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Skeletal muscle architecture is the structural property of whole muscles that dominates their function. This review describes the basic architectural properties of human upper and lower extremity muscles. The designs of various muscle groups in humans and other species are analyzed from the point of view of optimizing function. Muscle fiber arrangement and motor unit arrangement is discussed in terms of the control of movement. Finally, the ability of muscles to change their architecture in response to immobilization, eccentric exercise, and surgical tendon transfer is reviewed. Future integrative physiological studies will provide insights into the mechanisms by which such adaptations occur. It is likely that muscle fibers transduce both stress and strain and respond by modifying sarcomere number in a way more suited to the new biomechanical environment.

Contractile properties of rabbit tibialis anterior muscles were measured after eccentric contraction to investigate the mechanism of muscle injury. In the first experiment, two groups of muscles were strained 25% of the muscle fiber length at identical rates. However, because the timing of the imposed length change relative to muscle activation was different, the groups experienced dramatically different muscle forces. Because muscle maximum tetanic tension and other contractile parameters measured after 30 min of cyclic activity with either strain timing pattern were identical (P > 0.4), we concluded that muscle damage was equivalent despite very different imposed forces. This result was supported by a second experiment in which the same protocol was performed at one-half the strain (12.5% muscle fiber length). Again, there was no difference in maximum tetanic tension after cyclic 12.5% strain with either strain timing. Data from both experiments were analyzed by two-way analysis of variance, which revealed a highly significant effect of strain magnitude (P < 0.001) but no significant effect of stretch timing (P > 0.7). We interpret these data to signify that it is not high force per se that causes muscle damage after eccentric contraction but the magnitude of the active strain (i.e., strain during active lengthening). This conclusion was supported by morphometric analysis showing equivalent area fractions of damaged muscle fibers that were observed throughout the muscle cross section. The active strain hypothesis is described in terms of the interaction between the myofibrillar cytoskeleton, the sarcomere, and the sarcolemma.

The mechanical properties of isolated single muscle fiber segments were measured in muscle cells obtained from patients undergoing surgery for correction of flexion contractures secondary to static perinatal encephalopathy (cerebral palsy). "Normal" muscle cells from patients with intact neuromuscular function were also mechanically tested. Fiber segments taken from subjects with spasticity developed passive tension at significantly shorter sarcomere lengths (1.84 +/- 0.05 microm, n = 15) than fibers taken from normal subjects (2.20 +/- 0.04 microm, n = 35). Elastic modulus of the stress-strain relationship in fibers from patients with spasticity (55.00 +/- 6.61 kPa) was almost double that measured in normal fibers (28.25 +/- 3.31 kPa). The fact that these muscle cells from patients with spasticity have a shorter resting sarcomere length and increased modulus compared with normal muscle cells suggests dramatic remodeling of intracellular or extracellular muscle structural components such as titin and collagen. Such changes in muscles of patients with spasticity may have implications for therapy.

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The passive mechanical properties of small muscle fiber bundles obtained from surgical patients with spasticity (n = 9) and patients without neuromuscular disorders (n = 21) were measured in order to determine the relative influence of intracellular and extracellular components. For both types of patient, tangent modulus was significantly greater in bundles compared to identical tests performed on isolated single cells (P < 0.05). However, the relative difference between bundles and single cells was much greater in normal tissue than spastic tissue. The tangent modulus of normal bundles (462.5 +/- 99.6 MPa) was 16 times greater than normal single cells (28.2 +/- 3.3 MPa), whereas the tangent modulus of spastic bundles (111.2 +/- 35.5 MPa) was only twice that of spastic muscle cells (55.0 +/- 6.6 MPa). This relatively small influence of the extracellular matrix (ECM) in spastic muscle was even more surprising because spastic muscle cells occupied a significantly smaller fraction of the total specimen area (38.5 +/- 13.6%) compared to normal muscle (95.0 +/- 8.8%). Based on these data, normal muscle ECM is calculated to have a modulus of 8.7 GPa, and the ECM from spastic muscle of only 0.20 GPa. These data indicate that spastic muscle, although composed of cells that are stiffer compared to normal muscle, contains an ECM of inferior mechanical strength. The present findings illustrate some of the profound changes that occur in skeletal muscle secondary to spasticity. The surgical implications of these results are discussed.

Exercise involving lengthening of an activated muscle can cause injury. Recent reports documented the mechanics of exercise-induced muscle injury as well as physiological and cellular events and manifestations of injury. Loss of the cytoskeletal protein desmin and loss of cellular integrity as evidenced by sarcolemmal damage occur early during heavy eccentric exercise. These studies indicate that the earliest events in muscle injury are mechanical in nature, while later events indicate that it may be more appropriate to conclude that intense exercise initiates a muscle remodeling process. We conclude that muscle injury after eccentric exercise is differently severe in muscles with different architecture, is fibre type-specific, primarily because of fibre strain in the acute phase, and is exacerbated by inflammation after the initial injury.