10.11: Alternative Text Descriptions

Figure 10.1.1: The Three Connective Tissue Layers

This image shows the structural organization of skeletal muscle in three progressively magnified sections. The top section shows an entire skeletal muscle surrounded by epimysium. Inside the muscle are bundles labeled muscle fascicles. The middle section enlarges one fascicle and shows multiple muscle fibers grouped together. These fibers are surrounded by perimysium at the fascicle level and endomysium around each individual muscle fiber. A satellite cell is shown along the outside of a muscle fiber. The bottom section enlarges a single muscle fiber, showing the sarcolemma surrounding the fiber and many myofibrils packed inside it. Curved arrows between sections indicate the progression from whole muscle to fascicle, to muscle fiber, to myofibril.

Skeletal muscle is organized in bundles. Inside a whole muscle, the long muscle cells, called muscle fibers, are grouped into smaller bundles called fascicles. Each fascicle is wrapped in perimysium, and each muscle fiber is wrapped in endomysium. The entire muscle is wrapped in epimysium. Together, these three connective tissue layers are called the mysia.

These connective tissue coverings help organize the muscle and transmit force. When muscle fibers contract, the pulling force passes through the endomysium, perimysium, and epimysium, then into a tendon or sometimes a broad flat tendon sheet called an aponeurosis. The tendon then connects to the periosteum of bone, allowing muscle contraction to produce movement.

The figure also supports the idea that skeletal muscle is richly supplied with blood vessels and nerve input. Each muscle fiber receives nutrients and oxygen through the blood supply and is controlled by a branch of a somatic motor neuron. This nerve signal is necessary for normal skeletal muscle contraction.

Figure 10.1.2: Structure of a Skeletal Muscle Fiber

This image illustrates the microscopic structure of a skeletal muscle fiber, moving through three levels of organization: the muscle fiber, the myofibrils inside the fiber, and the sarcomere, which is the functional unit of contraction.

The overall organization shows three nested levels of structure. The labels in the image include muscle fiber, nuclei, mitochondria, sarcolemma, myofibrils, sarcomere, Z disc, thin (actin) filaments, thick (myosin) filaments, A band, I band, H zone, M line, and sarcoplasmic reticulum. The figure emphasizes how the arrangement of these structures directly supports muscle contraction.

At the muscle fiber level, the image shows a long cylindrical cell labeled as a muscle fiber. This cell contains multiple nuclei, many mitochondria, and an outer membrane called the sarcolemma. The muscle fiber serves as the basic cellular unit of skeletal muscle, produces force through contraction, and depends on mitochondria for energy. The sarcolemma is the outer membrane of the muscle fiber. Its functions are to conduct electrical signals and initiate muscle contraction. Inside the muscle fiber are many myofibrils, which are cylindrical structures that contain the contractile machinery and shorten during contraction.

At the myofibril level, the image shows that each myofibril is made up of repeating units called sarcomeres. These repeating units create the striated, or striped, appearance of skeletal muscle and allow coordinated contraction along the length of the muscle fiber.

At the sarcomere level, the figure shows a segment between two Z discs. The Z disc forms the boundary at each end of a sarcomere and anchors the thin, or actin, filaments. The thin filaments extend from the Z disc toward the center and slide during contraction by interacting with myosin. The thick, or myosin, filaments are located in the center of the sarcomere and generate force by pulling actin inward. The A band is the darker region corresponding to the length of the thick filaments and remains relatively constant during contraction. The I band is the lighter region containing only thin filaments and shortens during contraction. The H zone is the central region containing only thick filaments and narrows or disappears during contraction. The M line is the center of the sarcomere and stabilizes the thick filaments. The sarcoplasmic reticulum is shown as a network surrounding the myofibrils. Its functions are to store and release calcium ions and regulate contraction.

Figure 10.1.3: Sarcomere

This image illustrates the organization of a sarcomere and enlarges the thick and thin filaments responsible for skeletal muscle contraction. At the top of the figure, a single sarcomere extends between two Z lines. Thin filaments extend inward from each Z line toward the center of the sarcomere, while thick filaments occupy the central region. The darker A band corresponds to the full length of the thick filaments, including areas where thick and thin filaments overlap. The lighter I bands are located near the Z lines and contain only thin filaments. At the center of the A band, the H zone contains only thick filaments, and the M line marks the midpoint where the thick filaments are anchored.

Below the sarcomere, the left side shows an enlarged portion of a thick filament composed of many myosin molecules packed together. Numerous myosin heads project outward from the filament's surface. A further enlargement depicts a single myosin molecule with a long coiled tail, a flexible hinge region, and two globular heads. The heads contain actin-binding sites that attach to actin during contraction and ATP-binding sites that provide the energy needed for movement.

The right side shows an enlarged portion of a thin filament. The thin filament consists primarily of actin subunits arranged as intertwined strands. Running along the actin filament is tropomyosin, a long regulatory protein that lies over the myosin-binding sites on actin. Attached at intervals to the filament is troponin, a regulatory protein complex that controls the position of tropomyosin. A further enlargement shows individual actin subunits and a myosin-binding site on the actin filament.

The figure demonstrates that the banding pattern of a sarcomere is produced by the arrangement of thick and thin filaments and that muscle contraction depends on interactions between myosin heads on the thick filaments and binding sites on actin within the thin filaments.

Figure 10.2.1: Motor End-Plate and Innervation

This image illustrates the neuromuscular junction, the site where a motor neuron communicates with a skeletal muscle fiber. The figure is arranged as a series of enlargements that progress from the overall nerve-muscle connection to a detailed view of neurotransmitter release and receptor activation.

At the top of the figure, a myelinated motor neuron approaches a skeletal muscle fiber. The axon branches into multiple axon terminals, each ending in a synaptic end bulb at the surface of the muscle fiber. The outer membrane of the muscle fiber is the sarcolemma, while the interior contains sarcoplasm and numerous cylindrical myofibrils. A red arrow indicates a nerve impulse, or action potential, traveling along the motor neuron toward a synaptic end bulb.

The middle enlargement focuses on a single synaptic end bulb positioned above the motor end plate, a specialized region of the sarcolemma. The synaptic end bulb contains many synaptic vesicles filled with acetylcholine (ACh). Some vesicles are shown fusing with the membrane of the nerve terminal and releasing ACh into the synaptic cleft, the narrow gap between the neuron and muscle fiber. The motor end plate contains folded regions of the sarcolemma that increase surface area for communication between the neuron and the muscle fiber.

The lower enlargement provides a close-up view of neurotransmitter release. Synaptic vesicles within the synaptic end bulb contain multiple molecules of ACh. Several vesicles are shown releasing ACh by exocytosis into the synaptic cleft. The released ACh molecules diffuse across the cleft and bind to ACh receptors located on the motor end plate. The figure shows ACh binding to a receptor and opening an ion channel. An arrow indicates sodium ions (Na+) moving through the open channel into the muscle fiber. This sequence illustrates how a nerve impulse reaching the synaptic end bulb triggers neurotransmitter release, receptor activation, and ion movement across the muscle membrane.

Overall, the figure demonstrates the structural relationship between a motor neuron and a skeletal muscle fiber and shows the sequence of events by which acetylcholine transmits a signal from the nervous system to the muscle cell at the neuromuscular junction.

Figure 10.2.2: The T-tubule Narrow

This image shows the triad structure in a skeletal muscle fiber. The instructional purpose is to identify the relationship between the sarcolemma, T-tubule, and sarcoplasmic reticulum in the region where excitation is linked to internal muscle signaling.

At the top, the sarcolemma is labeled as the outer membrane of the muscle fiber. Just beneath it, the figure shows inward extensions associated with the membrane system. Surrounding the myofibril region is a network labeled sarcoplasmic reticulum.

The central feature is the T-tubule, shown passing between two enlarged sacs of the sarcoplasmic reticulum labeled terminal cisternae. The label triad identifies this three-part arrangement: one T-tubule plus two terminal cisternae, one on each side.

Figure 10.2.3: Contraction of a Muscle Fiber

This image illustrates the process of excitation–contraction coupling in skeletal muscle, showing how a nerve signal leads to muscle contraction through a sequence of electrical, chemical, and mechanical events.

The diagram is arranged vertically in sequential steps. It progresses from the neuromuscular junction at the top, to electrical signaling in the muscle fiber, to calcium release and actin–myosin interaction, and finally to muscle shortening and force generation at the bottom. Arrows show the downward direction of the process.

Step 1: Neuromuscular junction - A motor neuron axon terminal contacts a skeletal muscle fiber. The axon terminal contains synaptic vesicles filled with acetylcholine (ACh), and the muscle fiber membrane is labeled the sarcolemma. An action potential arrives at the neuromuscular junction and causes ACh to be released from the synaptic end bulb.

Step 2: Chemical signaling and muscle action potential - ACh diffuses across the synaptic cleft and binds to receptors on the motor end plate of the sarcolemma. This binding opens sodium ion channels, allowing sodium ions to enter the muscle fiber. That produces a muscle action potential.

Step 3: Signal propagation through T-tubules - The sarcolemma forms T-tubules that extend into the muscle fiber. The muscle action potential travels along the sarcolemma and down the T-tubules, carrying the signal into the interior of the muscle fiber.

Step 4: Calcium release from the sarcoplasmic reticulum - The T-tubules are closely associated with the sarcoplasmic reticulum, which stores calcium ions (Ca²⁺). The electrical signal triggers release of calcium into the muscle cell, where it diffuses around the myofibrils.

Step 5: Molecular interaction between actin and myosin - Within the myofibrils, thin filaments (actin) and thick filaments (myosin) are shown, along with troponin on the actin filament. Calcium binds to troponin, which causes associated proteins to shift and expose binding sites on actin. Myosin heads then attach to actin. Using energy from ATP, myosin pulls the actin filaments inward. This process repeats across many sarcomeres.

Step 6: Muscle contraction - As the filaments slide, individual sarcomeres shorten. When many sarcomeres shorten together, the muscle fiber shortens and produces tension. The final part of the figure shows the whole muscle becoming shorter and thicker.

Figure 10.2.4: Relaxation of a Muscle Fiber

This image shows the process of skeletal muscle relaxation, illustrating how a muscle returns to its resting state after contraction. The diagram is arranged as a top-to-bottom sequence, linking decreasing calcium levels to reduced filament interaction, muscle fiber lengthening, and whole-muscle relaxation.

The overall organization progresses through five connected stages: ending stimulation at the neuromuscular junction, calcium reuptake into the sarcoplasmic reticulum, reduced activation of the thin filament, cessation of actin–myosin interaction, muscle fiber lengthening, and whole muscle relaxation. Arrows show the downward direction of change from an active contraction state toward relaxation.

Step 1: Neuromuscular junction - At the top of the image, a synaptic end bulb of a motor neuron lies above the muscle fiber membrane, and the muscle surface forms the motor end plate. This part of the diagram indicates that neural stimulation has already occurred, but at this stage the stimulation is ending, which initiates relaxation.

Step 2: Calcium reuptake into the sarcoplasmic reticulum - The sarcoplasmic reticulum is shown containing calcium ions, and arrows indicate calcium moving back into storage. This step shows that calcium ions are actively reabsorbed into the sarcoplasmic reticulum, a process that requires ATP. As calcium levels in the muscle cytoplasm decrease, the relaxation cycle begins.

Step 3: Reduced activation of thin filaments - A thin filament, or actin filament, is shown with regulatory proteins and reduced calcium in the surrounding area. As calcium detaches from troponin, associated proteins including tropomyosin shift to cover the myosin-binding sites on actin. This means the thin filament is no longer prepared for contraction.

Step 4: Cessation of thick and thin filament interaction - A myosin head is shown separated from the actin filament. The thick and thin filaments are no longer engaged. Cross-bridge formation stops, myosin heads detach from actin, and the sliding filament mechanism ceases.

Step 5: Muscle fiber lengthening - A cylindrical muscle fiber is shown with arrows pointing outward from both ends. Without active cross-bridge cycling, the sarcomeres return toward their resting length, and the muscle fiber elongates.

Step 6: Whole muscle relaxation - At the bottom of the image, the entire muscle is shown in a longer, less compact shape. The muscle relaxes and lengthens, and tension decreases. External forces, such as opposing muscles or gravity, help restore resting length.

Figure 10.2.5: The Sliding Filament Model of Muscle Contraction

This image shows two stacked views of a sarcomere, comparing its structure before contraction in the top panel and during contraction in the bottom panel. The figure highlights how the relative positions of thick (myosin) and thin (actin) filaments change to produce shortening.

The image is organized into two horizontal panels. The top panel shows a relaxed sarcomere, and the bottom panel shows a contracted sarcomere. In both panels, the sarcomere extends from one Z line to the other, with the M line at the center. Thick filaments are located in the middle, and thin filaments extend inward from the Z lines. In the bottom panel, black arrows point inward, indicating contraction.

Top panel: Relaxed sarcomere - In the top panel, the Z lines are located at the left and right ends of the sarcomere. Thin filaments extend inward from each Z line but do not fully overlap in the center. Thick filaments occupy the middle region. The H zone, which is the central region containing only thick filaments, is visible. The I bands, which are the regions containing only thin filaments near the Z lines, are relatively wide. This panel represents the sarcomere in a resting or relaxed state. There is relatively less overlap between actin and myosin, and the sarcomere is not shortened.

Bottom panel: Contracted sarcomere - In the bottom panel, the Z lines are closer together than in the top panel. Thin filaments have moved inward toward the center, increasing the overlap between actin and myosin filaments. The H zone is reduced or nearly absent, and the I bands are shorter than in the relaxed state. The A band remains the same width. This panel represents the sarcomere in a contracted state. Myosin has pulled actin filaments toward the center, increasing overlap and shortening the sarcomere.

Sliding filament mechanism - The image shows that thick filaments remain relatively stationary while thin filaments slide past them. The process is:

1. Myosin heads attach to actin
2. Myosin pulls actin toward the M line
3. Z lines move closer together
4. Sarcomere length decreases
5. Repeated shortening across many sarcomeres produces overall muscle contraction

Figure 10.2.6: The Cross-Bridge Cycle

This image shows the cross-bridge cycle, the repeating sequence of interactions between myosin in the thick filament and actin in the thin filament that produces muscle contraction. The diagram is arranged vertically and labeled in stages from (a) through (e).

The overall organization progresses from top to bottom in sequential steps. Each panel shows the thin filament across the top and the thick filament below it, with a myosin head projecting upward toward actin. Small labeled molecules include calcium ions, ADP, Pi, and ATP. Together, the panels show how calcium and ATP regulate attachment, pulling, release, and resetting of the myosin head.

Step (a): Thin filament activation - the thin filament is shown with actin and calcium present nearby, and the binding sites on actin are exposed. The myosin head is close to actin but not yet attached. This step shows that calcium allows regulatory proteins to expose the myosin-binding sites on actin, preparing the thin filament for cross-bridge formation.

Step (b): Cross-bridge formation - the myosin head attaches to actin, forming a cross-bridge. ADP and Pi remain attached to the myosin head. This indicates that myosin is in an energized state and has bound to actin in preparation for force generation.

Step (c): Power stroke - the myosin head pivots downward, and arrows show movement of the actin filament relative to myosin. ADP and Pi are released. This step represents the power stroke, in which the myosin head pulls the actin filament toward the center of the sarcomere, producing force and shortening.

Step (d): ATP binding and detachment - ATP binds to the myosin head, and the myosin head detaches from actin. This step shows that ATP binding breaks the cross-bridge and allows myosin to release actin. Without ATP, detachment cannot occur.

Step (e): Re-cocking of the myosin head - ATP is hydrolyzed into ADP and Pi, which remain attached to the myosin head. The myosin head returns to a cocked, energized position. This hydrolysis provides the energy needed to prepare myosin for the next cycle of attachment.

Functional integration - The main relationship shown in the figure is that the cross-bridge cycle repeats in a specific sequence:

1. Calcium exposes binding sites on actin
2. Myosin attaches to actin
3. Myosin pulls actin in the power stroke
4. ATP binds, causing detachment
5. ATP is hydrolyzed, resetting the myosin head

Figure 10.2.7: Biochemical Pathways

This image contains three labeled diagrams showing major biochemical pathways that produce ATP in muscle cells.

Panel (a) shows the creatine phosphate system. In resting muscle, ATP and creatine are used to form creatine phosphate and ADP. During muscle activity, the enzyme creatine kinase transfers a phosphate from creatine phosphate back to ADP, producing ATP that can be used for muscle contraction. The arrows show that this pathway can operate in opposite directions depending on whether the muscle is at rest or active.

Panel (b) shows glycolysis. Blood glucose and muscle glycogen both supply glucose, which enters glycolysis. Glycolysis produces ATP and pyruvate. When oxygen is available, pyruvate can enter aerobic respiration. When oxygen is not available, pyruvate is converted to lactic acid, which enters the blood. This panel emphasizes that glycolysis can supply ATP without oxygen, but it produces less ATP than aerobic respiration.

Panel (c) shows cellular respiration in mitochondria. Inputs include blood glucose, pyruvic acid, fatty acids, and oxygen. The outputs shown are ATP, heat, carbon dioxide, and water. This panel emphasizes that aerobic respiration produces a large amount of ATP compared with the other pathways.

Together, the three panels compare rapid ATP regeneration by the creatine phosphate system, short-term ATP production by glycolysis, and larger ATP production by aerobic respiration in mitochondria.

Figure 10.3.1: Types of Muscle Contractions

This image compares three types of muscle contraction using a biceps curl example. Each row shows the same arm muscle during a different kind of contraction, along with a matching movement example using a dumbbell. The purpose of the diagram is to distinguish concentric, eccentric, and isometric contractions by showing whether the muscle shortens, lengthens, or stays the same length while producing force.

In the top row, the labeled example is concentric contraction. The arm bends upward, the muscle becomes shorter and thicker, and the associated movement arrow curves upward during the lifting phase of the curl. This row shows that a concentric contraction occurs when the muscle contracts while shortening to produce movement.

In the middle row, the labeled example is eccentric contraction. The arm lowers the weight, the muscle becomes longer while still active, and the movement arrow curves downward. This row shows that an eccentric contraction occurs when the muscle elongates while controlling movement.

In the bottom row, the labeled example is isometric contraction. The arm position stays fixed while the muscle remains active, and the figure states no movement. This row shows that an isometric contraction occurs when the muscle contracts without changing overall length enough to move the joint.

All of these muscle activities are under the exquisite control of the nervous system. Neural control regulates concentric, eccentric and isometric contractions, muscle fiber recruitment, and muscle tone. A crucial aspect of nervous system control of skeletal muscles is the role of motor units.

Figure 10.3.2: The Ideal Length of a Sarcomere

This image shows the relationship between sarcomere length and muscle tension. The vertical axis is labeled Tension (percent of maximum) and ranges up to 100 percent. The horizontal axis is labeled Percentage sarcomere length. A single line rises from low tension at shorter sarcomere lengths, reaches a maximum plateau at intermediate lengths, and then declines back to zero at longer lengths.

The graph begins near 0 percent tension at a sarcomere length of about 60 percent. Tension rises steeply to about 80 percent near 80 percent sarcomere length, then reaches 100 percent tension around 95 to 110 percent sarcomere length. After that, tension decreases steadily as sarcomere length increases, reaching 0 percent tension again around 170 percent sarcomere length.

Below the graph are three labeled regions with small schematic drawings of filament overlap. The first region is Decreased length, showing excessive filament overlap at short sarcomere length. The second region is Increased length, showing more optimal overlap. The third region is No cross bridges, showing thin and thick filaments too far apart to interact.

Figure 10.3.3: The Phases of a Single Muscle Twitch

This image shows the time course of a single muscle twitch after one stimulus. The vertical axis is labeled Tension, and the horizontal axis is labeled Time (msec), extending from 0 to 100 milliseconds. A red arrow at time zero marks the single stimulus.

The graph divides the twitch into three labeled phases. The first is the latent period, shown at the far left over the first few milliseconds after the stimulus. During this phase, tension remains very low and has not yet risen significantly.

The second phase is the contraction period, shown from shortly after the latent period to about 25 to 30 milliseconds. During this interval, the curve rises steeply from near zero to its maximum tension. The peak occurs at approximately 28 to 30 milliseconds.

The third phase is the relaxation period, beginning after the peak and extending to about 100 milliseconds. During this phase, tension gradually declines back toward baseline. The decrease is more gradual than the earlier rise.

Figure 10.3.4: Two Tension-Versus-Time Graphs

This image compares wave summation and tetanus using two tension-versus-time graphs. In both graphs, the vertical axis is labeled Tension and the horizontal axis is labeled Time.

In graph (a), labeled Wave summation, the tension curve rises and falls in a repeating pattern, with each successive peak becoming higher than the one before it. The curve shows multiple contractions occurring before the muscle fully returns to baseline, so the overall tension builds in a step-like pattern. After the final and highest peak, the curve drops back down toward zero.

In graph (b), labeled Tetanus, the tension rises from zero to a high level and then remains elevated in a broad plateau for a period of time before falling back to baseline. This graph shows sustained contraction with little or no relaxation during the plateau.

Figure 10.3.5: Treppe

This image shows treppe on a graph of tension versus time. The vertical axis is labeled Tension, and the horizontal axis is labeled Time.

The curve shows a series of separate muscle twitches. Each twitch rises and falls back near baseline before the next twitch begins. Across the sequence, the peaks gradually become higher, showing that each successive twitch produces slightly greater tension than the one before it. Overall, the graph demonstrates that treppe is a staircase-like increase in tension during repeated, separate muscle twitches, with full or nearly full relaxation between contractions.

It is believed that treppe results from a higher concentration of Ca⁺⁺ in the sarcoplasm resulting from the steady stream of signals from the motor neuron. It can only be maintained with adequate ATP.

Figure 10.5.1: Marathoners

This image shows several individuals running together in what appears to be a competitive road race. They are moving forward on a paved street, each wearing athletic clothing such as sleeveless tops, shorts, and running shoes. Visible race bibs display numbers including 20, 41, 42, and 43. Some runners wear brightly colored jerseys, and others wear shirts featuring the names of running clubs or event sponsors. In the background, a few bicycles and buildings can be seen, indicating an urban race setting. The runners are positioned close to one another, suggesting they are in the midst of the event rather than at the start or finish line.

Figure 10.5.2: Hypertrophy

This image shows the back view of an individual performing a double‑biceps pose commonly seen in bodybuilding. The person is standing with both arms raised and bent at the elbows, fists clenched to showcase the upper arm muscles. Prominent definition is visible across the shoulders, upper arms, and back. The lighting emphasizes muscular contours, creating highlights across the shoulder blades, upper back, and arms. The background appears outdoors, with a large blurred structure or sign partially visible. The focus of the image is the muscular development displayed through the flexed pose.

Figure 10.5.3: Atrophy

This image shows two simplified side-view anatomical drawings of an upper arm and forearm. Both drawings include the same arm bones, but the muscle size differs to illustrate a comparison between normal muscle and atrophied muscle.

On the left, labeled Normal Muscle, the muscle has a larger, fuller belly and occupies more space along the upper arm. The muscle appears thicker between its attachment points.

On the right, labeled Atrophied Muscle, the muscle is thinner and narrower while keeping a similar general shape and attachment pattern. It occupies less space along the upper arm, illustrating a loss of muscle mass.

Sarco penia can be delayed to some extent by exercise, as training adds structural proteins and causes cellular changes that can offset the effects of atrophy. Increased exercise can produce greater numbers of cellular mitochondria, increase capillary density, and increase the mass and strength of connective tissue. The effects of age-related atrophy are especially pronounced in people who are sedentary, as the loss of muscle cells is displayed as functional impairments such as trouble with locomotion, balance, and posture. This can lead to a decrease in quality of life and medical problems, such as joint problems because the muscles that stabilize bones and joints are weakened. Problems with locomotion and balance can also cause various injuries due to falls.

Figure 10.6.1: Cardiac Muscle Tissue

This image is a microscopic view of muscle tissue. It shows many elongated, parallel muscle fibers running diagonally across the image. The fibers appear closely packed and separated by narrow spaces.

Multiple dark oval nuclei are visible within the fibers. The nuclei appear centrally located rather than pushed to the outer edge. The tissue does not appear arranged as broad bundles like a gross anatomy drawing; instead, it shows the fine cellular pattern seen in a histology image.

Figure 10.6.2: Cardiac Muscle

This image shows the structure of cardiac muscle tissue and highlights the specialized connections between cardiac muscle cells. The main image shows several cardiac muscle fibers arranged in branching bundles. Each fiber contains a central nucleus. A small capillary is shown near the muscle fibers, emphasizing the tissue’s blood supply. The fibers branch and join with neighboring fibers rather than forming long parallel cylinders.

The figure labels intercalated discs where neighboring cardiac muscle cells meet. A magnified inset on the right enlarges one of these junctions. In that inset, the intercalated disc appears as a folded boundary between adjacent cells. The inset labels desmosomes and gap junctions within the intercalated disc.

The desmosomes are shown as anchoring connections that help hold adjacent cells together. The gap junctions are shown as communication channels between cells. Together, these structures allow cardiac muscle cells to remain connected mechanically and to coordinate activity across the tissue.

Figure 10.7.1: Smooth Muscle Tissue

This image has two labeled parts that show smooth muscle tissue in both diagram form and microscopic view.

In panel (a), the figure shows two illustrations of smooth muscle fibers with autonomic neurons. On the left, the smooth muscle cells are arranged in parallel bundles. The cells are elongated and spindle-shaped, tapering at both ends, and each cell contains a single central nucleus. Autonomic nerve fibers run between the muscle cells. On the right, a second illustration shows smooth muscle cells arranged in a less regular cluster. These cells are also spindle-shaped with central nuclei, and autonomic neurons branch among them. The two illustrations emphasize different arrangements of smooth muscle tissue and its autonomic nerve supply.

In panel (b), a micrograph shows smooth muscle tissue under the microscope. The tissue contains elongated cells with centrally located nuclei and lacks visible striations. The cells appear closely packed and aligned in the same general direction.

Figure 10.7.2: Muscle Contraction

This image compares a relaxed smooth muscle cell on the left with a contracted smooth muscle cell on the right. The figure shows how dense bodies and intermediate filaments contribute to smooth muscle contraction.

Figure 10.7.3: Motor Units

This image illustrates how autonomic neurons communicate with smooth muscle cells through multiple varicosities distributed along an axon rather than through a single specialized neuromuscular junction.

On the left side of the figure, an enlarged portion of an autonomic neuron is shown. The axon contains a series of rounded swellings called varicosities. Each varicosity contains numerous vesicles filled with neurotransmitters, depicted as small circular structures within the swelling. A gray arrow indicates that this enlarged structure corresponds to the neuron shown on the right side of the figure.

On the right side, elongated smooth muscle cells are arranged in parallel bundles. Running between the smooth muscle cells is an autonomic neuron, shown as a branching fiber. Along the length of the neuron are multiple varicosities, each appearing as a bulb-like enlargement of the axon. The varicosities are positioned close to the surrounding smooth muscle cells rather than being concentrated at a single contact point.

The figure demonstrates that autonomic neurons can release neurotransmitters from many varicosities distributed along the axon. This arrangement allows signals from a single neuron to influence multiple neighboring smooth muscle cells over a broad area, rather than at a single specialized synapse.