A motor unit, which comprises the motor nerve and the muscle fibers it innervates, is responsible for the synchronized contraction of muscle cells when the motor nerve is stimulated. The size of motor units within a muscle varies based on the muscle's function.

The dystrophin-glycoprotein complex in skeletal muscle provides a structural link between the muscle cell's cytoskeleton and the extracellular matrix, which helps stabilize the sarcolemma and prevent contraction-induced injury. Duchenne's muscular dystrophy is associated with the loss of dystrophin. Electron micrographs illustrate the distribution of dystrophin in skeletal muscle of a normal patient and the loss of dystrophin in a patient with Duchenne's muscular dystrophy.

The activation of motor units with a small number of fibers in cardiac muscle facilitates fine motor control. The short duration of the skeletal muscle action potential allows for rapid contractions and increases tension in the muscle. Repetitive stimulation of the muscle to increase tension is referred to as tetany.

The neuromuscular junction formed by the α motor is an important component in muscle function.
A motor unit consists of the motor nerve and all the muscle fibers innervated by the nerve. The motor unit is the functional contractile unit because all the muscle cells within a motor unit contract synchronously when the motor nerve fires. The size of motor units within a muscle varies, depending on the function of the muscle.
• Fig. 12.5. A, Organization of the dystrophin-glycoprotein complex in skeletal muscle. The dystrophinglycoprotein complex provides a structural link between the cytoskeleton of the muscle cell and the extracellular matrix, which appears to stabilize the sarcolemma and hence prevents contraction-induced injury (rupture). Duchenne’s muscular dystrophy is associated with loss of dystrophin. Numbers in dystrophin indicate hinge regions (e.g., H1, H2) and spectrin-like repeat domains (e.g., 4, 8, 12). ABD, actin-binding domain; C, carboxy terminus; CC, coiled-coil domain; DBD, dystroglycan-binding domain; N, amino terminus; nNOSµ, neuronal nitric oxide synthase µ; SBS, syntrophin-binding site; SSPN, sarcospan; Syn, syntrophin. Electron micrographs of a longitudinal view (B) and a cross-sectional view (C) show the distribution of dystrophin in skeletal muscle of a normal patient (CTRL). Another cross-sectional view (D) shows the loss of dystrophin from skeletal muscle in a patient with Duchenne’s muscular dystrophy (DMD). (A, From Allen D, Whitehead N, Froehner S. Absence of dystrophin disrupts skeletal muscle signaling: roles of Ca2+, reactive oxygen species, and nitric oxide in the development of muscular dystrophy. Physiol Rev. 2016;96:253-305. B, From Anastasi G, et al. Costameric proteins in human skeletal muscle during muscular inactivity. J Anat. 2008;213:284-295. C and D, From Beekman C, et al. A sensitive, reproducible and objective immunofluorescence analysis method of dystrophin in individual fibers in samples from patients with Duchenne muscular dystrophy. PLoS One. 2014;9[9]:e107494.)
Activation of motor units with a small number of fibers cardiac muscle, in contrast, is approximately 200 msec. facilitates fine motor control. Activation of varying numbers The short duration of the skeletal muscle action potential of motor units within a muscle is one way in which the allows very rapid contractions of the fiber and provides tension developed by a muscle can be controlled (see yet another mechanism by which the force of contrac“Recruitment” in the section “Modulation of the Force of tion can be increased. Increasing tension by repetitive ”). stimulation of the muscle is called tetany (see the section
The neuromuscular junction formed by the α motor “