonstrate different stiffness characteristics. When a muscle is only slightly or moderately stretched, structural proteins (in particular titin ⁶²) contribute most of the passive tension within the muscle. When a muscle is more extensively stretched, however, the extracellular connective tissues—especially those that compose the tendon—contribute much of the passive tension.⁶⁸

The simple passive length-tension curve represents an important part of the overall force-generating capability of the musculotendinous unit. This capability is especially important at very long lengths where muscle fibers begin to lose their active force-generating capability because there is less overlap among the active proteins that generate force. The steepness of the passive length-tension curve varies among muscles depending on muscle architecture and fiber length.

Passive tension within stretched muscles serves many useful purposes, such as moving or stabilizing a joint against the forces of gravity, physical contact, or other activated muscles. Consider, for example, the passive elongation of the calf muscles and Achilles tendon at the end of the stance phase of fast-paced walking, just before push off. This passive tension assists with the transmission of muscular force through the foot and to the ground, thereby helping to initiate propulsion. Although passive tension within stretched muscles is typically useful, its functional effectiveness at times is limited because of (1) the slow adaptability of the tissue to rapidly changing external forces, and (2) the significant amount of initial lengthening that must occur before the tissue can generate sufficient passive tension.

Stretched muscle tissue exhibits the property of elasticity because it can temporarily store part of the energy that created the stretch. This stored energy, when released, can augment the overall force potential of a muscle. A stretched muscle also exhibits viscoelastic properties (see Chapter 1) because its passive resistance (stiffness) increases with increased velocity of stretch. Properties of both elasticity and viscoelasticity are important components of plyometric exercise.

Although the stored energy in a moderately stretched muscle may be relatively slight when compared with the full force potential of the muscle, it may help prevent a muscle from being damaged during maximal elongation.⁶⁹ Elasticity therefore can serve as a damping mechanism that protects the structural components of the muscle and tendon.

ACTIVE LENGTH-TENSION CURVE

Muscle tissue is uniquely designed to generate force actively (i.e., volitionally) in response to a stimulus from the nervous system. This section of the chapter describes the means by which a muscle generates active force. Active force is produced by an activated muscle fiber, that is, one that is being stimulated by the nervous system to contract. As diagramed in Figure 3-4, both active force and passive tension are ultimately transmitted to the bones that constitute the joint.

Muscle fibers are composed of many tiny strands called myofibrils (see Figure 3-1). Myofibrils contain the contractile (active) proteins of the muscle fiber and have a distinctive structure. Each myofibril is 1 to 2 µm in diameter and consists of many myofilaments. The two most important myofilaments within the myofibril are the proteins actin and myosin. As will be described, muscle contraction involves a complex physiologic and mechanical interaction between these two proteins. The regular organization of these filaments produces the characteristic banded appearance of the myofibril as seen under the microscope (Figure 3-6). The repeating functional subunits of the myofibril are the sarcomeres (Figure 3-7). The dark band within a single sarcomere, also called the A band, correspond to the presence of myosin—thick filaments. Myosin also contains projections, called myosin heads, which are arranged in pairs (Figure 3-8). The light bands, also called I bands, contain actin—thin filaments (see Figure 3-7). In a resting muscle fiber, actin filaments partially overlap the myosin filaments. Under an electron microscope, the bands reveal a more complex pattern that consists of an H band, M line, and Z discs (defined in Table 3-1). Actin and myosin are aligned within the sarcomere with the help of structural proteins, providing mechanical stability to the fiber during contraction and stretch.^62,105 By way of the structural proteins and the endomysium, myofibrils ultimately connect with the tendon. This elegant connective web, formed between the proteins and connective tissues, allows force to be distributed longitudinally and laterally within a muscle.^74,75

TABLE 3-1.

Defined Regions within a Sarcomere

Region	Description
A band	Dark bands caused by the presence of thick myosin myofilaments.
I bands	Light bands caused by the presence of thin actin myofilaments.
H band	Region within A band where actin and myosin do not overlap.
M line	Midregion thickening of thick myosin myofilaments in the center of H band.
Z discs	Connecting points between successive sarcomeres. Z discs help anchor the thin actin myofilaments.

FIGURE 3-6. Electron micrograph of myofibrils demonstrates the regularly banded organization of myofilaments—actin and myosin. (From Fawcett DW: The cell, Philadelphia, 1981, Saunders.)

FIGURE 3-7. On top are electron micrographs of two full sarcomeres within a myofibril. The drawings below show relaxed and contracted (stimulated) myofibrils, indicating the position of the thick (myosin) and thin (actin) filaments. Detail of the regular, banded organization of the myofibril shows the position of the A band, I band, H band, M line, and Z discs. Relaxed and contracted states are shown to illustrate the changes that occur during shortening. (Modified from Standring S: Gray’s anatomy: the anatomical basis of clinical practice, ed 39, New York, 2005, Churchill Livingstone. Photographs by Brenda Russell, Department of Physiology and Biophysics, University of Illinois at Chicago. Original art by Lesley Skeates.)

FIGURE 3-8. Further detail of a sarcomere showing the crossbridge structure formed by the myosin heads and their attachment to the actin filaments. Note that the actin filament also contains the proteins troponin and tropomyosin. Troponin is responsible for exposing the actin filament to the myosin head, thereby allowing crossbridge formation. (From Levy MN, Koeppen BM, Stanton BA: Berne and Levy principles of physiology, ed 4, St Louis, 2006, Mosby.)

As described earlier, the sarcomere is the fundamental active force generator within the muscle fiber. Understanding the contractile events that take place in an individual sarcomere provides the basis for understanding the contraction process across the entire muscle. The contraction process is simply repeated from one sarcomere to the next. The model for describing active force generation within the sarcomere is called the sliding filament hypothesis and was developed independently by Hugh Huxley ⁵⁴ and Andrew Huxley (no relation).⁵³ In this model, active force is generated as actin filaments slide past myosin filaments, causing approximation of the Z discs and narrowing of the H band. This action results in a progressive overlap of the actin and myosin filaments, which, in effect, produces a shortening of each sarcomere, although the active proteins themselves do not actually shorten (Figure 3-9). Each myosin head attaches to an adjacent actin filament, forming a crossbridge. The amount of force generated within each sarcomere therefore depends on the number of simultaneously formed crossbridges. The greater the number of crossbridges, the greater the force generated within the sarcomere.

FIGURE 3-9. The sliding filament action showing myosin heads attaching and then releasing from the actin filament. This process is known as crossbridge cycling. Contractile force is generated during the power stroke of each crossbridge cycle. (From Guyton AC, Hall JE: Textbook of medical physiology, ed 10, Philadelphia, 2000, Saunders.)

As a consequence of the arrangement between the actin and myosin within a sarcomere, the amount of active force depends, in part, on the instantaneous length of the muscle fiber. A change in fiber length—from either active contraction or passive elongation—alters the amount of overlap between actin and myosin. The active length-tension curve for a sarcomere is presented in Figure 3-10. The ideal resting length of a muscle fiber (or individual sarcomere) is the length that allows the greatest number of crossbridges and therefore the greatest potential force. As the sarcomere is lengthened or shortened from its resting length, the number of potential crossbridges decreases so that lesser amounts of active force are generated, even under conditions of full activation or effort. The resulting active length-tension curve is described by an inverted U-shape with its peak at the ideal resting length.

FIGURE 3-10. Active length-tension curve of a sarcomere for four specified sarcomere lengths (upper right, A through D). Actin filaments (A) overlap so that the number of crossbridges is reduced. In B and C, actin and myosin filaments are positioned to allow an optimal number of crossbridges. In D, actin filaments are positioned out of the range of the myosin heads so that no crossbridges are formed. (From Guyton AC, Hall JE: Textbook of medical physiology, ed 10, Philadelphia, 2000, Saunders.)

The term length-force relationship is more appropriate for considering the terminology established in this text (see definitions of force and tension in the glossary of Chapter 1). The phrase length-tension is used, however, because of its wide acceptance in the physiology literature.

SPECIAL FOCUS 3-2 Muscle Proteins: an Expanding Area of Study for Muscle Physiologists

Thus far this chapter has focused primarily on the active proteins of actin and myosin within the sarcomere. More advanced study of this topic, however, reveals a far more complicated picture. Myosin, for example, is further classified into heavy chain or light chain proteins, with differing functions. The light chain myosin appears to have a more regulatory role in the contraction process, as do the proteins tropomyosin and troponin. Furthermore, other proteins serve an important structural or supportive role within or between the sarcomeres. The importance of these noncontractile proteins has been realized in recent decades. The information contained in Table 3-2 is intended primarily as background material and summarizes the most likely function of the more commonly studied muscle proteins. The interested reader may consult other sources for more detail on this topic.¹⁸

TABLE 3-2.

Summary of Functions of Selected Muscle Proteins

Adapted from Caiozzo VJ, Rourke B: The muscular system: structural and functional plasticity. In Tipton CM, ed: ACSM’s advanced exercise physiology, Philadelphia, 2006, Lippincott Williams & Wilkins.

SUMMATION OF ACTIVE FORCE AND PASSIVE TENSION: THE TOTAL LENGTH-TENSION CURVE

The active length-tension curve, when combined with the passive length-tension curve, yields the total length-tension curve of muscle. The combination of active force and passive tension allows for a large range of muscle forces over a wide range of muscle length. Consider the total length-tension curve for the muscle shown in Figure 3-11. At shortened lengths (a), below active resting length and below the length that generates passive tension, active force dominates the force-generating capability of the muscle. The force continues to rise as the muscle is lengthened (stretched) toward its resting length. As the muscle fiber is stretched beyond its resting length (b), passive tension begins to contribute so that the decrement in active force is offset by increased passive tension, effectively flattening this part of the total length-tension curve. This characteristic portion of the passive length-tension curve allows muscle to maintain high levels of force even as the muscle is stretched to a point at which active force generation is compromised. As the muscle fiber is further stretched (c), passive tension dominates the curve so that connective tissues are under near-maximal stress. High levels of passive tension are most apparent in muscles that are stretched across multiple joints. For example, as the wrist is actively and fully extended, the fingers passively flex slightly because of the stretch placed on the finger flexor muscles as they cross the front of the wrist. The amount of passive tension depends in part on the natural stiffness of the muscle. The shape of the total muscle length-tension curve therefore can vary considerably between muscles of different structure and function.⁸

FIGURE 3-11. Total length-tension curve for a typical muscle. At shortened lengths (a), all force is generated actively. As the muscle fiber is stretched beyond its resting length (b), passive tension begins to contribute to the total force. In (c) the muscle is further stretched, and passive tension accounts for most of the total force.

Isometric Muscle Force: Development of the Internal Torque–Joint Angle Curve

As defined in Chapter 1, isometric activation of a muscle produces force without a significant change in its length. This occurs naturally when the joint over which an activated muscle crosses is constrained from movement. Constraint often occurs from a force produced by an antagonistic muscle or an external source. Isometrically produced forces provide the necessary stability to the joints and body as a whole. The amplitude of an isometrically produced force from a given muscle reflects a summation of length-dependent active force and passive tension.

Maximal isometric force of a muscle is often used as a general indicator of a muscle’s peak strength and can indicate neuromuscular recovery after injury.57,84,110 In clinical settings it is not possible to directly measure length or force of maximally activated muscle. However, a muscle’s internal torque generation can be measured isometrically at several joint angles. Figure 3-12 shows the internal torque versus the joint angle curve (so-called “torque-angle curve”) of two muscle groups under isometric, maximal-effort conditions. (The torque-angle curve is the rotational equivalent of the total length-tension curve of a muscle group.) The internal torque produced isometrically by a muscle group can be determined by asking an individual to produce a maximal-effort contraction against a known external torque. As described in Chapter 4, an external torque can be determined by using an external force-sensing device (dynamometer) at a known distance from the joint’s axis of rotation. Because the measurement is performed during an isometric activation, the internal torque is assumed equal to the external torque. When a maximal-strength test is performed in conjunction with considerable encouragement provided by the tester, most healthy adults can achieve near-maximal activation of their muscle. Near-maximal activation is not always possible, however, in persons with pathology or trauma affecting their neuromuscular system.

FIGURE 3-12. Internal torque versus joint angle curve of two muscle groups under isometric, maximal-effort conditions. The shapes of the curves are very different for each muscle group. A, Internal torque of the elbow flexors is greatest at an angle of about 75 degrees of flexion. B, Internal torque of the hip abductors is greatest at a frontal plane angle of −10 degrees (i.e., 10 degrees of adduction).

SPECIAL FOCUS 3-3 Method of Measuring a Person’s Maximal Voluntary Muscle Activation

In normal clinical strength-testing situations, it is difficult to know for certain if a person is actually maximally activating a given muscle, even when maximal effort and good health are assumed. A measure of maximal voluntary activation can be assessed by applying a brief electrical stimulus to the motor nerve or directly over the skin of a muscle while the person is attempting a maximal voluntary contraction. Any increase in measured force that immediately follows the electrical stimulus indicates that not all the muscle fibers were volitionally activated. This technique is known as the interpolated stimulus technique.³⁵ The magnitude of voluntary activation is typically expressed as a percent of a muscle’s maximal activation potential (i.e., neural drive).

Most young healthy adults are able to achieve 95% to 100% of maximal isometric activation of the elbow flexor and dorsiflexors, although these values vary considerably among individuals and trials.5,35 The average level of maximal voluntary isometric activation can also vary among muscles.³⁵ Significantly lower levels of maximal voluntary activation have also been reported in muscles after trauma or disease, such as in the quadriceps muscle after anterior cruciate ligament injury¹⁰⁷ or in the diaphragm muscle in persons with asthma.⁶ Persons with multiple sclerosis have been shown to generate only 86% of maximum voluntary activation of their dorsiflexor muscles, compared with 96% activation in a healthy control group.⁸⁰

The shape of a maximal-effort torque-angle curve is very specific to each muscle group (compare Figure 3-12, A and B). The shape of each curve can yield important information about the physiologic and mechanical factors that determine the muscle groups’ torque. Consider the following two factors shown in Figure 3-13. First, muscle length changes as the joint angle changes. As previously described, a muscle’s force output—in both active and passive terms—is highly dependent on muscle length. Second, the changing joint angle alters the length of the muscle’s moment arm, or leverage.¹⁰⁴ For a given muscle force, a progressively larger moment arm creates a greater torque. Because both muscle length and leverage are altered simultaneously by rotation of the joint, it is not always possible to know which is more influential in determining the final shape of the torque-angle curve. A change in either variable—physiologic or mechanical—alters the clinical expression of a muscular-produced internal torque. Several clinically related examples are listed in Table 3-3.

TABLE 3-3.

Clinical Examples and Consequences of Changes in Mechanical or Physiologic Variables That Influence the Production of Internal Torque

FIGURE 3-13. Muscle length and moment arm have an impact on the maximal-effort torque for a given muscle. A, Muscle is at its near-greatest length, and muscle moment arm (brown line) is at its near-shortest length. B, Muscle length is shortened, and muscle moment arm length is greatest. (Modified from LeVeau BF: Williams and Lissner’s biomechanics of human motion, ed 3, Philadelphia, 1992, Saunders.)

The torque-angle curve of the hip abductors demonstrated in Figure 3-12, B depends primarily on muscle length, as shown by the linear reduction of maximal torque produced at progressively greater abduction angles of the hip. Regardless of the muscle group, however, the combination of high total muscle force (based on muscle length) and great leverage (based on moment arm length) results in the greatest relative internal torque.

In summary, the magnitude of isometric torque differs considerably based on the angle of the joint at the time of activation, even with maximal effort. Accordingly it is important that clinical measurements of isometric torque include the joint angle so that future comparisons are valid. The testing of isometric strength at different joint angles enables the characterizing of the functional range of a muscle’s strength. This information may be required to determine the suitability of a person for a certain task at the workplace, especially if the task requires a critical internal torque to be produced at certain joint angles.

SPECIAL FOCUS 3-4 Exploring the Reasons for the Unique “Signature” of a Muscle Group’s Isometric Torque-Angle Curve

Undoubtedly, the shape of a muscle group’s torque-angle curve is related to the functional demands placed on the muscles and the joint. For the elbow flexors, for example, the maximal internal torque potential is greatest in the midranges of elbow motion and least near full extension and flexion (see Figure 3-12, A). Not coincidentally, in the upright position the external torque caused by gravity acting on the forearm and hand-held objects is also greatest in the midranges of elbow motion and least at the extremes of elbow motion.

For the hip abductor muscles, the internal torque potential is greatest near neutral (0 degrees of abduction) (see Figure 3-12, B). This hip joint angle coincides with the approximate angle at which the hip abductor muscles are most needed for frontal plane stability in the single-limb support phase of walking. Large amounts of hip abduction torque are rarely functionally required in a position of maximal hip abduction.