Muscles Can Be Divided Into Three Main Groups According to Their Structure

Muscle Tissue

Muscles can be divided into three main groups according to their structure:

• Smooth muscle tissue.
• Skeletal muscle tissue.
• Cardiac (heart) muscle tissue.

Characteristics of muscle:

• excitability - responds to stimuli (e.g., nervous impulses)
• contractility - able to shorten in length
• extensibility - stretches when pulled
• elasticity - tends to return to original shape & length after contraction or extension

Functions of muscle:

• motion
• maintenance of posture
• heat production

Skeletal muscle is attached to the skeleton and moves the body and its components. It appears striated (striped) under the microscope and is under voluntary control. The biceps of the arm is an example of skeletal muscle. Cardiac muscle is only located in the heart. Cardiac muscle is also striated, but is not normally under voluntary control. Smooth muscle surrounds blood vessels and other passageways and alters the size of openings or passageways and propels material through body tubes. Smooth muscle is distributed throughout the body. It lacks striations and is involuntary. The respiratory and digestive tracts have layers of smooth muscle in their walls.

Skeletal Muscle Ultrastructure

• A skeletal muscle fiber is formed from the fusion of many embryonic cells during development to form slender cells that extend from one end of the muscle to the other. Each muscle fiber normally has one nerve fiber that extends to the cell membrane, forming the neuromuscular junction. There is a 100-nanometer space, the synaptic cleft, between the nerve fiber and the muscle fiber.
• The muscle cell membrane forms inward projections, the transversetubules, associated with the cell's smooth endoplasmic reticulum (sarcoplasmic reticulum). The sarcoplasmic reticulum stores calcium and surrounds bundles of contractile proteins. The contractile proteins, which do the work of contraction, are parallel and arranged in an overlapping pattern that gives rise to the muscle striations. The pattern of striations is repeated many times down the length of the muscle fiber in segments called sarcomeres.
• The proteins of the sarcomere are grouped in thick filaments and thin filaments. Contraction occurs when thick and thin filaments slide past each other, pulling the muscle ends closer together. A thick filament is a bundle of approximately two hundred myosin proteins. A portion of each myosin protein projects outward to form myosin heads.

• Thin filaments overlap the thick filaments and are composed of three types of protein molecules. The main protein is actin. Three hundred to four hundred molecules of globular actin (G actin) link like beads in a necklace to form a strand called fibrous actin (F actin). Two such "necklaces" are then intertwined into a loose double helix. In the groove between the two F-actins, much like a string, is the protein tropomoysin. Each G- actin contains an active site to bind the myosin head. When the muscle is at rest, tropomyosin covers the active sites of actin. Attached to tropomyosin is troponin, a small complex of three polypeptides. This structural arrangement allows muscle to contract.

Muscle Contraction

• Muscle contraction begins when the nerve fiber releases the neurotransmitter acetylcholine into the synaptic cleft. Acetylcholine moves across the synaptic cleft and binds to receptors on the muscle fiber. This indirectly initiates an action potential , a change of electrical charge at the membrane that is similar to events in a neuron. The action potential spreads across and into the muscle fiber via the transverse tubules and triggers the release of calcium from the sarcoplasmic reticulum. Next, calcium binds to troponin, causing the troponin to change shape. Since troponin is attached to tropomysin, as troponin changes shape the tropomysin is pulled away from the active sites of actin, which become exposed. The myosin head, which was previously blocked by tropomysin, now binds to the active site of actin, forming a cross-bridge between the thick and thin filament.
• Myosin pulls the thin filament past the myosin as the myosin head repeatedly flexes, lets go of the actin, extends and attaches to a new active site, and flexes again. As the many myosin heads continue to repeat this process, thin filaments slide past the thick filaments and the sarcomere is shortened. Shortening of all sarcomeres within the muscle fiber results in contraction of the whole fiber.
• Muscle relaxes and returns to its original form when tropomyosin covers up the active sites of actin, preventing the formation of cross-bridges. Relaxation also involves the destruction of acetylcholine by acetylcholinesterase in the synaptic cleft, ending muscle stimulation, and the re-uptake of calcium into the sarcoplasmic reticulum. Without calcium, troponin returns to its original shape, pulling tropomyosin back over the active sites of actin. Myosin no longer forms cross-bridges, so the muscle relaxes.
• Depolarization of the T-tubule membrane causes a release of calcium ions from the sarcoplasmic reticulum, triggering muscle contraction.
• Myosin heads in a myosin thick filament cluster to the outside, with the tails lining up inside. The heads on either end point in opposite directions. During muscle contraction, the heads pull actin filaments together toward the center bare zone, contracting the muscle fiber.

Energy (ATP) Requirements

• The contraction of muscle fibers requires a large amount of energy in the form of adenosine triphosphate (ATP). ATP is made available through various mechanisms. A limited amount of ATP is stored in the muscle cell. ATP is also produced by a phosphate transfer from creatine phosphate to ADP; muscles do store larger amounts of creatine phosphate. The stored ATP and the ATP created from creatine phosphate are available for immediate use and provide approximately enough ATP for about six seconds of exercise.
• Additional ATP can be produced through anaerobic and aerobic metabolism. Aerobic respiration provides a larger production of ATP but depends on sufficient oxygen delivery. Myoglobin, a protein in muscle cells that binds oxygen, contributes some of the oxygen for aerobic respiration. Aerobic ATP production also requires mitochondria . Muscles packed with mitochondria give meat a darker color ("dark meat") than muscles with fewer mitochondria ("white meat"). Anaerobic fermentation provides less energy but can produce ATP in the absence of oxygen. A serious drawback of anaerobic fermentation is the production of lactic acid, a product that can alter cell pH . Both processes can use glucose released from glycogen, which is stored in muscles as a reserve fuel.

Muscle Fatigue

• A decrease in the ability of muscle to contract is muscle fatigue. Muscle fatigue can result from short burst of maximum effort, such as a 50-meter swim, or sustained long-term activities such as marathon running. The cause of fatigue depends on the activity. Fatigue from short, extensive burst of activity can result from depletion of ATP or buildup of lactic acid. Muscle fatigue from sustained activities can result from depletion of fuel molecules or depletion of acetylcholine at the neuromuscular junction.

Hypertrophy and Conditioning

• Through training, a muscle can become larger (hypertrophy) and have greater endurance. A muscle grows mainly by increasing the number of thin and thick filaments within the fibers. Growth results from repeated contractions of muscle, as in weight lifting. Muscle conditioning is the increased ability of the muscle to perform a task, either because of greater strength or better fatigue-resistance. Many changes in muscle performance, however, result from changes in the cardiovascular and respiratory systems, enabling them to deliver fuel and oxygen to muscle fibers more efficiently. Many changes specific to muscle fibers involve enhancing energy production, including an increase in number of mitochondria and myoglobin and greater storage of glycogen.

• Diseases affecting muscle can result from loss of neurons that stimulate the muscle, such as polio; changes in the neuromuscular junction that result in loss of ability to stimulate the muscle, such as myasthenia gravis (an autoimmune disease); or loss of structural integrity of the muscle fiber, such as muscular dystrophy. All result in decreased ability of the muscle to contract and sometimes the complete loss of the muscle's function.

• SMOOTH MUSCLE

• Smooth muscle is responsible for the contractility of hollow organs, such as blood vessels, the gastrointestinal tract, the bladder, or the uterus. Its structure differs greatly from that of skeletal muscle, although it can develop isometric force per cross-sectional area that is equal to that of skeletal muscle. However, the speed of smooth muscle contraction is only a small fraction of that of skeletal muscle.
• Structure: The most striking feature of smooth muscle is the lack of visible cross striations (hence the name smooth). Smooth muscle fibers are much smaller (2-10 m in diameter) than skeletal muscle fibers (10-100 m ). It is customary to classify smooth muscle as single-unit and multi-unit smooth muscle (Fig. SM1). The fibers are assembled in different ways. The muscle fibers making up the single-unit muscle are gathered into dense sheets or bands. Though the fibers run roughly parallel, they are densely and irregularly packed together, most often so that the narrower portion of one fiber lies against the wider portion of its neighbor. These fibers have connections, the plasma membranes of two neighboring fibers form gap junctions that act as low resistance pathway for the rapid spread of electrical signals throughout the tissue. The multi-unit smooth muscle fibers have no interconnecting bridges. They are mingled with connective tissue fibers.

• Electron micrographs of smooth muscle reveal that the actin filaments are organized through attachment to the dense bodies that contain a-actinin, a Z-band protein in skeletal muscle. Thus, it is assumed that the dense bodies function as Z-lines. The ratio of thin to thick filaments is much higher in smooth muscle (~15:1) than in skeletal muscle (~6:1). Smooth muscle is rich in intermediate filaments that contain two specific proteins, desmin and vimentin.
• Innervation and stimulation: Smooth muscle is primarily under the control of autonomic nervous system, whereas skeletal muscle is under the control of the somatic nervous system. The single-unit smooth muscle has pacemaker regions where contractions are spontaneously and rhythmically generated. The fibers contract in unison, that is the single unit of smooth muscle is syncytial. The fibers of multi-unit smooth muscle are innervated by sympathetic and parasympathetic nerve fibers and respond independently from each other upon nerve stimulation.
• Nerve stimulation in smooth muscle causes membrane depolarization, like in skeletal muscle. Excitation, the electrochemical event occurring at the membrane is followed by the mechanical event, contraction. In the case of smooth muscle, this excitation-contraction coupling is termed electromechanical coupling; the link for the coupling is Ca2+ that permeates from the extracellular space into the intracellular water of smooth muscle. There is another excitation mechanism in smooth muscle, which is independent of the membrane potential change; it is based on receptor activation by drugs or hormones followed by muscle contraction. This is termed pharmacomechanical coupling. The link is Ca2+ that is released from an internal source, the sarcoplasmic reticulum.
• The role of mechanical events of smooth muscle in the wall of hollow organs is twofold: 1) Its tonic contraction maintains organ dimensions against imposed load. 2) Force development and muscle shortening, like in skeletal muscle.

The heart is the pump that keeps blood circulating throughout the body and thereby transports nutrients, breakdown products, antibodies, hormones, and gases to and from the tissues. The heart consists mostly of muscle; the myocardial cells (collectively termed the myocardium) are arranged in ways that set it apart from other types of muscle. The outstanding characteristics of the action of the heart are its contractility, which is the basis for its pumping action, and the rhythmicity of the contraction.

Heart muscle differs from its counterpart, skeletal muscle, in that it exhibits rhythmic contractions. The amount of blood pumped by the heart per minute (the cardiac output) varies to meet the metabolic needs of the peripheral tissues (muscle, kidney, brain, skin, liver, heart, and gastrointestinal tract). The cardiac output is determined by the contractile force developed by the heart cells (myocytes), as well as by the frequency at which they are activated (rhythmicity). The factors affecting the frequency and force of heart muscle contraction are critical in determining the normal pumping performance of the heart and its response to changes in demand.

Structure and organization

The heart is a network of highly branched cardiac cells 110 μm in length and 15 μm in width, which are connected end to end by intercalated discs. The cells are organized into layers of myocardial tissue that are wrapped around the chambers of the heart. The contraction of the individual heart cells produces force and shortening in these bands of muscle, with a resultant decrease in the heart chamber size and the consequent ejection of the blood into the pulmonary and systemic vessels. Important components of each heart cell involved in excitation and metabolic recovery processes are the plasma membrane and transverse tubules in registration with the Z lines, the longitudinal sarcoplasmic reticulum and terminal cisternae, and the mitochondria. The thick (myosin) and thin (actin, troponin, and tropomyosin) protein filaments are arranged into contractile units (that is, the sarcomere extending from

Z line to Z line) that have a characteristic cross-striated pattern similar to that seen in skeletal muscle.

The frequency of contraction

The rate at which the heart contracts and the synchronization of atrial and ventricular contraction required for the efficient pumping of blood depend on the electrical properties of the myocardial cells and on the conduction of electrical information from one region of the heart to another. Each of the phases of the action potential is caused by time-dependent changes in the permeability of the plasma membrane to (K+), (Na+), and (Ca2+). The resting potential of the myocytes of the ventricle (phase 4) begins with the outside of the cell being positive—i.e., having a greater concentration of positive ions. Atrial and ventricular myocytes are normally quiescent (nonrhythmic); however, when the resting membrane potential is depolarized to a critical potential (Ecrit), a self-generating action potential follows, leading to muscle contraction. Phase 0, the upstroke, is associated with a sudden increase in membrane permeability to Na+. Phases 1, 2, and 3 result from changes in membrane permeability and conductance to Na+, K+, and Ca2+.

The electrical activity of heart muscle cells differs substantially from that of skeletal muscle cells in that phases 1, 2, and 3 are considerably prolonged (200 milliseconds versus 5 milliseconds, respectively). Another significant difference in excitability is that heart muscle cannot be tetanized (i.e., induced to spasm) by the application of repetitive stimuli (see above striated muscle), thus ensuring the completion of the contraction/relaxation cycle and the effective pumping of blood.

Because atrial and ventricular cells are normally quiescent, exhibiting action potentials only after the muscle is depolarized to the critical membrane potential (Ecrit), the source of the rhythmic contractions of the heart must be sought elsewhere. In contrast to atrial and ventricular myocytes, the myocytes of the sinoatrial (SA) node, the atrioventricular (AV) node, the bundle branches, and the Purkinje Fiber system are made up of specialized cardiac muscle cells that exhibit a spontaneous upward drift in the resting potential toward Ecrit, resulting in the generation of the action potential with all of its phases. The normal rhythmicity of cells from each of these regions depends on the rate at which spontaneous depolarization occurs and the resting membrane potential from which it starts. The region with the fastest intrinsic rate, the SA node, sets the pace for the whole heart. The pacemaker activity is propagated to the rest of the heart by means of the low electrical resistance pathways through the muscle cells (e.g., intercalated disks) and the presence of specialized conducting tissue (e.g., bundle branches and the Purkinje system). The time course of activation and the shape of the action potentials in different parts of the heart are responsible for the synchronous activation and contraction of the muscles of the atrium followed by those of the ventricle.

The normal rhythm of the heart (i.e., the heart rate) can be altered by neural activity. The heart is innervated by sympathetic and parasympathetic nerves, which have a profound effect on the resting potential and the rate of diastolic depolarization in the SA nodal region. The activity of the sympathetic nervous system may be increased by the activation of the sympathetic nerves innervating the heart or by the secretion of epinephrine and norepinephrine from the adrenal gland. This decreases the resting potential of the myocytes of the SA node while increasing the rate of diastolic depolarization. The result is an increase in the heart rate. Conversely, stimulating the parasympathetic nervous system (vagal nerves to the heart) increases the resting potential and decreases the rate of diastolic depolarization; under these circumstances the heart rate slows. The sympathetic nervous system is activated under conditions of fright or vigorous activity (the so-called fight-or-flight reaction), where the increase in force and rate of heart contraction are easily felt; the parasympathetic system exerts its influence during periods of rest.