{"id":528,"date":"2025-06-19T22:21:49","date_gmt":"2025-06-19T22:21:49","guid":{"rendered":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/?post_type=chapter&p=528"},"modified":"2025-08-05T23:59:07","modified_gmt":"2025-08-05T23:59:07","slug":"muscle-tissue","status":"publish","type":"chapter","link":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/chapter\/muscle-tissue\/","title":{"raw":"Muscle Tissue","rendered":"Muscle Tissue"},"content":{"raw":"
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Focus Questions\u2014to Guide Your Reading of This Chapter<\/p>\r\n\r\n<\/header>\r\n

\r\n
    \r\n \t
  1. What are the five key properties of muscle tissue? How do these properties facilitate muscle function?<\/li>\r\n \t
  2. Explain the structure of muscle tissue. How does force generation translate from the sarcomere to the whole organ?<\/li>\r\n \t
  3. How is muscle force modulated?<\/li>\r\n<\/ol>\r\n<\/div>\r\n<\/div>\r\n

    11.1 Introduction<\/h1>\r\n

    Muscles are the motors of the vertebrate body. But muscles do more than just move us about\u2014they also work in conjunction with the skeletal system to provide body support as well as play a role in the movement of material through the body, such as moving blood through the vasculature or producing pressure changes in the chest to drive air in and out of the lungs. What\u2019s more, muscles enable vertebrate bodies to accomplish incredible feats: The shaker muscles of rattlesnake tails can maintain contraction frequencies of up to 100 Hz for hours. During migrations, eels can swim for months with minimal energy expenditure (four to six times less than that of salmon!). And the smooth muscles of the uterine wall can generate sustained intrauterine pressures of 80\u2013100 mmHg during labor!<\/p>\r\n

    This chapter will begin with a brief introduction to muscle development and then transition into an examination of the tissue-level structure of muscle. As we discuss the tissue-level structure of muscle, we\u2019ll highlight how this structure facilitates muscle function (namely, contraction).<\/p>\r\n\r\n

    11.2 Muscle Development<\/h1>\r\n

    Generally speaking, muscle cells develop from mesenchymal cells from the paraxial mesoderm (myotome). While these cells are actively dividing, they are known as myoblasts and are the precursors to mature muscle cells known as myocytes<\/strong> (just like we\u2019ve seen before with the precursors of bone cells called osteoblasts and precursors of cartilage cells called chondroblasts). When cell division stops, the myoblasts<\/strong> begin to elongate and differentiate into myocytes.<\/p>\r\n

    Depending on the location in the body, the muscle tissue type, and the ultimate function of the muscle that is developing, the myocytes can form and organize in very different ways. For example, in skeletal muscle, the myoblasts line up longitudinally and fuse together. This produces long, single cells with several hundred nuclei positioned along the outer edge of the cell membrane. This structure is called a syncytium<\/strong> and can produce individual myocytes as long as 30 cm in some animals! Because of the unique, elongated shape of the skeletal muscle myocytes, they are often called muscle fibers.<\/p>\r\n\r\n

    11.3 Structure and Function of Muscle<\/h1>\r\n

    Muscle Tissue Types<\/h2>\r\n

    Muscle tissue is specialized for contraction. This tissue type is composed primarily of myocytes (\u201cmyo\u201d = muscle, \u201ccyt\u201d = cell; so \u201cmyocytes\u201d = \u201cmuscle cells\u201d). The cells are considered excitable cells, meaning they respond to electrical or chemical stimulation. The cytoplasm of myocytes is filled with bundles of proteins called myofilaments<\/strong>, which give muscle cells their distinctive appearance. Muscle cells can take one of two forms:<\/p>\r\n\r\n

      \r\n \t
    1. Striated<\/strong><\/span>: having alternating light and dark bands formed by regions of myofilament overlap; this gives them a \u201cstripey\u201d appearance (think: striations = striped; see Figures 11.1A and 11.1C).<\/li>\r\n \t
    2. Smooth<\/strong><\/span>: lacking striations; these muscle cells also contain myofilaments, but the myofilaments are arranged as irregular bundles, so they don\u2019t overlap to form striations (Figure 11.1B).<\/li>\r\n<\/ol>\r\n

      In muscle tissue, a small amount of extracellular matrix surrounds each muscle cell and is called endomysium<\/strong> or external lamina; the endomysium functions to hold the muscle cells together in the tissue. We\u2019ll revisit this later in the chapter when we talk about gross muscle anatomy. Beyond this general distinction in appearance, we can further classify muscle tissue based on function. There are three types of muscle tissue (Figure 11.1):<\/p>\r\n\r\n

        \r\n \t
      1. Smooth muscle<\/strong><\/li>\r\n \t
      2. Cardiac muscle<\/strong><\/li>\r\n \t
      3. Skeletal muscle<\/strong><\/li>\r\n<\/ol>\r\n[caption id=\"\" align=\"aligncenter\" width=\"585\"]\"\" -
        Figure 11.1\u2014Three types of muscle tissue and their distinguishing features.[\/caption]\r\n

        Smooth muscle tissue, as its name implies, is composed of smooth muscle cells; contraction of this tissue is involuntary, meaning that we have no conscious control over contraction of this muscle type. We find smooth muscle tissue in the hollow organs of the digestive tract, blood vessels, eyes, skin, and the ducts of some glands. Smooth muscle tissue usually contains specialized junctions (\u201cgap junctions\u201d) between cells to facilitate cell-to-cell communication. There are two types of smooth muscle:<\/p>\r\n\r\n

          \r\n \t
        1. Unitary smooth muscle<\/strong><\/span>: This type of smooth muscle undergoes spontaneous, rhythmic contractions that are generated myogenically (i.e., from within the muscle). This type of smooth muscle is found in the digestive tract, uterus, and urinary ducts.<\/li>\r\n \t
        2. Multiunit smooth muscle<\/strong><\/span>: This type of smooth muscle is neurogenic<\/strong><\/span> (i.e., contraction is stimulated by the nervous system). Multiunit contractions allow more refined regulation of control; this type of smooth muscle is typically found in walls of blood vessels, irises of eyes, and sperm ducts.<\/li>\r\n<\/ol>\r\n

          Cardiac muscle tissue is composed of striated muscle cells called cardiac muscle cells; this type of muscle is found only in the heart. Contraction of cardiac muscle tissue is involuntary (like smooth muscle). Cardiac muscle cells are relatively short and branched; they are also uninucleate (one nucleus per cell). A key characteristic of cardiac muscle tissue is the presence of intercalated discs<\/strong>: Within the intercalated discs, we find junctions (i.e., places where neighboring cells connect) that enable rapid cell communication, which helps coordinate heart muscle contraction.<\/p>\r\n

          Skeletal muscle is also composed of striated muscle cells, and this muscle tissue type is found mostly attached to skeletal elements. Contraction of skeletal muscle is voluntary and occurs via electrical stimulation from the nervous system. Skeletal muscle is composed of long, thin muscle cells arranged in parallel\u2014these are often called muscle fibers and are formed by myoblasts (immature muscle cells). Because of their incredible length, muscle fibers are multinucleated<\/strong><\/span>\u2014meaning they have multiple nuclei. This chapter will focus primarily on skeletal muscle.<\/p>\r\n

          Even though these three muscle types have their differences, they all perform the same general function, which is to generate a force called muscle tension<\/strong><\/span>. Muscle tension functions in generating movement as well as maintaining posture, stabilizing joints, generating heat, and regulating the flow of substances through hollow organs. To accomplish the task of generating muscle tension, muscle cells must convert chemical energy in the form of ATP (adenosine triphosphate) into the mechanical energy of muscle tension. And this task requires that muscles have a set of particular properties, including the following:<\/p>\r\n\r\n

            \r\n \t
          1. Contractility<\/strong><\/span>: ability to contract or the drawing together of the proteins within a muscle cell (rather than necessarily the shortening of the cell)<\/li>\r\n \t
          2. Excitability<\/strong><\/span>: ability to respond to chemical, mechanical, or electrical stimuli<\/li>\r\n \t
          3. Conductivity<\/strong><\/span>: ability to transfer electrical change across the entire length of the cell\u2019s plasma membrane<\/li>\r\n \t
          4. Extensibility<\/strong><\/span>: ability to stretch up to three times their resting length without being damaged or rupturing<\/li>\r\n \t
          5. Elasticity<\/strong><\/span>: ability to return to the cell\u2019s original shape after being stretched<\/li>\r\n<\/ol>\r\n

            As you might imagine, given the tight relationship between form and function, these unique functions of muscle cells come with a bit of unique cellular structure. Muscle cells have the same organelles as other cells, but they also possess some key structural differences (Figure 11.2), which come with their own new set of terms, including the following:<\/p>\r\n\r\n

              \r\n \t
            1. Sarcolemma<\/strong><\/span>: phospholipid bilayer surrounding a muscle cell that houses specialized proteins that assist with cell function; analogous to the plasma membrane<\/li>\r\n \t
            2. Sarcoplasm<\/strong><\/span>: located within the muscle cell, contains cytosol and organelles, and is analogous to cytoplasm of other cell types<\/li>\r\n \t
            3. Sarcoplasmic reticulum<\/strong><\/span>: modified smooth endoplasmic reticulum that forms a weblike network around each myofibril and functions in the storage and release of calcium ions\u2014a critical component of muscle contraction<\/li>\r\n \t
            4. Myofibril<\/strong><\/span>: cylindrical organelle involved in muscle contraction that is composed of bundles of specialized proteins and is the most abundant organelle in skeletal muscle cells<\/li>\r\n<\/ol>\r\n[caption id=\"\" align=\"aligncenter\" width=\"624\"]\"\" -
              Figure 11.2\u2014Myocyte anatomy.[\/caption]\r\n

              Let\u2019s unpack the sarcolemma a bit more. Unlike other cells whose plasma membranes are restricted to the exterior surface of a cell, the sarcolemma actually forms inward extensions called transverse tubules<\/strong><\/span> or T-tubules<\/strong><\/span> (Figure 11.3). These T-tubules extend deep into the cell and surround each myofibril, creating a tunnel-like network within the cell. Because T-tubules are continuous with the exterior of the cell, they are filled with extracellular fluid. Inside the cell, the T-tubules are flanked on either side by enlarged portions of the sarcoplasmic reticulum called the terminal cisternae<\/strong><\/span>. Together, the T-tubule and two terminal cisternae are known as a triad<\/strong><\/span>. The triad is an important structure in the process of muscle contraction.<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"523\"]\"\" -
              Figure 11.3\u2014Anatomy of the sarcoplasmic reticulum.[\/caption]\r\n

              Let\u2019s look deeper still and consider the structure of individual myofibrils. A single myofibril is composed of hundreds to thousands of protein bundles called myofilaments<\/strong><\/span> (Figures 11.4 and 11.5<\/a>). Myofilaments are made up of one or more of three types of proteins:<\/p>\r\n\r\n

                \r\n \t
              1. Contractile proteins<\/strong><\/span>: produce tension<\/li>\r\n \t
              2. Regulatory proteins<\/strong><\/span>: control timing of muscle fiber contraction<\/li>\r\n \t
              3. Structural proteins<\/strong><\/span>: hold myofilaments in place and ensure structural stability of myofibrils and the muscle fiber<\/li>\r\n<\/ol>\r\n

                Of the myofilaments, there are three types:<\/p>\r\n\r\n

                  \r\n \t
                1. Thick<\/strong><\/span> filaments<\/li>\r\n \t
                2. Thin<\/strong><\/span> filaments<\/li>\r\n \t
                3. Elastic<\/strong><\/span> filaments<\/li>\r\n<\/ol>\r\n

                  Thick filaments are composed of many molecules of the contractile protein myosin<\/strong><\/span>. Myosin\u2019s structure has two globular heads and two intertwined polypeptide chains that compose the tail. The heads attach to the tail via a flexible neck. Thick filaments are arranged such that the heads, which contain a site for binding to thin filaments, are positioned at the ends of the filament and the tails are in the middle.<\/p>\r\n

                  Thin filaments are made up of both contractile and regulatory proteins:<\/p>\r\n\r\n

                    \r\n \t
                  1. Actin:<\/strong><\/span> contractile protein with an active site for binding to myosin head (thick filament); multiple actin subunits string together to form two intertwining strands and form the largest part of the thin filament<\/li>\r\n \t
                  2. Tropomyosin:<\/strong><\/span> long, ropelike regulatory protein that spirals around the actin strands and covers the actin active sites<\/li>\r\n \t
                  3. Troponin:<\/strong><\/span> small, globular regulatory protein that holds tropomyosin in place<\/li>\r\n<\/ol>\r\n

                    Tropomyosin and troponin function in switching on and off (or \u201cregulating\u201d) muscle contraction by controlling whether the active site on the actin subunits is available to interact with the myosin heads of the thick filament.<\/p>\r\n

                    Elastic filaments are composed of a single large structural protein called titin<\/strong><\/span>. Titin is coil shaped, allowing it to stretch (\u201cextensibility\u201d) and recoil (\u201celasticity\u201d). This filament runs through the core of thick filaments and helps stabilize thick filament structure and resist excessive stretching. Because of its ability to recoil, elastic filaments enable muscle fibers to return to their original lengths after stretching.<\/p>\r\n

                    Myofibrils are patterned by the arrangement of thick and thin myofilaments; there are regions of the myofibril where only thin or thick filaments are present and regions where the two overlap. You\u2019ll recall that one of the characteristics of skeletal muscle fibers is that they are striated\u2014these light and dark bands (\u201cstriations\u201d) are produced by the repeated overlapping arrangement of thick and thin filaments within discrete units called sarcomeres<\/strong>. The anatomy of the sarcomere is as follows (Figures 11.4 and 11.5<\/a>):<\/p>\r\n\r\n

                      \r\n \t
                    1. Zone of overlap<\/strong><\/span>: where thick and thin filaments overlap; this is where tension is generated during muscle contraction.<\/li>\r\n \t
                    2. I <\/strong>band<\/strong><\/span>: light regions of a striation; only thin filaments are found here.<\/li>\r\n \t
                    3. A band<\/strong><\/span>: dark regions of a striation; this is the portion of the sarcomere that contains thick filaments. The edges of the A band actually contain both thick and thin filaments, as they overlap here, but the center of the A band is composed only of thick filaments (a region known as the H zone).<\/li>\r\n \t
                    4. M line<\/strong><\/span>: a dark line running down the center of the A band; this consists of structural proteins that function in holding thick filaments in place and serve as an anchoring point for the elastic filaments.<\/li>\r\n \t
                    5. Z disc <\/strong>(sometimes also called the Z line)<\/strong><\/span>: a dark line running down the center of the I band. The Z disc is also composed of structural proteins that function to anchor the thin filaments in place and serve as attachment sites for the elastic filaments. The Z discs attach myofibrils to one another across the diameter of the muscle fiber.<\/li>\r\n<\/ol>\r\n[caption id=\"\" align=\"aligncenter\" width=\"490\"]\"\" -
                      Figure 11.4\u2014Anatomy and organization of the muscle fiber and myofibrils.[\/caption]\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"541\"]\"\" -
                      Figure 11.5\u2014Anatomy and organization of the sarcomere. Note overlap of thick and thin filaments, allowing for interaction between the two proteins and the engagement of the sliding filament mechanism.[\/caption]\r\n

                      The sarcomere is the functional unit of the contraction in skeletal muscle and spans from one Z disc to the next Z disc; therefore, each sarcomere is composed of one A band and two half-I bands. There are many sarcomeres in each myofibril, and the particular arrangement of the sarcomere elements is crucial to allowing skeletal muscle contraction to occur, as we will see in the next section (Muscle Contraction<\/span><\/span>).<\/p>\r\n\r\n

                      \r\n

                      Box 11.1<\/span>\u2014A New Organizational Design in Skeletal Muscle Fibers<\/strong><\/p>\r\n

                      The structure of the sarcomere\u2014indeed, of the entire myofibril of skeletal muscle\u2014has been incredibly well conserved across vertebrate taxa. However, recent work by Eric Parmentier<\/strong><\/a> and Marc Thiry<\/strong> has identified a novel sarcomere architecture in the sound-producing muscles of the cusk eel (Parophidion vassali<\/em><\/span>; Figure 11.6). Parmentier and Thiry suggest that this peculiar sarcomere structure may be an adaptation that circumvents the trade-off between speed and force often observed in skeletal muscle (i.e., muscle contraction is typically fast or strong but rarely both). In this species, myofilaments have a branched, Y-shaped structure; each of these branches connects to a neighboring myofibril. This branched structure provides a mechanism for increasing the number of crossbridges that can form during muscle contraction, thus amplifying force production. Furthermore, cusk eel sarcomeres have wider Z discs than typically observed in vertebrate muscle. The larger Z disc may contribute to consistent sound features during high-speed contraction.<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"483\"]\"\" -
                      Figure 11.6\u2014Cusk eel. Photo credit: NOAA via @DeepSeaImage.[\/caption]\r\n

                      Interestingly, this isn\u2019t the only mechanism for sound production in fishes that involves funky musculature. Verity Cook<\/strong><\/a> and colleagues, at Charit\u00e9 University in Berlin, found that one of the world\u2019s smallest fish\u2014Danionella cerebrum<\/em><\/span>\u2014can actually produce a drumming sound over 140 dB. These fish accomplish this amazing feat through the use of a specialized muscle that pulls a rib into a small piece of indented cartilage. When the rib is released, it springs back and strikes the swim bladder to create a noise as loud as the bang of a firecracker!<\/p>\r\n\r\n<\/div>\r\n

                      Muscle Contraction<\/h2>\r\n

                      I mentioned that the structure of the sarcomere is critical for the muscle contraction to occur, but why? How does it happen?<\/p>\r\n

                      The widely accepted model for skeletal muscle contraction is the sliding filament theory. In the sliding filament theory, thin filaments slide past thick filaments and generate tension throughout the sarcomere. During contraction, the I bands and H zone narrow, but the A band does not change. This occurs because the myosin heads of the thick filaments bind to the thin filaments and pull them toward the M line. This brings the Z discs closer together and shortens the sarcomere as a unit. Something important to note here: None of the filaments themselves get shorter! The thin filaments are simply pulled toward the M line. And because the sarcomeres are arranged end-to-end within the myofibril, simultaneous contraction of the sarcomeres results in contraction of the whole muscle fiber (Figure 11.7).<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"500\"]\"\" -
                      Figure 11.7\u2014Relative position of the thick and thin filaments during sarcomere contraction. Note that the filaments themselves do not change length; rather, they change their position relative to each other (i.e., the zone of overlap increases in size).[\/caption]\r\n\r\n

                      \r\n

                      Box 11.2<\/span>\u2014Winding Filament Theory<\/strong><\/p>\r\n

                      Even though the sliding filament theory tends to be the established model for explaining muscle contraction, it fails to account for some aspects of muscle function, including how force is amplified during stretching and depressed during shortening. Dr. Kiisa Nishikawa<\/strong><\/a> and colleagues have been working to shed light on some of these less understood aspects of muscle contraction, and their work has led to the development of the winding filament theory<\/strong><\/span>. This theory focuses on the function of titin, a large elastic protein found in the sarcomeres of skeletal muscle. In the winding filament theory, titin binds to the thin filaments, thus increasing its stiffness. In addition, as the crossbridge cycle is activated and thin filaments are pulled toward the M line (as described in the sliding filament theory), titin is simultaneously wound around the thin filaments. The combination of these two events allows the sarcomere to store potential energy during contraction, which can then be released during shortening. The winding filament theory builds upon the foundation of the sliding filament theory by adding an explanation of the mechanism that allows for force enhancement during muscle stretching and force depression during shortening. It also provides a framework for the development of testable predictions as research of the mechanisms of muscle contraction at the sarcomere level continues.<\/p>\r\n\r\n<\/div>\r\n

                      Now, even though this is an anatomy textbook, it\u2019s difficult to understand muscle function (i.e., contraction) without pulling in some physiology. This is because muscle contraction is really dependent on the property of excitability. And even though contraction takes place in the sarcomere, the events leading to contraction begin with electrical changes across the sarcolemma. In muscle cells, the cytosol and extracellular fluid (ECF) are electrically neutral away from the plasma membrane (i.e., there are equal numbers of positive and negative ions). But at the sarcolemma, we find a thin layer of negative ions in the cytosol and a thin layer of positive ions in the ECF. This separation of positive and negative ions creates an electrical gradient, which represents a source of potential energy. For this reason, this gradient is often called an electrical potential<\/strong><\/span>.<\/p>\r\n

                      If we compare the electrical potential of two points\u2014say, one side of a muscle cell versus the other\u2014the difference between the potentials at these two points is called a voltage<\/strong><\/span>. When we talk about membrane potential, we\u2019re referring to this difference in electrical potential across the plasma membrane. For muscle fibers at rest, a typical resting membrane potential is around \u221285 mV. This resting membrane potential can change as ions cross the sarcolemma.<\/p>\r\n

                      This brings us to action potentials<\/strong><\/span>, which are quick, temporary changes in the membrane potential in a single region of the sarcolemma. Action potentials are generated by the opening and closing of channels, which control movement of ions across the membrane.<\/p>\r\n

                      But why does it matter that these ions cross back and forth and generate action potential? Well, the generation of action potentials is critical for long-distance signaling in the cell. You\u2019ll recall from earlier in this chapter that one of the key properties of muscle cells is conductivity<\/strong><\/span>, or the ability to transfer electrical changes rapidly across the sarcolemma. The action potentials don\u2019t just stay in one spot in the cell\u2014they are conducted throughout the sarcolemma, including the T-tubules. And this arrival of an action potential at the T-tubules is what initiates a muscle contraction and enables a muscle fiber to contract as a unit!<\/p>\r\n

                      Now, we cannot have skeletal muscle contraction without stimulation from the nervous system, so to really understand muscle contraction, we also need a basic understanding of the relationship between the nervous system and the muscular system. The nervous system will be covered in greater detail in other chapters of this book, so the nervous system information we cover now is really just a generalized introduction to select components of that system for the purposes of understanding muscle function.<\/p>\r\n

                      All skeletal muscle is innervated<\/strong><\/span>, meaning that it is connected to a neuron (motor neuron)<\/strong>. Each motor neuron communicates with several muscle fibers via a connection called a synapse<\/strong><\/span>. And the number of muscle fibers innervated by a single motor neuron depends a lot on where we look in the body and whether the structure in question executes gross (i.e., large-scale) movements or precise (i.e., fine-scale) movements. Generally speaking, we see a single motor neuron innervating many fibers in places like the trunk of the body, where gross motion occurs, and few fibers in places like the eyes, hands, and fingers, where precise motion occurs.<\/p>\r\n

                      The specific term for a synapse between a motor neuron and a muscle fiber is neuromuscular junction<\/strong><\/span> (\u201cneuro\u201d = nerve, \u201cmuscular\u201d = muscle, \u201cjunction\u201d = place where two things meet). The neuromuscular junction is where communication between the nerve and a muscle fiber takes place, which is accomplished through transmission of a signal called a nerve impulse<\/strong><\/span>. The neuromuscular junction is made up of three parts (Figure 11.8):<\/p>\r\n\r\n

                        \r\n \t
                      1. Axon terminal<\/strong><\/span>: the swollen end of the axon (part of motor neuron). The axon terminal contains synaptic vesicles, which house neurotransmitters<\/strong> (i.e., chemicals used to cause change in the cell the neuron communicates with; e.g., acetylcholine<\/strong>).<\/li>\r\n \t
                      2. Synaptic cleft<\/strong><\/span>: the space between the axon terminal and the motor end plate.<\/li>\r\n \t
                      3. Motor end plate<\/strong><\/span>: a specialized region of the sarcolemma that houses receptors for neurotransmitters.<\/li>\r\n<\/ol>\r\n[caption id=\"\" align=\"aligncenter\" width=\"728\"]\"\" -
                        Figure 11.8\u2014Anatomy of the neuromuscular junction.[\/caption]\r\n

                        OK, we are finally ready to talk about muscle contraction. The process of muscle contraction can be broken down into three parts:<\/p>\r\n\r\n

                          \r\n \t
                        1. Excitation phase<\/li>\r\n \t
                        2. Excitation\u2013contraction coupling<\/li>\r\n \t
                        3. Contraction phase<\/li>\r\n<\/ol>\r\n

                          During the excitation phase<\/strong><\/span>, a signal is transmitted from the motor neuron to the sarcolemma of the muscle fiber through the release of acetylcholine<\/strong><\/span> (ACh<\/strong><\/span>), a neurotransmitter. This generates a response in the muscle fiber called an end-plate potential<\/strong><\/span>.<\/p>\r\n

                          In order to actually produce a muscle contraction, multiple end-plate potentials must be generated. But the ACh released into the synapse is quickly broken down by an enzyme called acetylcholinesterase<\/strong> (AChE). So in order to produce the multiple end-plate potentials necessary for contraction to occur, the motor neuron must continue to generate action potentials and release new ACh molecules.<\/p>\r\n

                          Upon the generation of the end-plate potential, the second phase of muscle contraction\u2014excitation\u2013contraction coupling<\/strong><\/span>\u2014is initiated. During this phase, the end-plate potential is propagated across the sarcolemma and down through the T-tubules, which initiates the release of calcium ions from the sarcoplasmic reticulum into the sarcoplasm of the muscle fiber.<\/p>\r\n

                          The stage is now set to initiate the third phase of generating a muscle contraction\u2014the contraction phase<\/strong><\/span>. The calcium ions that were released from the sarcoplasmic reticulum bind to troponin, the globular, regulatory protein found in the thin filaments that we discussed earlier in the chapter. This binding of calcium causes the troponin to shift position, which enables tropomyosin\u2014the long, regulatory protein in thin filament\u2014to move and expose the active sites on the actin subunits. Once these active sites are exposed, the myosin heads from the thick filaments can bind to the actin on the thin filaments, and the sliding filament mechanism is engaged. When the sliding filament mechanism is engaged in multiple sarcomeres along the length of the muscle fiber and in multiple muscle fibers in the muscle, whole organ contraction takes place. Now, muscles cannot just contract and stop there\u2014they also have to relax. Muscle relaxation has two components:<\/p>\r\n\r\n

                            \r\n \t
                          1. Release of ACh stops and any ACh left in the synapse is broken down by AChE.<\/li>\r\n \t
                          2. Calcium ion concentrations in the sarcoplasm return to resting level and troponin and tropomyosin return to their resting positions, thus blocking the active sites on the thin filament.<\/li>\r\n<\/ol>\r\n

                            One very important thing to note is that muscles cannot lengthen themselves (i.e., muscles can only \u201cpull\u201d on structures, they cannot \u201cpush\u201d)! For this reason, muscle groups that act about joints are typically organized as antagonist pairs or antagonist groups, such that the contraction of one muscle or group of muscles moves a body part in one direction, and contraction of the opposing muscle or group of muscles moves the body part in the opposite direction (and thereby relengthens the first set of muscles). So even though muscles cannot actually lengthen themselves, they can be passively relengthened after shortening because they contain parts that behave elastically. In other words, they will return to their original length after being stretched or shortened. These elastic components include connective tissue within the muscle, parallel to the fibers, called parallel elastic components<\/strong>, and the tendons that attach muscle to bone, called series elastic components<\/strong>. These elastic components help save energy by reducing the force that muscles have to exert to produce opposing motions.<\/p>\r\n

                            Let\u2019s consider an example: My triceps brachii, located on the posterior side of my humerus, extends the elbow when it contracts; the biceps group (which includes biceps brachii, brachialis, and brachioradialis) on the anterior side of my humerus flexes the elbow and relengthens the triceps so it can contract again (Figure 11.9).<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"516\"]\"\" -
                            Figure 11.9\u2014Antagonist muscle groups of the arm.[\/caption]\r\n

                            I described these antagonist pairs as muscle groups, and that is because oftentimes there are multiple muscles in a position to produce a similar motion when they contract across a joint. These muscles that can work together are called synergists<\/strong><\/span> or agonists<\/strong><\/span>. This redundancy of muscles crossing joints and producing similar actions allows for more refined control of joint motions; there are also some additional mechanisms for modulating muscle actions and movements, as we\u2019ll see shortly.<\/p>\r\n\r\n

                            Muscle Tension<\/h2>\r\n

                            Let\u2019s turn our attention to muscle tension for a bit now. When muscle tissue contracts, it produces tension<\/strong><\/span>. The smallest possible muscle contraction is called a muscle twitch<\/strong><\/span>, which is simply the response of a muscle fiber to a single motor neuron action potential. Every muscle twitch produces tension, which translates to some degree of force production and varies from fiber to fiber. The tension produced during a twitch is influenced by several factors, including<\/p>\r\n\r\n

                              \r\n \t
                            1. Timing and frequency of stimulation<\/li>\r\n \t
                            2. Resting fiber length<\/li>\r\n \t
                            3. Muscle fiber type<\/li>\r\n<\/ol>\r\n

                              Let\u2019s look at each of these factors and see how they can influence tension production of muscle fibers. We\u2019ll start with timing and frequency of stimulation.<\/p>\r\n

                              Generally speaking, repeated stimulation of a muscle fiber produces twitches with progressively greater tension. The reason for this is that the sarcoplasmic reticulum pumps don\u2019t have enough time to pump all the calcium ions back into the sarcoplasmic reticulum, which results in increasing calcium ion concentrations in the sarcoplasm with each stimulus. This increasing tension is known as wave summation, because the waves of contraction add together.<\/p>\r\n

                              Depending on the frequency of stimulation, or how quickly the stimulation is occurring, our muscle fiber can wind up in one of two states (Figure 11.10):<\/p>\r\n\r\n

                                \r\n \t
                              1. Unfused tetanus<\/strong><\/span> (or incomplete tetanus<\/strong><\/span>): occurs when fiber is stimulated at a frequency of about 50 times per second. This frequency allows partial relaxation between each contraction, so tension increases and decreases slightly with each twitch until a level of maximal tension is reached.<\/li>\r\n \t
                              2. Fused tetanus<\/strong><\/span> (or complete tetanus<\/strong><\/span>): occurs when a fiber is stimulated at a higher frequency\u2014typically around 80\u2013100 times per second. In this state, the fiber does not have time to relax between contractions, and as a result, tension remains constant at a maximal level.<\/li>\r\n<\/ol>\r\n[caption id=\"\" align=\"aligncenter\" width=\"709\"]\"\" -
                                Figure 11.10\u2014Unfused versus fused tetanus. Note the difference in the frequency of stimulation and how that affects the muscle fiber\u2019s ability to relax (or not) between stimuli and the corresponding impact on generating maximum tension.[\/caption]\r\n

                                Our second factor\u2014resting fiber length<\/strong><\/span>\u2014brings us to the concept of length-tension relationships. The length-tension relationship<\/strong> is a principle that states that the number of crossbridges that can form in a sarcomere depends on the length of the sarcomere prior to contraction<\/em><\/span>. The optimal length of the sarcomere is the length at which the most crossbridges can form, and the number of crossbridges that can form directly influences the amount of tension the fiber can produce (generally, more crossbridges lead to greater force production and vice versa; Figure 11.11).<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"515\"]\"\" -
                                Figure 11.11\u2014Length-tension relationship. As sarcomere length increases or decreases, the zone of overlap changes size and affects how the thick and thin filaments interact with each other. Because the number of crossbridges is maximized and there is minimal interference of the Z disc at an intermediate length, this is the length of the sarcomere at which tension production peaks.[\/caption]\r\n\r\n

                                \r\n

                                Box 11.3<\/span>\u2014Wrist Posture, Sarcomere Length, and Grip Strength<\/strong><\/p>\r\n

                                Let\u2019s illustrate this concept with a quick experiment. Flex your wrist 90 degrees. Now try to squeeze your pen\/pencil\/hand dynamometer hard. It\u2019s a little tough, right? This is because your flexed wrist position has shortened the muscles of the forearm, causing a great deal of overlap of the thick and thin filaments in the sarcomeres. Since there is so much overlap, there is not much room for the thick and thin filaments to slide past one another before hitting the Z disc. This results in the formation of very few functional crossbridges, and as a result, the muscle generates less tension.<\/p>\r\n

                                Let\u2019s try again\u2014but hyperextend your wrist this time (90 degrees in the other direction). Now try to squeeze your pen\/pencil\/dynamometer. Still tough, right? This time, the muscle is stretched, and there isn\u2019t enough overlap for the thick and thin filaments to connect properly. Again, this leads to the formation of fewer crossbridges and the production of less tension.<\/p>\r\n

                                Last, extend your wrist normally and squeeze your pen\/pencil\/dynamometer. You should notice that your grip strength is strongest in this position. This is because the muscle is at its natural resting length, and the sarcomeres are at optimal length with just the right amount of overlap of the thick and thin filaments; this arrangement maximizes crossbridge formation and increases tension production.<\/p>\r\n

                                As you can see, the optimal length of the sarcomere is actually an intermediate length. So it\u2019s a little bit like a Goldilocks situation: Less tension is produced when the sarcomere is too short and when the sarcomere is too long. But when the sarcomere is \u201cjust<\/em><\/span> right,\u201d the muscle is able to maximize tension\u2014and by extension, force\u2014production.<\/p>\r\n\r\n<\/div>\r\n

                                Recall the elastic filaments that make up part of the myofibril. These filaments enable the myofibril to be stretched, resulting in differing lengths of the myofibril and its sarcomeres. This, in turn, affects the degree of overlap of the thick and thin filaments in the sarcomere\u2019s zone of overlap. Therefore, the size of the zone of overlap is largely dependent upon the position of the muscle prior to contraction.<\/p>\r\n

                                The third factor that can affect the generation of tension is fiber type.<\/p>\r\n\r\n

                                Muscle Fiber Types<\/h2>\r\n

                                In some muscles, the muscle fibers are supplied by multiple connections from the nerve cells (i.e., they contain multiple motor end plates). These muscles are called tonic muscles<\/strong><\/span>, and the force of the contraction in this type of muscle fiber is controlled by how quickly the nerve impulses arrive in sequence (frequency<\/strong><\/span>). Tonic muscles typically contract slowly but are really hard to fatigue. Tonic muscles are uncommon in fishes, birds, and mammals. When observed in mammals, they are typically small and restricted to places requiring fine control, like the muscles that move the eyeball. However, tonic fibers are much more common in amphibians and reptiles and have been shown to contribute to sustained force production by the jaw muscles of some species, enabling them to subdue prey (e.g., horned frogs) or engage in long-lasting courtship behaviors (e.g., alligator lizards).<\/p>\r\n

                                In contrast, most skeletal muscles have fibers with only a single connection to a nerve cell (i.e., a single motor end plate). These are called twitch muscles<\/strong><\/span>. In twitch muscles, the nerve impulses spread easily throughout the fiber, so once the threshold impulse level is reached, the fiber will contract in an \u201call or nothing\u201d fashion and then relax. However, if the fibers are stimulated several times in rapid succession, the forces from each twitch will be summed up to a maximum, which is called tetanic force<\/strong><\/span>. Twitch muscles tend to be large muscles with several motor units, so forces can be modulated by varying the number of motor units stimulated as well as the frequency of stimulation.<\/p>\r\n

                                Twitch fibers differ in structure and function, and as a result of these differences, some fibers twitch more rapidly than others. Whether a muscle fiber is considered a \u201cfast\u201d or \u201cslow\u201d fiber is largely determined by the level of myosin ATPase activity in the cell (this is the enzyme that hydrolyzes ATP to drive the power stroke of contraction).<\/p>\r\n

                                Muscle fibers with high ATPase activity are called fast-twitch fibers<\/strong><\/span> because they go through contraction cycles relatively quickly. Fast-twitch fibers tend to be found in body parts that need to move rapidly (e.g., the muscles that move the eyes). In contrast, fibers with low myosin ATPase activity are called slow-twitch fibers<\/strong><\/span> and tend to be found in muscles that require slow sustained contractions (e.g., postural muscles of the back).<\/p>\r\n

                                When we consider twitch speed in conjunction with a fiber\u2019s primary energy source, we find that skeletal muscle can be categorized into two \u201ctype\u201d classes:<\/p>\r\n\r\n

                                  \r\n \t
                                1. Type I fibers<\/strong><\/span>: These are slow-twitch fibers with small diameters, high myoglobin concentration, many mitochondria, and a well-developed blood supply. Myoglobin is an oxygen-binding protein found in vertebrate muscle. The high myoglobin content of Type I fibers makes them red in appearance, so muscles with many Type I fibers are sometimes called red muscle<\/strong><\/span>. These muscle fibers are also sometimes referred to as slow-oxidative <\/strong>(SO)<\/strong> fibers<\/strong><\/span> due to their slow contraction times and reliance on oxidative or aerobic metabolism (requires oxygen).<\/li>\r\n \t
                                2. Type II fibers<\/strong><\/span>: These are fast-twitch fibers with large diameters that contract quickly but also fatigue quickly compared to Type I fibers. Type II fibers rely primarily on anaerobic energy production, so they are characterized by having fewer myoglobin and mitochondria compared to Type I fibers. The lack of myoglobin in Type II fibers gives them a light color, so they are sometimes called white muscle<\/strong><\/span>. These muscle fibers are also sometimes referred to as fast-glycolytic <\/strong>(FG)<\/strong> fibers<\/strong><\/span>, because they contract more rapidly and rely on glycolytic or anaerobic metabolism (does not require oxygen).<\/li>\r\n<\/ol>\r\n

                                  Up to this point, we\u2019ve been considering muscle tension at the fiber level, so let\u2019s zoom out a bit now and consider tension at the organ level. Recall from earlier that muscle fibers are innervated by motor neurons, and a single motor neuron may innervate multiple fibers. We refer to this motor neuron and all the fibers it innervates as a motor unit<\/strong><\/span>.<\/p>\r\n

                                  In humans, the average motor unit is made up of one motor neuron and about 150 muscle fibers, but this can vary depending on the part of the body and its function. For example, in areas that require precise movements, like the hand, we find motor units innervating as few as 10 muscle fibers. In contrast, areas of the body with large, powerful muscles, such as in the back, have motor units that innervate upward of 2,000\u20133,000 fibers. All the muscle fibers in a motor unit are of the same type, though, resulting in slow motor units and fast motor units. When a whole muscle begins a contraction, not all the motor units immediately engage. In fact, the slow motor units typically activate first and are later joined by fast motor units if additional tension is required to complete a task\u2014this is called recruitment<\/strong><\/span>.<\/p>\r\n\r\n

                                  11.4 Summary<\/h1>\r\n

                                  In this chapter, we introduced muscles as the motors of the vertebrate body. By looking at muscle development as well as the tissue-level structure of muscle, we were able to gain an understanding of the microscopic organization of muscle as well as how this structure facilitates muscle contraction.<\/p>\r\n\r\n

                                  \r\n

                                  Application Questions<\/p>\r\n\r\n<\/header>\r\n

                                  \r\n
                                    \r\n \t
                                  1. In domesticated chickens, the breast meat tends to be \u201cwhite\u201d meat, whereas the thigh meat tends to be \u201cdark\u201d meat.\r\n
                                      \r\n \t
                                    1. Given what you now know about muscle fiber types and their characteristics, why do you suspect this is the case?<\/li>\r\n \t
                                    2. What do these differences indicate about muscle function in the breast versus the thigh of these birds?<\/li>\r\n \t
                                    3. Do you think this pattern might differ in a migratory game bird, such as ducks? Why or why not?<\/li>\r\n<\/ol>\r\n<\/li>\r\n \t
                                    4. You are at the gym and notice that you have an easier time lifting weights when your arm is in a particular position, compared to other positions. In the context of the length-tension relationship and muscle function, explain why this is the case.<\/li>\r\n<\/ol>\r\n<\/div>\r\n<\/div>\r\n

                                      11.5 Further Reading<\/h1>\r\n
                                        \r\n \t
                                      1. Abbott B. C., and X. M. Aubert. \u201cThe force exerted by active striated muscle during and after change of length.\u201d Journal of Physiology<\/em><\/span> 117 (1952): 77\u201386.<\/li>\r\n \t
                                      2. Cook, Verity A., Antonia H. Groneberg, Maximillian Hoffmann, Mykola Kadobianskyi, Johannes Veith, Lisanne Schulze, J\u00f6rg Henninger, Ralf Britz, and Benjamin Judkewitz. \u201cUltrafast sound production mechanism in one of the smallest vertebrates.\u201d Proceedings of the National Academy of Sciences <\/em>U.S.A<\/em>.<\/em><\/span> 121 (2024): e2314017121.<\/li>\r\n \t
                                      3. Nishikawa, Kiisa C., Jena A. Monroy, Theodore E. Uyeno, Sang Hoon Yeo, Dinesh K. Pai, and Stan L. Lindstedt. \u201cIs titin a \u2018winding filament\u2019? A new twist on muscle contraction.\u201d Proceedings of the Royal Society B<\/em><\/span>. 279 (2012): 981\u2013990.<\/li>\r\n \t
                                      4. Parmentier, Eric, and Marc Thiry. \u201cA new organisational design in skeletal muscle fibres.\u201d Cell and Tissue Research<\/em><\/span> 393 (2023): 111\u2013117.<\/li>\r\n<\/ol>\r\n

                                        11.6 References<\/h1>\r\n
                                          \r\n \t
                                        1. Abbott B. C., and X. M. Aubert. \u201cThe force exerted by active striated muscle during and after change of length.\u201d Journal of Physiology<\/em><\/span> 117 (1952): 77\u201386.<\/li>\r\n \t
                                        2. Amerman, Erin C. Human Anatomy and Physiology<\/em><\/span>, 1st ed. Boston: Pearson, 2016.<\/li>\r\n \t
                                        3. Cook, Verity A., Antonia H. Groneberg, Maximillian Hoffmann, Mykola Kadobianskyi, Johannes Veith, Lisanne Schulze, J\u00f6rg Henninger, Ralf Britz, and Benjamin Judkewitz. \u201cUltrafast sound production mechanism in one of the smallest vertebrates.\u201d Proceedings of the National Academy of Sciences <\/em>U.S.A<\/em>.<\/em><\/span> 121 (2024): e2314017121.<\/li>\r\n \t
                                        4. Marieb, Elaine N., and Katja Hoehn. Human Anatomy and Physiology<\/em><\/span>, 10th ed. Boston: Pearson, 2016.<\/li>\r\n \t
                                        5. McKinley, Michael P., Valerie D. O\u2019Loughlin, and Elizabeth E. Pennefather-O\u2019Brien. Human Anatomy<\/em><\/span>, 5th ed. New York: McGraw Hill Education, 2015.<\/li>\r\n \t
                                        6. Nishikawa, Kiisa C., Jena A. Monroy, Theodore E. Uyeno, Sang Hoon Yeo, Dinesh K. Pai, and Stan L. Lindstedt. \u201cIs titin a \u2018winding filament\u2019? A new twist on muscle contraction.\u201d Proceedings of the Royal Society B<\/em><\/span>. 279 (2012): 981\u2013990.<\/li>\r\n \t
                                        7. Parmentier, Eric, and Marc Thiry. \u201cA new organisational design in skeletal muscle fibres.\u201d Cell and Tissue Research<\/em><\/span> 393 (2023): 111\u2013117.<\/li>\r\n<\/ol>","rendered":"
                                          \n
                                          \n

                                          Focus Questions\u2014to Guide Your Reading of This Chapter<\/p>\n<\/header>\n

                                          \n
                                            \n
                                          1. What are the five key properties of muscle tissue? How do these properties facilitate muscle function?<\/li>\n
                                          2. Explain the structure of muscle tissue. How does force generation translate from the sarcomere to the whole organ?<\/li>\n
                                          3. How is muscle force modulated?<\/li>\n<\/ol>\n<\/div>\n<\/div>\n

                                            11.1 Introduction<\/h1>\n

                                            Muscles are the motors of the vertebrate body. But muscles do more than just move us about\u2014they also work in conjunction with the skeletal system to provide body support as well as play a role in the movement of material through the body, such as moving blood through the vasculature or producing pressure changes in the chest to drive air in and out of the lungs. What\u2019s more, muscles enable vertebrate bodies to accomplish incredible feats: The shaker muscles of rattlesnake tails can maintain contraction frequencies of up to 100 Hz for hours. During migrations, eels can swim for months with minimal energy expenditure (four to six times less than that of salmon!). And the smooth muscles of the uterine wall can generate sustained intrauterine pressures of 80\u2013100 mmHg during labor!<\/p>\n

                                            This chapter will begin with a brief introduction to muscle development and then transition into an examination of the tissue-level structure of muscle. As we discuss the tissue-level structure of muscle, we\u2019ll highlight how this structure facilitates muscle function (namely, contraction).<\/p>\n

                                            11.2 Muscle Development<\/h1>\n

                                            Generally speaking, muscle cells develop from mesenchymal cells from the paraxial mesoderm (myotome). While these cells are actively dividing, they are known as myoblasts and are the precursors to mature muscle cells known as myocytes<\/strong> (just like we\u2019ve seen before with the precursors of bone cells called osteoblasts and precursors of cartilage cells called chondroblasts). When cell division stops, the myoblasts<\/strong> begin to elongate and differentiate into myocytes.<\/p>\n

                                            Depending on the location in the body, the muscle tissue type, and the ultimate function of the muscle that is developing, the myocytes can form and organize in very different ways. For example, in skeletal muscle, the myoblasts line up longitudinally and fuse together. This produces long, single cells with several hundred nuclei positioned along the outer edge of the cell membrane. This structure is called a syncytium<\/strong> and can produce individual myocytes as long as 30 cm in some animals! Because of the unique, elongated shape of the skeletal muscle myocytes, they are often called muscle fibers.<\/p>\n

                                            11.3 Structure and Function of Muscle<\/h1>\n

                                            Muscle Tissue Types<\/h2>\n

                                            Muscle tissue is specialized for contraction. This tissue type is composed primarily of myocytes (\u201cmyo\u201d = muscle, \u201ccyt\u201d = cell; so \u201cmyocytes\u201d = \u201cmuscle cells\u201d). The cells are considered excitable cells, meaning they respond to electrical or chemical stimulation. The cytoplasm of myocytes is filled with bundles of proteins called myofilaments<\/strong>, which give muscle cells their distinctive appearance. Muscle cells can take one of two forms:<\/p>\n

                                              \n
                                            1. Striated<\/strong><\/span>: having alternating light and dark bands formed by regions of myofilament overlap; this gives them a \u201cstripey\u201d appearance (think: striations = striped; see Figures 11.1A and 11.1C).<\/li>\n
                                            2. Smooth<\/strong><\/span>: lacking striations; these muscle cells also contain myofilaments, but the myofilaments are arranged as irregular bundles, so they don\u2019t overlap to form striations (Figure 11.1B).<\/li>\n<\/ol>\n

                                              In muscle tissue, a small amount of extracellular matrix surrounds each muscle cell and is called endomysium<\/strong> or external lamina; the endomysium functions to hold the muscle cells together in the tissue. We\u2019ll revisit this later in the chapter when we talk about gross muscle anatomy. Beyond this general distinction in appearance, we can further classify muscle tissue based on function. There are three types of muscle tissue (Figure 11.1):<\/p>\n

                                                \n
                                              1. Smooth muscle<\/strong><\/li>\n
                                              2. Cardiac muscle<\/strong><\/li>\n
                                              3. Skeletal muscle<\/strong><\/li>\n<\/ol>\n
                                                \"\"
                                                –
                                                Figure 11.1\u2014Three types of muscle tissue and their distinguishing features.<\/figcaption><\/figure>\n

                                                Smooth muscle tissue, as its name implies, is composed of smooth muscle cells; contraction of this tissue is involuntary, meaning that we have no conscious control over contraction of this muscle type. We find smooth muscle tissue in the hollow organs of the digestive tract, blood vessels, eyes, skin, and the ducts of some glands. Smooth muscle tissue usually contains specialized junctions (\u201cgap junctions\u201d) between cells to facilitate cell-to-cell communication. There are two types of smooth muscle:<\/p>\n

                                                  \n
                                                1. Unitary smooth muscle<\/strong><\/span>: This type of smooth muscle undergoes spontaneous, rhythmic contractions that are generated myogenically (i.e., from within the muscle). This type of smooth muscle is found in the digestive tract, uterus, and urinary ducts.<\/li>\n
                                                2. Multiunit smooth muscle<\/strong><\/span>: This type of smooth muscle is neurogenic<\/strong><\/span> (i.e., contraction is stimulated by the nervous system). Multiunit contractions allow more refined regulation of control; this type of smooth muscle is typically found in walls of blood vessels, irises of eyes, and sperm ducts.<\/li>\n<\/ol>\n

                                                  Cardiac muscle tissue is composed of striated muscle cells called cardiac muscle cells; this type of muscle is found only in the heart. Contraction of cardiac muscle tissue is involuntary (like smooth muscle). Cardiac muscle cells are relatively short and branched; they are also uninucleate (one nucleus per cell). A key characteristic of cardiac muscle tissue is the presence of intercalated discs<\/strong>: Within the intercalated discs, we find junctions (i.e., places where neighboring cells connect) that enable rapid cell communication, which helps coordinate heart muscle contraction.<\/p>\n

                                                  Skeletal muscle is also composed of striated muscle cells, and this muscle tissue type is found mostly attached to skeletal elements. Contraction of skeletal muscle is voluntary and occurs via electrical stimulation from the nervous system. Skeletal muscle is composed of long, thin muscle cells arranged in parallel\u2014these are often called muscle fibers and are formed by myoblasts (immature muscle cells). Because of their incredible length, muscle fibers are multinucleated<\/strong><\/span>\u2014meaning they have multiple nuclei. This chapter will focus primarily on skeletal muscle.<\/p>\n

                                                  Even though these three muscle types have their differences, they all perform the same general function, which is to generate a force called muscle tension<\/strong><\/span>. Muscle tension functions in generating movement as well as maintaining posture, stabilizing joints, generating heat, and regulating the flow of substances through hollow organs. To accomplish the task of generating muscle tension, muscle cells must convert chemical energy in the form of ATP (adenosine triphosphate) into the mechanical energy of muscle tension. And this task requires that muscles have a set of particular properties, including the following:<\/p>\n

                                                    \n
                                                  1. Contractility<\/strong><\/span>: ability to contract or the drawing together of the proteins within a muscle cell (rather than necessarily the shortening of the cell)<\/li>\n
                                                  2. Excitability<\/strong><\/span>: ability to respond to chemical, mechanical, or electrical stimuli<\/li>\n
                                                  3. Conductivity<\/strong><\/span>: ability to transfer electrical change across the entire length of the cell\u2019s plasma membrane<\/li>\n
                                                  4. Extensibility<\/strong><\/span>: ability to stretch up to three times their resting length without being damaged or rupturing<\/li>\n
                                                  5. Elasticity<\/strong><\/span>: ability to return to the cell\u2019s original shape after being stretched<\/li>\n<\/ol>\n

                                                    As you might imagine, given the tight relationship between form and function, these unique functions of muscle cells come with a bit of unique cellular structure. Muscle cells have the same organelles as other cells, but they also possess some key structural differences (Figure 11.2), which come with their own new set of terms, including the following:<\/p>\n

                                                      \n
                                                    1. Sarcolemma<\/strong><\/span>: phospholipid bilayer surrounding a muscle cell that houses specialized proteins that assist with cell function; analogous to the plasma membrane<\/li>\n
                                                    2. Sarcoplasm<\/strong><\/span>: located within the muscle cell, contains cytosol and organelles, and is analogous to cytoplasm of other cell types<\/li>\n
                                                    3. Sarcoplasmic reticulum<\/strong><\/span>: modified smooth endoplasmic reticulum that forms a weblike network around each myofibril and functions in the storage and release of calcium ions\u2014a critical component of muscle contraction<\/li>\n
                                                    4. Myofibril<\/strong><\/span>: cylindrical organelle involved in muscle contraction that is composed of bundles of specialized proteins and is the most abundant organelle in skeletal muscle cells<\/li>\n<\/ol>\n
                                                      \"\"
                                                      –
                                                      Figure 11.2\u2014Myocyte anatomy.<\/figcaption><\/figure>\n

                                                      Let\u2019s unpack the sarcolemma a bit more. Unlike other cells whose plasma membranes are restricted to the exterior surface of a cell, the sarcolemma actually forms inward extensions called transverse tubules<\/strong><\/span> or T-tubules<\/strong><\/span> (Figure 11.3). These T-tubules extend deep into the cell and surround each myofibril, creating a tunnel-like network within the cell. Because T-tubules are continuous with the exterior of the cell, they are filled with extracellular fluid. Inside the cell, the T-tubules are flanked on either side by enlarged portions of the sarcoplasmic reticulum called the terminal cisternae<\/strong><\/span>. Together, the T-tubule and two terminal cisternae are known as a triad<\/strong><\/span>. The triad is an important structure in the process of muscle contraction.<\/p>\n

                                                      \"\"
                                                      –
                                                      Figure 11.3\u2014Anatomy of the sarcoplasmic reticulum.<\/figcaption><\/figure>\n

                                                      Let\u2019s look deeper still and consider the structure of individual myofibrils. A single myofibril is composed of hundreds to thousands of protein bundles called myofilaments<\/strong><\/span> (Figures 11.4 and 11.5<\/a>). Myofilaments are made up of one or more of three types of proteins:<\/p>\n

                                                        \n
                                                      1. Contractile proteins<\/strong><\/span>: produce tension<\/li>\n
                                                      2. Regulatory proteins<\/strong><\/span>: control timing of muscle fiber contraction<\/li>\n
                                                      3. Structural proteins<\/strong><\/span>: hold myofilaments in place and ensure structural stability of myofibrils and the muscle fiber<\/li>\n<\/ol>\n

                                                        Of the myofilaments, there are three types:<\/p>\n

                                                          \n
                                                        1. Thick<\/strong><\/span> filaments<\/li>\n
                                                        2. Thin<\/strong><\/span> filaments<\/li>\n
                                                        3. Elastic<\/strong><\/span> filaments<\/li>\n<\/ol>\n

                                                          Thick filaments are composed of many molecules of the contractile protein myosin<\/strong><\/span>. Myosin\u2019s structure has two globular heads and two intertwined polypeptide chains that compose the tail. The heads attach to the tail via a flexible neck. Thick filaments are arranged such that the heads, which contain a site for binding to thin filaments, are positioned at the ends of the filament and the tails are in the middle.<\/p>\n

                                                          Thin filaments are made up of both contractile and regulatory proteins:<\/p>\n

                                                            \n
                                                          1. Actin:<\/strong><\/span> contractile protein with an active site for binding to myosin head (thick filament); multiple actin subunits string together to form two intertwining strands and form the largest part of the thin filament<\/li>\n
                                                          2. Tropomyosin:<\/strong><\/span> long, ropelike regulatory protein that spirals around the actin strands and covers the actin active sites<\/li>\n
                                                          3. Troponin:<\/strong><\/span> small, globular regulatory protein that holds tropomyosin in place<\/li>\n<\/ol>\n

                                                            Tropomyosin and troponin function in switching on and off (or \u201cregulating\u201d) muscle contraction by controlling whether the active site on the actin subunits is available to interact with the myosin heads of the thick filament.<\/p>\n

                                                            Elastic filaments are composed of a single large structural protein called titin<\/strong><\/span>. Titin is coil shaped, allowing it to stretch (\u201cextensibility\u201d) and recoil (\u201celasticity\u201d). This filament runs through the core of thick filaments and helps stabilize thick filament structure and resist excessive stretching. Because of its ability to recoil, elastic filaments enable muscle fibers to return to their original lengths after stretching.<\/p>\n

                                                            Myofibrils are patterned by the arrangement of thick and thin myofilaments; there are regions of the myofibril where only thin or thick filaments are present and regions where the two overlap. You\u2019ll recall that one of the characteristics of skeletal muscle fibers is that they are striated\u2014these light and dark bands (\u201cstriations\u201d) are produced by the repeated overlapping arrangement of thick and thin filaments within discrete units called sarcomeres<\/strong>. The anatomy of the sarcomere is as follows (Figures 11.4 and 11.5<\/a>):<\/p>\n

                                                              \n
                                                            1. Zone of overlap<\/strong><\/span>: where thick and thin filaments overlap; this is where tension is generated during muscle contraction.<\/li>\n
                                                            2. I <\/strong>band<\/strong><\/span>: light regions of a striation; only thin filaments are found here.<\/li>\n
                                                            3. A band<\/strong><\/span>: dark regions of a striation; this is the portion of the sarcomere that contains thick filaments. The edges of the A band actually contain both thick and thin filaments, as they overlap here, but the center of the A band is composed only of thick filaments (a region known as the H zone).<\/li>\n
                                                            4. M line<\/strong><\/span>: a dark line running down the center of the A band; this consists of structural proteins that function in holding thick filaments in place and serve as an anchoring point for the elastic filaments.<\/li>\n
                                                            5. Z disc <\/strong>(sometimes also called the Z line)<\/strong><\/span>: a dark line running down the center of the I band. The Z disc is also composed of structural proteins that function to anchor the thin filaments in place and serve as attachment sites for the elastic filaments. The Z discs attach myofibrils to one another across the diameter of the muscle fiber.<\/li>\n<\/ol>\n
                                                              \"\"
                                                              –
                                                              Figure 11.4\u2014Anatomy and organization of the muscle fiber and myofibrils.<\/figcaption><\/figure>\n
                                                              \"\"
                                                              –
                                                              Figure 11.5\u2014Anatomy and organization of the sarcomere. Note overlap of thick and thin filaments, allowing for interaction between the two proteins and the engagement of the sliding filament mechanism.<\/figcaption><\/figure>\n

                                                              The sarcomere is the functional unit of the contraction in skeletal muscle and spans from one Z disc to the next Z disc; therefore, each sarcomere is composed of one A band and two half-I bands. There are many sarcomeres in each myofibril, and the particular arrangement of the sarcomere elements is crucial to allowing skeletal muscle contraction to occur, as we will see in the next section (Muscle Contraction<\/span><\/span>).<\/p>\n

                                                              \n

                                                              Box 11.1<\/span>\u2014A New Organizational Design in Skeletal Muscle Fibers<\/strong><\/p>\n

                                                              The structure of the sarcomere\u2014indeed, of the entire myofibril of skeletal muscle\u2014has been incredibly well conserved across vertebrate taxa. However, recent work by Eric Parmentier<\/strong><\/a> and Marc Thiry<\/strong> has identified a novel sarcomere architecture in the sound-producing muscles of the cusk eel (Parophidion vassali<\/em><\/span>; Figure 11.6). Parmentier and Thiry suggest that this peculiar sarcomere structure may be an adaptation that circumvents the trade-off between speed and force often observed in skeletal muscle (i.e., muscle contraction is typically fast or strong but rarely both). In this species, myofilaments have a branched, Y-shaped structure; each of these branches connects to a neighboring myofibril. This branched structure provides a mechanism for increasing the number of crossbridges that can form during muscle contraction, thus amplifying force production. Furthermore, cusk eel sarcomeres have wider Z discs than typically observed in vertebrate muscle. The larger Z disc may contribute to consistent sound features during high-speed contraction.<\/p>\n

                                                              \"\"
                                                              –
                                                              Figure 11.6\u2014Cusk eel. Photo credit: NOAA via @DeepSeaImage.<\/figcaption><\/figure>\n

                                                              Interestingly, this isn\u2019t the only mechanism for sound production in fishes that involves funky musculature. Verity Cook<\/strong><\/a> and colleagues, at Charit\u00e9 University in Berlin, found that one of the world\u2019s smallest fish\u2014Danionella cerebrum<\/em><\/span>\u2014can actually produce a drumming sound over 140 dB. These fish accomplish this amazing feat through the use of a specialized muscle that pulls a rib into a small piece of indented cartilage. When the rib is released, it springs back and strikes the swim bladder to create a noise as loud as the bang of a firecracker!<\/p>\n<\/div>\n

                                                              Muscle Contraction<\/h2>\n

                                                              I mentioned that the structure of the sarcomere is critical for the muscle contraction to occur, but why? How does it happen?<\/p>\n

                                                              The widely accepted model for skeletal muscle contraction is the sliding filament theory. In the sliding filament theory, thin filaments slide past thick filaments and generate tension throughout the sarcomere. During contraction, the I bands and H zone narrow, but the A band does not change. This occurs because the myosin heads of the thick filaments bind to the thin filaments and pull them toward the M line. This brings the Z discs closer together and shortens the sarcomere as a unit. Something important to note here: None of the filaments themselves get shorter! The thin filaments are simply pulled toward the M line. And because the sarcomeres are arranged end-to-end within the myofibril, simultaneous contraction of the sarcomeres results in contraction of the whole muscle fiber (Figure 11.7).<\/p>\n

                                                              \"\"
                                                              –
                                                              Figure 11.7\u2014Relative position of the thick and thin filaments during sarcomere contraction. Note that the filaments themselves do not change length; rather, they change their position relative to each other (i.e., the zone of overlap increases in size).<\/figcaption><\/figure>\n
                                                              \n

                                                              Box 11.2<\/span>\u2014Winding Filament Theory<\/strong><\/p>\n

                                                              Even though the sliding filament theory tends to be the established model for explaining muscle contraction, it fails to account for some aspects of muscle function, including how force is amplified during stretching and depressed during shortening. Dr. Kiisa Nishikawa<\/strong><\/a> and colleagues have been working to shed light on some of these less understood aspects of muscle contraction, and their work has led to the development of the winding filament theory<\/strong><\/span>. This theory focuses on the function of titin, a large elastic protein found in the sarcomeres of skeletal muscle. In the winding filament theory, titin binds to the thin filaments, thus increasing its stiffness. In addition, as the crossbridge cycle is activated and thin filaments are pulled toward the M line (as described in the sliding filament theory), titin is simultaneously wound around the thin filaments. The combination of these two events allows the sarcomere to store potential energy during contraction, which can then be released during shortening. The winding filament theory builds upon the foundation of the sliding filament theory by adding an explanation of the mechanism that allows for force enhancement during muscle stretching and force depression during shortening. It also provides a framework for the development of testable predictions as research of the mechanisms of muscle contraction at the sarcomere level continues.<\/p>\n<\/div>\n

                                                              Now, even though this is an anatomy textbook, it\u2019s difficult to understand muscle function (i.e., contraction) without pulling in some physiology. This is because muscle contraction is really dependent on the property of excitability. And even though contraction takes place in the sarcomere, the events leading to contraction begin with electrical changes across the sarcolemma. In muscle cells, the cytosol and extracellular fluid (ECF) are electrically neutral away from the plasma membrane (i.e., there are equal numbers of positive and negative ions). But at the sarcolemma, we find a thin layer of negative ions in the cytosol and a thin layer of positive ions in the ECF. This separation of positive and negative ions creates an electrical gradient, which represents a source of potential energy. For this reason, this gradient is often called an electrical potential<\/strong><\/span>.<\/p>\n

                                                              If we compare the electrical potential of two points\u2014say, one side of a muscle cell versus the other\u2014the difference between the potentials at these two points is called a voltage<\/strong><\/span>. When we talk about membrane potential, we\u2019re referring to this difference in electrical potential across the plasma membrane. For muscle fibers at rest, a typical resting membrane potential is around \u221285 mV. This resting membrane potential can change as ions cross the sarcolemma.<\/p>\n

                                                              This brings us to action potentials<\/strong><\/span>, which are quick, temporary changes in the membrane potential in a single region of the sarcolemma. Action potentials are generated by the opening and closing of channels, which control movement of ions across the membrane.<\/p>\n

                                                              But why does it matter that these ions cross back and forth and generate action potential? Well, the generation of action potentials is critical for long-distance signaling in the cell. You\u2019ll recall from earlier in this chapter that one of the key properties of muscle cells is conductivity<\/strong><\/span>, or the ability to transfer electrical changes rapidly across the sarcolemma. The action potentials don\u2019t just stay in one spot in the cell\u2014they are conducted throughout the sarcolemma, including the T-tubules. And this arrival of an action potential at the T-tubules is what initiates a muscle contraction and enables a muscle fiber to contract as a unit!<\/p>\n

                                                              Now, we cannot have skeletal muscle contraction without stimulation from the nervous system, so to really understand muscle contraction, we also need a basic understanding of the relationship between the nervous system and the muscular system. The nervous system will be covered in greater detail in other chapters of this book, so the nervous system information we cover now is really just a generalized introduction to select components of that system for the purposes of understanding muscle function.<\/p>\n

                                                              All skeletal muscle is innervated<\/strong><\/span>, meaning that it is connected to a neuron (motor neuron)<\/strong>. Each motor neuron communicates with several muscle fibers via a connection called a synapse<\/strong><\/span>. And the number of muscle fibers innervated by a single motor neuron depends a lot on where we look in the body and whether the structure in question executes gross (i.e., large-scale) movements or precise (i.e., fine-scale) movements. Generally speaking, we see a single motor neuron innervating many fibers in places like the trunk of the body, where gross motion occurs, and few fibers in places like the eyes, hands, and fingers, where precise motion occurs.<\/p>\n

                                                              The specific term for a synapse between a motor neuron and a muscle fiber is neuromuscular junction<\/strong><\/span> (\u201cneuro\u201d = nerve, \u201cmuscular\u201d = muscle, \u201cjunction\u201d = place where two things meet). The neuromuscular junction is where communication between the nerve and a muscle fiber takes place, which is accomplished through transmission of a signal called a nerve impulse<\/strong><\/span>. The neuromuscular junction is made up of three parts (Figure 11.8):<\/p>\n

                                                                \n
                                                              1. Axon terminal<\/strong><\/span>: the swollen end of the axon (part of motor neuron). The axon terminal contains synaptic vesicles, which house neurotransmitters<\/strong> (i.e., chemicals used to cause change in the cell the neuron communicates with; e.g., acetylcholine<\/strong>).<\/li>\n
                                                              2. Synaptic cleft<\/strong><\/span>: the space between the axon terminal and the motor end plate.<\/li>\n
                                                              3. Motor end plate<\/strong><\/span>: a specialized region of the sarcolemma that houses receptors for neurotransmitters.<\/li>\n<\/ol>\n
                                                                \"\"
                                                                –
                                                                Figure 11.8\u2014Anatomy of the neuromuscular junction.<\/figcaption><\/figure>\n

                                                                OK, we are finally ready to talk about muscle contraction. The process of muscle contraction can be broken down into three parts:<\/p>\n

                                                                  \n
                                                                1. Excitation phase<\/li>\n
                                                                2. Excitation\u2013contraction coupling<\/li>\n
                                                                3. Contraction phase<\/li>\n<\/ol>\n

                                                                  During the excitation phase<\/strong><\/span>, a signal is transmitted from the motor neuron to the sarcolemma of the muscle fiber through the release of acetylcholine<\/strong><\/span> (ACh<\/strong><\/span>), a neurotransmitter. This generates a response in the muscle fiber called an end-plate potential<\/strong><\/span>.<\/p>\n

                                                                  In order to actually produce a muscle contraction, multiple end-plate potentials must be generated. But the ACh released into the synapse is quickly broken down by an enzyme called acetylcholinesterase<\/strong> (AChE). So in order to produce the multiple end-plate potentials necessary for contraction to occur, the motor neuron must continue to generate action potentials and release new ACh molecules.<\/p>\n

                                                                  Upon the generation of the end-plate potential, the second phase of muscle contraction\u2014excitation\u2013contraction coupling<\/strong><\/span>\u2014is initiated. During this phase, the end-plate potential is propagated across the sarcolemma and down through the T-tubules, which initiates the release of calcium ions from the sarcoplasmic reticulum into the sarcoplasm of the muscle fiber.<\/p>\n

                                                                  The stage is now set to initiate the third phase of generating a muscle contraction\u2014the contraction phase<\/strong><\/span>. The calcium ions that were released from the sarcoplasmic reticulum bind to troponin, the globular, regulatory protein found in the thin filaments that we discussed earlier in the chapter. This binding of calcium causes the troponin to shift position, which enables tropomyosin\u2014the long, regulatory protein in thin filament\u2014to move and expose the active sites on the actin subunits. Once these active sites are exposed, the myosin heads from the thick filaments can bind to the actin on the thin filaments, and the sliding filament mechanism is engaged. When the sliding filament mechanism is engaged in multiple sarcomeres along the length of the muscle fiber and in multiple muscle fibers in the muscle, whole organ contraction takes place. Now, muscles cannot just contract and stop there\u2014they also have to relax. Muscle relaxation has two components:<\/p>\n

                                                                    \n
                                                                  1. Release of ACh stops and any ACh left in the synapse is broken down by AChE.<\/li>\n
                                                                  2. Calcium ion concentrations in the sarcoplasm return to resting level and troponin and tropomyosin return to their resting positions, thus blocking the active sites on the thin filament.<\/li>\n<\/ol>\n

                                                                    One very important thing to note is that muscles cannot lengthen themselves (i.e., muscles can only \u201cpull\u201d on structures, they cannot \u201cpush\u201d)! For this reason, muscle groups that act about joints are typically organized as antagonist pairs or antagonist groups, such that the contraction of one muscle or group of muscles moves a body part in one direction, and contraction of the opposing muscle or group of muscles moves the body part in the opposite direction (and thereby relengthens the first set of muscles). So even though muscles cannot actually lengthen themselves, they can be passively relengthened after shortening because they contain parts that behave elastically. In other words, they will return to their original length after being stretched or shortened. These elastic components include connective tissue within the muscle, parallel to the fibers, called parallel elastic components<\/strong>, and the tendons that attach muscle to bone, called series elastic components<\/strong>. These elastic components help save energy by reducing the force that muscles have to exert to produce opposing motions.<\/p>\n

                                                                    Let\u2019s consider an example: My triceps brachii, located on the posterior side of my humerus, extends the elbow when it contracts; the biceps group (which includes biceps brachii, brachialis, and brachioradialis) on the anterior side of my humerus flexes the elbow and relengthens the triceps so it can contract again (Figure 11.9).<\/p>\n

                                                                    \"\"
                                                                    –
                                                                    Figure 11.9\u2014Antagonist muscle groups of the arm.<\/figcaption><\/figure>\n

                                                                    I described these antagonist pairs as muscle groups, and that is because oftentimes there are multiple muscles in a position to produce a similar motion when they contract across a joint. These muscles that can work together are called synergists<\/strong><\/span> or agonists<\/strong><\/span>. This redundancy of muscles crossing joints and producing similar actions allows for more refined control of joint motions; there are also some additional mechanisms for modulating muscle actions and movements, as we\u2019ll see shortly.<\/p>\n

                                                                    Muscle Tension<\/h2>\n

                                                                    Let\u2019s turn our attention to muscle tension for a bit now. When muscle tissue contracts, it produces tension<\/strong><\/span>. The smallest possible muscle contraction is called a muscle twitch<\/strong><\/span>, which is simply the response of a muscle fiber to a single motor neuron action potential. Every muscle twitch produces tension, which translates to some degree of force production and varies from fiber to fiber. The tension produced during a twitch is influenced by several factors, including<\/p>\n

                                                                      \n
                                                                    1. Timing and frequency of stimulation<\/li>\n
                                                                    2. Resting fiber length<\/li>\n
                                                                    3. Muscle fiber type<\/li>\n<\/ol>\n

                                                                      Let\u2019s look at each of these factors and see how they can influence tension production of muscle fibers. We\u2019ll start with timing and frequency of stimulation.<\/p>\n

                                                                      Generally speaking, repeated stimulation of a muscle fiber produces twitches with progressively greater tension. The reason for this is that the sarcoplasmic reticulum pumps don\u2019t have enough time to pump all the calcium ions back into the sarcoplasmic reticulum, which results in increasing calcium ion concentrations in the sarcoplasm with each stimulus. This increasing tension is known as wave summation, because the waves of contraction add together.<\/p>\n

                                                                      Depending on the frequency of stimulation, or how quickly the stimulation is occurring, our muscle fiber can wind up in one of two states (Figure 11.10):<\/p>\n

                                                                        \n
                                                                      1. Unfused tetanus<\/strong><\/span> (or incomplete tetanus<\/strong><\/span>): occurs when fiber is stimulated at a frequency of about 50 times per second. This frequency allows partial relaxation between each contraction, so tension increases and decreases slightly with each twitch until a level of maximal tension is reached.<\/li>\n
                                                                      2. Fused tetanus<\/strong><\/span> (or complete tetanus<\/strong><\/span>): occurs when a fiber is stimulated at a higher frequency\u2014typically around 80\u2013100 times per second. In this state, the fiber does not have time to relax between contractions, and as a result, tension remains constant at a maximal level.<\/li>\n<\/ol>\n
                                                                        \"\"
                                                                        –
                                                                        Figure 11.10\u2014Unfused versus fused tetanus. Note the difference in the frequency of stimulation and how that affects the muscle fiber\u2019s ability to relax (or not) between stimuli and the corresponding impact on generating maximum tension.<\/figcaption><\/figure>\n

                                                                        Our second factor\u2014resting fiber length<\/strong><\/span>\u2014brings us to the concept of length-tension relationships. The length-tension relationship<\/strong> is a principle that states that the number of crossbridges that can form in a sarcomere depends on the length of the sarcomere prior to contraction<\/em><\/span>. The optimal length of the sarcomere is the length at which the most crossbridges can form, and the number of crossbridges that can form directly influences the amount of tension the fiber can produce (generally, more crossbridges lead to greater force production and vice versa; Figure 11.11).<\/p>\n

                                                                        \"\"
                                                                        –
                                                                        Figure 11.11\u2014Length-tension relationship. As sarcomere length increases or decreases, the zone of overlap changes size and affects how the thick and thin filaments interact with each other. Because the number of crossbridges is maximized and there is minimal interference of the Z disc at an intermediate length, this is the length of the sarcomere at which tension production peaks.<\/figcaption><\/figure>\n
                                                                        \n

                                                                        Box 11.3<\/span>\u2014Wrist Posture, Sarcomere Length, and Grip Strength<\/strong><\/p>\n

                                                                        Let\u2019s illustrate this concept with a quick experiment. Flex your wrist 90 degrees. Now try to squeeze your pen\/pencil\/hand dynamometer hard. It\u2019s a little tough, right? This is because your flexed wrist position has shortened the muscles of the forearm, causing a great deal of overlap of the thick and thin filaments in the sarcomeres. Since there is so much overlap, there is not much room for the thick and thin filaments to slide past one another before hitting the Z disc. This results in the formation of very few functional crossbridges, and as a result, the muscle generates less tension.<\/p>\n

                                                                        Let\u2019s try again\u2014but hyperextend your wrist this time (90 degrees in the other direction). Now try to squeeze your pen\/pencil\/dynamometer. Still tough, right? This time, the muscle is stretched, and there isn\u2019t enough overlap for the thick and thin filaments to connect properly. Again, this leads to the formation of fewer crossbridges and the production of less tension.<\/p>\n

                                                                        Last, extend your wrist normally and squeeze your pen\/pencil\/dynamometer. You should notice that your grip strength is strongest in this position. This is because the muscle is at its natural resting length, and the sarcomeres are at optimal length with just the right amount of overlap of the thick and thin filaments; this arrangement maximizes crossbridge formation and increases tension production.<\/p>\n

                                                                        As you can see, the optimal length of the sarcomere is actually an intermediate length. So it\u2019s a little bit like a Goldilocks situation: Less tension is produced when the sarcomere is too short and when the sarcomere is too long. But when the sarcomere is \u201cjust<\/em><\/span> right,\u201d the muscle is able to maximize tension\u2014and by extension, force\u2014production.<\/p>\n<\/div>\n

                                                                        Recall the elastic filaments that make up part of the myofibril. These filaments enable the myofibril to be stretched, resulting in differing lengths of the myofibril and its sarcomeres. This, in turn, affects the degree of overlap of the thick and thin filaments in the sarcomere\u2019s zone of overlap. Therefore, the size of the zone of overlap is largely dependent upon the position of the muscle prior to contraction.<\/p>\n

                                                                        The third factor that can affect the generation of tension is fiber type.<\/p>\n

                                                                        Muscle Fiber Types<\/h2>\n

                                                                        In some muscles, the muscle fibers are supplied by multiple connections from the nerve cells (i.e., they contain multiple motor end plates). These muscles are called tonic muscles<\/strong><\/span>, and the force of the contraction in this type of muscle fiber is controlled by how quickly the nerve impulses arrive in sequence (frequency<\/strong><\/span>). Tonic muscles typically contract slowly but are really hard to fatigue. Tonic muscles are uncommon in fishes, birds, and mammals. When observed in mammals, they are typically small and restricted to places requiring fine control, like the muscles that move the eyeball. However, tonic fibers are much more common in amphibians and reptiles and have been shown to contribute to sustained force production by the jaw muscles of some species, enabling them to subdue prey (e.g., horned frogs) or engage in long-lasting courtship behaviors (e.g., alligator lizards).<\/p>\n

                                                                        In contrast, most skeletal muscles have fibers with only a single connection to a nerve cell (i.e., a single motor end plate). These are called twitch muscles<\/strong><\/span>. In twitch muscles, the nerve impulses spread easily throughout the fiber, so once the threshold impulse level is reached, the fiber will contract in an \u201call or nothing\u201d fashion and then relax. However, if the fibers are stimulated several times in rapid succession, the forces from each twitch will be summed up to a maximum, which is called tetanic force<\/strong><\/span>. Twitch muscles tend to be large muscles with several motor units, so forces can be modulated by varying the number of motor units stimulated as well as the frequency of stimulation.<\/p>\n

                                                                        Twitch fibers differ in structure and function, and as a result of these differences, some fibers twitch more rapidly than others. Whether a muscle fiber is considered a \u201cfast\u201d or \u201cslow\u201d fiber is largely determined by the level of myosin ATPase activity in the cell (this is the enzyme that hydrolyzes ATP to drive the power stroke of contraction).<\/p>\n

                                                                        Muscle fibers with high ATPase activity are called fast-twitch fibers<\/strong><\/span> because they go through contraction cycles relatively quickly. Fast-twitch fibers tend to be found in body parts that need to move rapidly (e.g., the muscles that move the eyes). In contrast, fibers with low myosin ATPase activity are called slow-twitch fibers<\/strong><\/span> and tend to be found in muscles that require slow sustained contractions (e.g., postural muscles of the back).<\/p>\n

                                                                        When we consider twitch speed in conjunction with a fiber\u2019s primary energy source, we find that skeletal muscle can be categorized into two \u201ctype\u201d classes:<\/p>\n

                                                                          \n
                                                                        1. Type I fibers<\/strong><\/span>: These are slow-twitch fibers with small diameters, high myoglobin concentration, many mitochondria, and a well-developed blood supply. Myoglobin is an oxygen-binding protein found in vertebrate muscle. The high myoglobin content of Type I fibers makes them red in appearance, so muscles with many Type I fibers are sometimes called red muscle<\/strong><\/span>. These muscle fibers are also sometimes referred to as slow-oxidative <\/strong>(SO)<\/strong> fibers<\/strong><\/span> due to their slow contraction times and reliance on oxidative or aerobic metabolism (requires oxygen).<\/li>\n
                                                                        2. Type II fibers<\/strong><\/span>: These are fast-twitch fibers with large diameters that contract quickly but also fatigue quickly compared to Type I fibers. Type II fibers rely primarily on anaerobic energy production, so they are characterized by having fewer myoglobin and mitochondria compared to Type I fibers. The lack of myoglobin in Type II fibers gives them a light color, so they are sometimes called white muscle<\/strong><\/span>. These muscle fibers are also sometimes referred to as fast-glycolytic <\/strong>(FG)<\/strong> fibers<\/strong><\/span>, because they contract more rapidly and rely on glycolytic or anaerobic metabolism (does not require oxygen).<\/li>\n<\/ol>\n

                                                                          Up to this point, we\u2019ve been considering muscle tension at the fiber level, so let\u2019s zoom out a bit now and consider tension at the organ level. Recall from earlier that muscle fibers are innervated by motor neurons, and a single motor neuron may innervate multiple fibers. We refer to this motor neuron and all the fibers it innervates as a motor unit<\/strong><\/span>.<\/p>\n

                                                                          In humans, the average motor unit is made up of one motor neuron and about 150 muscle fibers, but this can vary depending on the part of the body and its function. For example, in areas that require precise movements, like the hand, we find motor units innervating as few as 10 muscle fibers. In contrast, areas of the body with large, powerful muscles, such as in the back, have motor units that innervate upward of 2,000\u20133,000 fibers. All the muscle fibers in a motor unit are of the same type, though, resulting in slow motor units and fast motor units. When a whole muscle begins a contraction, not all the motor units immediately engage. In fact, the slow motor units typically activate first and are later joined by fast motor units if additional tension is required to complete a task\u2014this is called recruitment<\/strong><\/span>.<\/p>\n

                                                                          11.4 Summary<\/h1>\n

                                                                          In this chapter, we introduced muscles as the motors of the vertebrate body. By looking at muscle development as well as the tissue-level structure of muscle, we were able to gain an understanding of the microscopic organization of muscle as well as how this structure facilitates muscle contraction.<\/p>\n

                                                                          \n
                                                                          \n

                                                                          Application Questions<\/p>\n<\/header>\n

                                                                          \n
                                                                            \n
                                                                          1. In domesticated chickens, the breast meat tends to be \u201cwhite\u201d meat, whereas the thigh meat tends to be \u201cdark\u201d meat.\n
                                                                              \n
                                                                            1. Given what you now know about muscle fiber types and their characteristics, why do you suspect this is the case?<\/li>\n
                                                                            2. What do these differences indicate about muscle function in the breast versus the thigh of these birds?<\/li>\n
                                                                            3. Do you think this pattern might differ in a migratory game bird, such as ducks? Why or why not?<\/li>\n<\/ol>\n<\/li>\n
                                                                            4. You are at the gym and notice that you have an easier time lifting weights when your arm is in a particular position, compared to other positions. In the context of the length-tension relationship and muscle function, explain why this is the case.<\/li>\n<\/ol>\n<\/div>\n<\/div>\n

                                                                              11.5 Further Reading<\/h1>\n
                                                                                \n
                                                                              1. Abbott B. C., and X. M. Aubert. \u201cThe force exerted by active striated muscle during and after change of length.\u201d Journal of Physiology<\/em><\/span> 117 (1952): 77\u201386.<\/li>\n
                                                                              2. Cook, Verity A., Antonia H. Groneberg, Maximillian Hoffmann, Mykola Kadobianskyi, Johannes Veith, Lisanne Schulze, J\u00f6rg Henninger, Ralf Britz, and Benjamin Judkewitz. \u201cUltrafast sound production mechanism in one of the smallest vertebrates.\u201d Proceedings of the National Academy of Sciences <\/em>U.S.A<\/em>.<\/em><\/span> 121 (2024): e2314017121.<\/li>\n
                                                                              3. Nishikawa, Kiisa C., Jena A. Monroy, Theodore E. Uyeno, Sang Hoon Yeo, Dinesh K. Pai, and Stan L. Lindstedt. \u201cIs titin a \u2018winding filament\u2019? A new twist on muscle contraction.\u201d Proceedings of the Royal Society B<\/em><\/span>. 279 (2012): 981\u2013990.<\/li>\n
                                                                              4. Parmentier, Eric, and Marc Thiry. \u201cA new organisational design in skeletal muscle fibres.\u201d Cell and Tissue Research<\/em><\/span> 393 (2023): 111\u2013117.<\/li>\n<\/ol>\n

                                                                                11.6 References<\/h1>\n
                                                                                  \n
                                                                                1. Abbott B. C., and X. M. Aubert. \u201cThe force exerted by active striated muscle during and after change of length.\u201d Journal of Physiology<\/em><\/span> 117 (1952): 77\u201386.<\/li>\n
                                                                                2. Amerman, Erin C. Human Anatomy and Physiology<\/em><\/span>, 1st ed. Boston: Pearson, 2016.<\/li>\n
                                                                                3. Cook, Verity A., Antonia H. Groneberg, Maximillian Hoffmann, Mykola Kadobianskyi, Johannes Veith, Lisanne Schulze, J\u00f6rg Henninger, Ralf Britz, and Benjamin Judkewitz. \u201cUltrafast sound production mechanism in one of the smallest vertebrates.\u201d Proceedings of the National Academy of Sciences <\/em>U.S.A<\/em>.<\/em><\/span> 121 (2024): e2314017121.<\/li>\n
                                                                                4. Marieb, Elaine N., and Katja Hoehn. Human Anatomy and Physiology<\/em><\/span>, 10th ed. Boston: Pearson, 2016.<\/li>\n
                                                                                5. McKinley, Michael P., Valerie D. O\u2019Loughlin, and Elizabeth E. Pennefather-O\u2019Brien. Human Anatomy<\/em><\/span>, 5th ed. New York: McGraw Hill Education, 2015.<\/li>\n
                                                                                6. Nishikawa, Kiisa C., Jena A. Monroy, Theodore E. Uyeno, Sang Hoon Yeo, Dinesh K. Pai, and Stan L. Lindstedt. \u201cIs titin a \u2018winding filament\u2019? A new twist on muscle contraction.\u201d Proceedings of the Royal Society B<\/em><\/span>. 279 (2012): 981\u2013990.<\/li>\n
                                                                                7. Parmentier, Eric, and Marc Thiry. \u201cA new organisational design in skeletal muscle fibres.\u201d Cell and Tissue Research<\/em><\/span> 393 (2023): 111\u2013117.<\/li>\n<\/ol>\n","protected":false},"author":13,"menu_order":11,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["vanessa-hiliard"],"pb_section_license":""},"chapter-type":[],"contributor":[62],"license":[],"part":3,"_links":{"self":[{"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/pressbooks\/v2\/chapters\/528"}],"collection":[{"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/wp\/v2\/users\/13"}],"version-history":[{"count":19,"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/pressbooks\/v2\/chapters\/528\/revisions"}],"predecessor-version":[{"id":1012,"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/pressbooks\/v2\/chapters\/528\/revisions\/1012"}],"part":[{"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/pressbooks\/v2\/parts\/3"}],"metadata":[{"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/pressbooks\/v2\/chapters\/528\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/wp\/v2\/media?parent=528"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/pressbooks\/v2\/chapter-type?post=528"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/wp\/v2\/contributor?post=528"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.palni.org\/comparativevertebrateandhumananatomy\/wp-json\/wp\/v2\/license?post=528"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}