Module 3
Skeletal and Muscular Systems
a. Bone: Mineralized Connective Tissue
Bone is a connective tissue, so it is a blend of living cells and a matrix that
contains fibers. Bones are covered by a sturdy two-layer membrane called the periosteum
(meaning “around the bone”). The membrane’s outer layer is dense connective tissue, and
the inner layer contains bone cells called osteoblasts (“bone formers”). As bone develops,
the osteoblasts secrete collagen and some elastin, as well as carbohydrates and other
proteins. With time, this matrix around osteoblasts hardens when salts of the mineral
calcium are deposited in it. Each osteoblast is trapped in a space, or lacuna, in the matrix
(lacuna means hole). At this point their bone-forming function ends and they are called
osteocytes (osteo 5 bone; cyte 5 cell).
Bone tissue, composed of minerals and collagen, forms the structural framework
of the human skeleton, providing support, protection, and mobility to the body. The
unique composition and organization of bone tissue contribute to its remarkable strength,
resilience, and adaptability in withstanding mechanical stresses associated with various
activities.
Minerals, primarily calcium and phosphate, play a critical role in imparting
hardness and rigidity to bone tissue, giving it its characteristic density and strength. These
mineral components form hydroxyapatite crystals, which are deposited within the
collagen matrix of bone and contribute to its mineralized structure. The mineral phase of
bone provides compressive strength and resistance to deformation, allowing bones to bear
weight and withstand external forces without collapsing or fracturing.
However, it is the collagen component of bone tissue that confers its remarkable
tensile strength and flexibility, enabling bones to resist bending, stretching, and shearing
forces. Collagen, a fibrous protein arranged in a helical structure, forms a network of
fibers within the bone matrix, providing structural integrity and resilience to mechanical
loading. The interplay between collagen fibers and mineralized matrix gives bone tissue
its unique combination of strength and flexibility, allowing it to bend without breaking
and absorb energy during impact.
The hierarchical organization of collagen fibers within bone tissue further
enhances its mechanical properties, with fibers arranged in parallel arrays at multiple
length scales. At the nanoscale, collagen molecules assemble into fibrils, which in turn
aggregate to form fibers, bundles, and lamellae at higher levels of organization. This
hierarchical structure allows bone tissue to distribute and dissipate mechanical forces
efficiently, minimizing the risk of fracture or damage.
Moreover, the dynamic nature of bone tissue enables it to respond and adapt to
changes in mechanical loading through a process known as remodeling. Osteoblasts,
specialized bone-forming cells, deposit new bone tissue in response to mechanical stress,
reinforcing areas subjected to increased strain. Conversely, osteoclasts, bone-resorbing
cells, remove old or damaged bone tissue in regions experiencing reduced stress,
maintaining optimal bone strength and architecture over time.
In addition to its mechanical function, bone tissue serves as a reservoir for
essential minerals, such as calcium and phosphorus, which are mobilized to maintain
systemic mineral homeostasis. Furthermore, bone tissue houses bone marrow, a vital site
for hematopoiesis (blood cell production) and the storage of fat and immune cells.
In summary, the interplay between minerals and collagen in bone tissue endows it
with both hardness and strength, allowing it to withstand the mechanical stresses
associated with everyday activities. The unique structural and mechanical properties of
bone tissue highlight its remarkable adaptation to the diverse demands of the
musculoskeletal system and underscore its essential role in supporting and protecting the
body.
Bones contain two kinds of tissue, compact bone and spongy bone. Shows where
these tissues are in a long bone such as the femur (thighbone). As its name suggests,
compact bone is a dense tissue that looks solid and smooth. In a long bone, it forms the
bone’s shaft and the outer part of its two ends. A cavity inside the shaft contains bone
marrow.
Compact bone tissue forms in thin, circular layers around small central canals.
Each set of layers is called an osteon (os-tee-ahn; sometimes called a Haversian system).
The canals connect with each other and serve as channels for blood vessels and nerves
that transport substances to and from osteocytes. Osteocytes also extend slender cell
processes into narrow channels called canaliculi that run between lacunae. These “little
canals” allow nutrients to move through the hard matrix from osteocyte to osteocyte.
Wastes can be removed the same way.
The bone tissue inside a long bone’s shaft and at its ends looks like a sponge.
Tiny, flattened struts are fused together to make up this spongy bone tissue, which looks
lacy and delicate but actually is quite firm and strong.
An early embryo has a rubbery skeleton that consists of cartilage and membranes.
Yet, after only about 2 months of life in the womb, this flexible framework is
transformed into a bony skeleton. Once again, we can look at the development of a long
bone as an example. As you can see at the top, a cartilage “model” provides the pattern
for each long bone. Once the outer membrane is in place on the model, the bone forming
osteoblasts become active and a bony “collar” forms around the cartilage shaft. Then the
cartilage inside the shaft calcifies, and blood vessels, nerves, and elements including
osteoblasts begin to infiltrate the forming bone. Soon, the marrow cavity forms and
osteoblasts produce the matrix that will become mineralized with calcium.
Each end of a long bone is called an epiphysis (e-pif-uhsis). As long as a person is
growing, each epiphysis is separated from the bone shaft by an epiphyseal plate of
cartilage. Human growth hormone (GH) prevents the plates from calcifying, so the bone
can lengthen. When growth stops, usually when people reach their late teens or early
twenties, bone replaces the cartilage plates.
Calcium is constantly entering and leaving our bones. Calcium is deposited when
osteoblasts form bone, and it is withdrawn when “bone breaker” cells called osteoclasts
break down the matrix of bone tissue. This ongoing calcium recycling is called bone
remodeling, and it has several important functions.
Regularly breaking down “old” bone and replacing it with fresh tissue helps keep
bone resilient, so it is less likely to become brittle and break. When a bone is subjected to
mechanical stress, such as load-bearing exercise, the remodeling process is adjusted so
that more bone is deposited than removed. That is why the bones of regular exercisers are
denser and stronger than the bones of couch potatoes. On the other hand, when the body
must heal a broken bone, osteoclasts release more calcium than usual from bone matrix.
Osteoblasts then use the calcium to repair the injured bone tissue.
A child’s body requires lots of calcium to meet the combined demands of bone
growth and other needs for the calcium stored in bones. Along with dietary calcium,
remodeling helps meet the demand. For example, the diameter of a growing child’s
thighbones increases as osteoblasts form bone at the surface of each shaft. At the same
time, however, osteoclasts break down a small amount of bone tissue inside the shaft.
Thus the child’s thighbones become thicker and stronger to support the increasing body
weight, but they don’t get too heavy.
Bone remodeling also plays a key role in maintaining homeostasis of the blood
level of calcium. Neither our nervous system nor our muscles can function properly
unless the blood level of calcium stays within a narrow range. When the level falls below
this range, a hormone called PTH stimulates osteoclasts to break down bone and release
calcium to the blood. If the level rises too high, another hormone, calcitonin, stimulates
osteoblasts to deposit calcium in bone tissue. Notice that this control mechanism is an
example of negative feedback. You will read more about it, when we take a closer look at
hormones.
b. The Skeletal System: The Body’s Bony Framework
An adult’s skeleton contains 206 bones. These bones vary in size and shape, from
bones in the ear that are the size of a watch battery to massive thighbones. Some, like the
thighbone, are long and slender. Others, like the ankle bones, are quite short. Still others,
such as the sternum (breastbone), are flat, and still others, such as spinal vertebrae, are
“irregular.” All bones contain bone tissue, however, and other connective tissue lines
their surfaces and internal cavities. At joints there is cartilage where one bone meets or
“articulates” with another. Other tissues associated with bones include nervous tissue and
epithelium, which occurs in the walls of blood vessels that carry substances to and from
bones. Clearly, bones are complex organs!
Some bones, such as long bones, have cavities that contain bone marrow, a type
of connective tissue. In children most marrow-containing bones have red bone marrow, in
which blood cells form. With time, however, much of this red marrow is replaced by
fatrich yellow marrow, where no blood cells form. For this reason, most of an adult’s
blood cells form in red bone marrow in irregular bones, such as the hip bone, and in flat
bones, such as the sternum. If you lose a lot of blood, yellow marrow in your long bones
can convert to red marrow, which makes red blood cells.
The skeletal system consists of bones along with joints, cartilages, and straplike
ligaments that hold our bones together. The bones are organized into an axial skeleton
and an appendicular skeleton. The bones of the axial skeleton form the body’s vertical,
head-to-toe axis. The appendicular (“hanging”) skeleton includes bones of the limbs,
shoulders, and hips. Ligaments connect bones at joints. Ligaments are composed of
elastic connective tissue, so they are stretchy and resilient like thick rubber bands.
Tendons are cords or straps that attach muscles to bones or to other muscles. They are
built of connective tissue packed with collagen fibers, which make tendons strong.
Bones contribute to homeostasis in many ways. For instance, bones that support
and anchor skeletal muscles help maintain or change the positions of our body parts.
Some form hard compartments that enclose and protect other organs; for example, the
skull encloses and protects the brain, and the rib cage protects the lungs. As noted in,
bones also serve as a “pantry” where the body can store calcium. Because the calcium in
bone is in the form of the compound calcium phosphate, bone also is a storage depot for
phosphorus.
c. The Axial Skeleton
Your skull consists of more than two dozen bones that are divided into several
groups. By tradition many of them have names derived from Latin, but their roles are
easy to grasp. For example, the cranium, or brain case, includes eight bones that together
surround and protect your brain. Frontal bone makes up the forehead and upper ridges of
the eye sockets. It contains sinuses, which are air spaces lined with mucous membrane.
Sinuses make the skull lighter, which translates into less weight for the spine and neck
muscles to support. But channels connect them to the nasal passages, and their ability to
produce mucus can mean misery for anyone who has a cold or pollen allergies. A
bacterial infection in the nasal passages can spread to the sinuses, causing sinusitis.
Temporal bones form the lower sides of the cranium and surround the ear canals,
which are tunnels that lead to the middle and inner ear. Inside the middle ear are tiny
bones that function in hearing. On the sides of your head, in front of each temporal bone,
a sphenoid bone extends inward to form part of the inner eye socket. The ethmoid bone
also forms part of the inner socket and helps support the nose. Two parietal bones above
and behind the temporal bones form much of the skull as they sweep upward and meet at
the top of the head. An occipital bone forms the back and base of the skull. It also
encloses an opening, the foramen magnum (“large hole”). Here, the spinal cord emerges
from the base of the brain and enters the spinal column. Other openings are channels for
nerves and blood vessels. For instance, the jugular veins, which carry blood leaving the
brain, pass through openings between the occipital bone and each temporal bone.
Facial bones, many of which you can easily feel with your fingers. The largest is
your lower jaw, or mandible. The upper jaw consists of two maxillary bones, each called
a maxilla. Two zygomatic bones form the middle of the hard bumps we call
“cheekbones” and the outer parts of the eye sockets. A small, flattened lacrimal bone fills
out the inner eye socket. Tear ducts pass between this bone and the maxillary bones and
drain into the nasal cavity—one reason why your nose runs when you cry. Tooth sockets
in the upper and lower jaws also contain the teeth.
Palatine bones make up part of the floor and side wall of the nasal cavity.
(Extensions of these bones, together with the maxillary bones, form the back of the hard
palate, the “roof” of your mouth.) A vomer bone forms part of the nasal septum, a thin
“wall” that divides the nasal cavity into two.
The flexible, curved vertebral column—your backbone or spine—runs from the
base of the skull to the hip bones (pelvic girdle). This arrangement transmits the weight
of a person’s torso to the lower limbs. As a result, people who gain too much weight may
develop problems with their knees and ankles because those joints are not designed to
bear such a heavy load. The vertebrae are stacked and have bony projections that form a
protected channel for the delicate spinal cord. As sketched, humans have seven cervical
vertebrae in the neck, twelve thoracic vertebrae in the chest area, and five lumbar
vertebrae in the lower back. During the course of human evolution, five other vertebrae
have become fused to form the sacrum, and several more have become fused to form the
coccyx, or “tailbone.” Counting these, there are thirty-three vertebrae in all.
Roughly a quarter of your spine’s length consists of intervertebral disks—
compressible pads of fibrocartilage sandwiched between vertebrae. The disks serve as
shock absorbers and flex points. They are thickest between cervical vertebrae and
between lumbar vertebrae. Severe or rapid shocks, as well as changes due to aging, can
cause a disk to herniate or “slip.” If the slipped disk ruptures, its jellylike core may
squeeze out, making matters worse. And if the changes compress neighboring nerves or
the spinal cord, the result can be excruciating pain and the loss of mobility that often
comes with pain. Depending on the situation, treatment can range from bed rest and use
of painkilling drugs to surgery.
In addition to protecting the spinal cord, absorbing shocks, and providing
flexibility, the vertebral column also serves as an attachment point for twelve pairs of
ribs, which in turn serve as a scaffolding for the thoracic cavity, the body cavity of the
upper torso. The upper ribs also attach to the paddle-shaped sternum. As you will read in
later, this rib cage helps protect the lungs, heart, and other internal organs and is vitally
important in breathing.
d. The Appendicular Skeleton
Append means “to hang,” and the appendicular skeleton includes the bones of
“hanging” body parts such as your arms, hands, legs, and feet. It also includes a pectoral
girdle at each shoulder and the pelvic girdle at the hips.
Each pectoral girdle has a large, flat shoulder blade—a scapula—and a long,
slender collarbone, or clavicle, that connects to the breastbone (sternum). The rounded
shoulder end of the humerus, the long bone of the upper arm, fits into an open socket in
the scapula. Your arms can move in a great many ways; they can swing in wide circles
and back and forth, lift objects, or tug on a rope. Such freedom of movement is possible
because muscles only loosely attach the pectoral girdles and upper limbs to the rest of the
body. Although the arrangement is sturdy enough under normal conditions, it is
vulnerable to strong blows. Fall on an outstretched arm and you might fracture your
clavicle or dislocate your shoulder. In all but the elderly the collarbone is the bone most
frequently broken.
Each of your upper limbs includes thirty separate bones. The humerus connects
with two bones of the forearm—the radius (on the thumb side) and the ulna (on the
“pinky finger” side). The upper end of the ulna joins the lower end of the humerus to
form the elbow joint. The bony bump sometimes (mistakenly) called the “wrist bone” is
the lower end of the ulna.
The radius and ulna join the hand at the wrist joint, where they meet eight small,
curved carpal bones. Ligaments attach these bones to the long bones. Blood vessels,
nerves, and tendons pass in sheaths over the wrist; when a blow, constant pressure, or
repetitive movement (such as typing) damages these tendons, the result can be a painful
disorder called carpal tunnel syndrom. The bones of the hand, the five metacarpals, end at
the knuckles. Phalanges are the bones of the fingers.
For most of us, our shoulders and arms are much more flexible than our hips and
legs. Why? Although there are similarities in the basic “design” of both girdles, this
lower part of the appendicular skeleton is adapted to bear the body’s entire weight when
we are standing. The pelvic girdle is much more massive than the combined pectoral
girdles, and it is attached to the axial skeleton by extremely strong ligaments. It forms an
open basin: A pair of coxal bones attach to the lower spine (sacrum) in back, then curve
forward and meet at the pubic arch. (“Hip bones” are actually the upper iliac regions of
the coxal bones.) This combined structure is the pelvis. In females the pelvis is broader
than in males, and it shows other structural differences that are evolutionary adaptations
for childbearing. A forensic scientist or paleontologist examining skeletal remains can
easily establish the sex of the deceased if a pelvis is present.
The legs contain the body’s largest bones. In terms of length, the thighbone, or
femur, ranks number one. It is also extremely strong. When you run or jump, your femurs
routinely withstand stresses of several tons per square inch (aided by contracting leg
muscles). The femur’s ball-like upper end fits snugly into a deep socket in the coxal (hip)
bone. The other end connects with one of the bones of the lower leg, the thick, load-
bearing tibia on the inner (big toe) side. A slender fibula parallels the tibia on the outer
(little toe) side. The tibia is your shinbone. A triangular kneecap, the patella, helps protect
the knee joint. As Susanna’s story in the introduction noted, however, athletes often
damage their knees.
The ankle and foot bones correspond closely to those of the wrist and hand. Tarsal
bones make up the ankle and heel, and the foot contains five long bones, the metatarsals.
The largest metatarsal, leading to the big toe, is thicker and stronger than the others to
support a great deal of body weight. Like fingers, the toes contain phalanges.
e. Joints: Connections between Bones
There are three main types of joints in the skeletal system. In the most common
type of joint, called a synovial joint, adjoining bones are separated by a cavity. The
articulating ends of the bones are covered with a cushioning layer of cartilage, and they
are stabilized by ligaments. A capsule of dense connective tissue surrounds the bones of a
synovial joint. The synovial membrane that lines the inner surface of the capsule contains
cells that secrete a lubricating synovial fluid into the joint cavity.
Synovial joints are built to allow movement. In hingelike synovial joints such as
the knee and elbow, the motion is limited to simple flexing and extending (straightening).
The ball-and-socket joints at the hips are known as freely movable joints because they are
capable of a wider range of movements: They can rotate and move in different planes—
for instance, up-down or side-to-side.
In a cartilaginous joint, cartilage fills the space between bones, so only slight
movement is possible. The intervertebral disks between vertebrae are examples. Similar
joints occur between the breastbone and some of the ribs. There is no cavity in a fibrous
joint, and fibrous connective tissue unites the bones. An adult’s fibrous joints generally
don’t allow movement.
Examples are the fibrous joints that hold your teeth in their sockets. In a fetus,
fibrous joints loosely connect the flat skull bones. During childbirth, these loose
connections allow the bones to slide over each other, preventing skull fractures. A
newborn baby’s skull still has fibrous joints and soft areas called fontanels. With time the
joints harden into sutures. Much later in life the skull bones may fuse completely.
f. Disorders of the Skeleton
As we age, bone tissue may break down faster than it is renewed. This steady
deterioration is called osteoporosis. When it occurs, the backbone, pelvis (hip bones), and
other bones lose mass. Osteoporosis is most common in women past menopause,
although men can be affected, too. Deficiencies of calcium and sex hormones, smoking,
and a sedentary lifestyle all may contribute to osteoporosis. Exercise (to stimulate bone
deposits) and taking in plenty of calcium can help minimize bone loss. Medications can
slow or even help reverse the bone loss.
Sports injuries, obesity, and simply getting older are among the causes of
osteoarthritis. In this disorder, years of mechanical stress or disease wear away the
cartilage covering the bone ends of freely movable joints. Often, the arthritic joint is
painfully inflamed, and surgeons now routinely replace seriously arthritic hips, knees,
and shoulders.
Rheumatoid arthritis (RA) is a complex autoimmune disorder characterized by
chronic inflammation of the joints, leading to pain, swelling, stiffness, and eventual joint
damage. While the exact cause of RA remains unclear, it is believed to result from a
combination of genetic, environmental, and immunological factors that contribute to
immune system dysfunction and aberrant inflammatory responses within the joints.
In individuals with rheumatoid arthritis, the immune system malfunctions and
mistakenly identifies the synovial membrane, the tissue lining the joints, as foreign or
abnormal. This triggers an immune response characterized by the activation of
inflammatory cells, such as T lymphocytes, B lymphocytes, and macrophages, and the
release of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α),
interleukin-1 (IL-1), and interleukin-6 (IL-6).
The sustained activation of the immune system and chronic inflammation within
the synovial membrane lead to the progressive destruction of cartilage, bone, and other
joint structures. This inflammatory cascade disrupts the delicate balance between
cartilage synthesis and degradation, resulting in cartilage breakdown and erosion.
Moreover, the release of enzymes and proteases by inflammatory cells further contributes
to joint damage by degrading extracellular matrix components, such as collagen and
proteoglycans.
In addition to its effects on joint tissues, rheumatoid arthritis can also cause
systemic manifestations and complications affecting various organs and systems
throughout the body. Extra-articular manifestations of RA may include rheumatoid
nodules, subcutaneous lumps that develop over bony prominences or tendons, as well as
systemic inflammation affecting the lungs, heart, blood vessels, skin, eyes, and other
organs.
The progression and severity of rheumatoid arthritis can vary widely among
individuals, with some experiencing mild symptoms and others facing significant
disability and impairment in daily functioning. Factors such as genetic predisposition,
disease duration, presence of autoantibodies (e.g., rheumatoid factor and anti-citrullinated
protein antibodies), and environmental triggers (e.g., smoking, infections) can influence
the course and outcome of the disease.
Management of rheumatoid arthritis typically involves a multidisciplinary
approach aimed at controlling inflammation, alleviating symptoms, preserving joint
function, and improving overall quality of life. Treatment strategies may include the use
of disease-modifying anti-rheumatic drugs (DMARDs), such as methotrexate,
hydroxychloroquine, and biologic agents targeting specific inflammatory pathways.
Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, physical therapy,
occupational therapy, and lifestyle modifications may also be recommended to manage
pain, reduce inflammation, and improve joint mobility.
In recent years, advances in understanding the pathophysiology of rheumatoid
arthritis have led to the development of targeted therapies that aim to modulate specific
components of the immune system involved in disease pathogenesis. These targeted
biologic therapies, including TNF inhibitors, interleukin-6 receptor antagonists, and Janus
kinase (JAK) inhibitors, have revolutionized the management of RA and significantly
improved outcomes for many patients.
Despite these advances, rheumatoid arthritis remains a chronic and often
debilitating condition that requires ongoing monitoring, treatment optimization, and
patient education to effectively manage symptoms and prevent long-term joint damage
and disability. Continued research into the underlying mechanisms of RA and the
development of novel therapeutic approaches hold promise for further improving
outcomes and quality of life for individuals living with this challenging autoimmune
disorder.
Repetitive movements can cause inflammation when they damage the soft tissue
associated with joints. Tendinitis, the underlying cause of conditions such as “tennis
elbow,” develops when tendons and synovial membranes around joints such as the elbow
and shoulders become inflamed.
Today one of the most common repetitive motion injuries is carpal tunnel
syndrome. The “carpal tunnel” is a slight hollow between a wrist ligament and the
underside of the wrist’s eight carpal bones. Squeezed into this tunnel are several tendons
and a nerve that services parts of the hand. Chronic overuse, such as long hours typing at
a computer keyboard, can inflame the tendons. When the swollen tendons press on the
nerve, the result can be pain, numbness, and tingling in fingers. Simply avoiding the
offending motion can help relieve carpal tunnel syndrome. In more serious cases
injections of an antiinflammatory drug are helpful. Sometimes, however, the wrist
ligament must be surgically cut to relieve the pressure.
Synovial joints such as our knees, hips, and shoulders get a lot of use, so it’s not
surprising that they are vulnerable to mechanical stresses. Stretch or twist a joint
suddenly and too far, and you strain it. Do something that makes a small tear in its
ligaments or tendons and you will have a sprain. In fact, a sprained ankle is the most
common joint injury. Sprains hurt mainly because of swelling and bleeding from broken
small blood vessels. Applying cold (such as an ice pack, 30 minutes on, then 30 minutes
off) for the first 24 hours will minimize these effects; after that, doctors usually advise
applying heat, such as a heating pad. The warmth speeds healing by increasing blood
circulation to the injured tissue.
A blow can dislocate a joint—that is, the two bones will no longer be in contact.
During collision sports such as football, a blow to a knee often tears a ligament. If the
torn part is not reattached within ten days, phagocytic cells in the knee joint’s synovial
fluid will attack and destroy the damaged tissue.
Most bone breaks can be classed as either a simple or closed fracture, a complete
fracture, or a compound fracture. As you can probably tell from the drawings, a simple
fracture is the least serious injury because the bone ends don’t do much damage to the
surrounding soft tissue. A complete fracture, in which the bone separates into two pieces
and soft tissue is damaged, is more serious. Worse is a compound fracture, in part
because broken ends or shards of bone puncture the skin, creating an open wound and the
chance of infection. A surgeon may have difficulty reattaching all the pieces of a bone
that has been shattered in this way.
When a bone breaks into pieces, the pieces must quickly be reset into their normal
alignment. Otherwise it’s unlikely that the bone will heal properly. Its functioning may be
impaired for the rest of a person’s life. In addition to the pins and casts that may be used
to hold healing bones in place, the injured area may be stimulated with electricity, which
speeds healing.
Joint and bone injuries, whether resulting from trauma, overuse, or degenerative
conditions, indeed tend to heal more rapidly in younger individuals compared to older
adults. This difference in healing ability is attributed to various factors related to age-
related changes in tissue structure, cellular function, and overall health status.
During youth and adolescence, bones and joints are in a dynamic state of growth
and development, characterized by high metabolic activity, robust blood supply, and
efficient tissue repair mechanisms. In younger individuals, bone tissue is more porous
and vascular, allowing for rapid exchange of nutrients, oxygen, and signaling molecules
essential for the healing process. Moreover, younger individuals typically have higher
levels of growth factors and hormones, such as growth hormone and insulin-like growth
factor 1 (IGF-1), which promote cell proliferation, differentiation, and tissue
regeneration.
In contrast, aging is associated with gradual changes in bone and joint structure
and function, collectively referred to as musculoskeletal aging. These changes include
decreased bone density and strength, alterations in cartilage composition and elasticity,
and diminished capacity for tissue repair and regeneration. As individuals age, bone
remodeling becomes less efficient, leading to a gradual loss of bone mass and increased
susceptibility to fractures and osteoporosis. Similarly, the cartilage in joints undergoes
degenerative changes, such as thinning, fibrillation, and loss of proteoglycans,
contributing to joint stiffness, pain, and dysfunction.
Moreover, lifestyle factors and habits, such as smoking cigarettes, can exacerbate
age-related declines in musculoskeletal health and impair the body's ability to repair and
regenerate damaged tissues. Smoking is known to have deleterious effects on bone
metabolism, including decreased bone mineral density, impaired bone formation, and
delayed fracture healing. The toxic components of cigarette smoke, such as nicotine and
carbon monoxide, disrupt osteoblast function, inhibit collagen synthesis, and promote
osteoclast activity, leading to accelerated bone loss and compromised bone quality.
In addition to smoking, other modifiable risk factors, such as poor nutrition,
sedentary lifestyle, obesity, and chronic diseases (e.g., diabetes, rheumatoid arthritis), can
also negatively impact musculoskeletal health and impair healing processes. Conversely,
adopting healthy lifestyle habits, such as regular exercise, balanced nutrition, smoking
cessation, and adequate sleep, can promote optimal bone and joint health and enhance the
body's capacity for tissue repair and regeneration.
Furthermore, advances in medical technology and rehabilitation strategies have
enabled healthcare providers to optimize the management of joint and bone injuries in
individuals of all ages. Treatments such as physical therapy, orthopedic surgery,
regenerative medicine interventions (e.g., stem cell therapy, platelet-rich plasma), and
pharmacological agents (e.g., bone-forming medications, analgesics) can help facilitate
healing, reduce pain, and restore function in individuals with musculoskeletal injuries or
conditions.
In conclusion, while joint and bone injuries may heal faster in younger individuals
due to their enhanced regenerative capacity and metabolic activity, age-related changes
and lifestyle factors can impair the body's ability to repair itself. By understanding the
mechanisms underlying musculoskeletal aging and implementing strategies to mitigate
modifiable risk factors, individuals can optimize their musculoskeletal health and
promote more effective healing of joint and bone injuries throughout the lifespan.
Some skeletal disorders are inherited, and a few cause lifelong difficulties. An
example is osteogenesis imperfecta or OI. In this incurable disease, the collagen in bone
tissue is defective, so the bones are extremely brittle and break easily. Children with OI
must have surgeries to set the fractures and often have stunted growth.
Bones (and bone marrow) can become infected when a bacterial infection
elsewhere spreads (via the bloodstream) or when the microbe enters an open wound.
Antibiotics usually can cure the problem, although severe cases may require surgery to
clean out the affected bone tissue.
The bone cancer called osteosarcoma strikes people young and old. It often
develops in a long bone in a limb, or in a joint such as the hip or knee. The most common
treatment of a primary bone cancer is amputation of the limb involved. Like many other
types of cancer, bone cancer often is curable if caught early. Unfortunately, many bone
cancer cases involve cancer that has spread from another site in the body. In the series of
bone scans shown below, red “hot spots” show the progression (left to right) of a
patient’s bone cancer.
g. The Body’s Three Kinds of Muscle
Introduced the three basic kinds of muscle tissue—skeletal muscle, smooth
muscle, and cardiac muscle. Smooth and cardiac muscle occur with other tissues that
form organs such as the bladder and the heart. Skeletal muscle makes up the muscular
system, which interacts with the skeleton to move body parts. Together these three types
of muscle tissue make up about 50 percent of the body. In all of them, cells specialized to
contract bring about some type of movement.
Most of the body’s muscle tissue is skeletal muscle. Its long, thin cells are often
called muscle “fibers. And unlike other body cells, skeletal muscle fibers have more than
one nucleus. As you may remember from, the internal structure of muscle fibers gives
them a striated, or striped, appearance, and bundles of them form skeletal muscles.
Smooth muscle, a type of involuntary muscle tissue, plays a critical role in the
function of hollow organs and tubular structures throughout the body. Unlike skeletal
muscle, which is under conscious control and responsible for voluntary movements,
smooth muscle functions autonomously, regulating the contraction and relaxation of
organs and vessels to facilitate essential physiological processes such as digestion,
circulation, and urinary excretion.
Smooth muscle is characterized by its unique morphology and arrangement within
the body. The cells of smooth muscle, known as myocytes or fibers, are spindle-shaped
and smaller in size compared to skeletal muscle cells. Unlike skeletal muscle fibers,
which exhibit a striated appearance due to the organized arrangement of contractile
proteins (actin and myosin filaments), smooth muscle fibers lack this striated pattern,
giving them a smooth and uniform appearance under the microscope. This absence of
striations is the basis for the name "smooth" muscle tissue.
Another distinguishing feature of smooth muscle is its organization into
interconnected networks or sheets within the walls of hollow organs and tubes. These
sheets of smooth muscle cells are arranged in layers, allowing for coordinated
contractions and relaxation of the organ or vessel. Gap junctions and adherens junctions
facilitate communication and mechanical coupling between adjacent smooth muscle cells,
enabling synchronous contraction and coordinated function.
Smooth muscle is found in a wide range of anatomical structures throughout the
body, including the walls of blood vessels (arteries, veins, and capillaries), airways
(bronchioles), gastrointestinal tract (esophagus, stomach, intestines), urinary system
(bladder, ureters), reproductive system (uterus, fallopian tubes), and other hollow organs
(gallbladder, uterus). In each of these locations, smooth muscle performs specialized
functions tailored to the specific requirements of the organ or tissue.
The contraction and relaxation of smooth muscle are regulated by a variety of
factors, including neural, hormonal, and local chemical signals. Autonomic nerve fibers
of the sympathetic and parasympathetic nervous systems innervate smooth muscle tissue,
modulating its activity in response to physiological demands. Hormonal factors such as
adrenaline (epinephrine), acetylcholine, and various vasoactive peptides also influence
smooth muscle function by binding to specific receptors on the surface of smooth muscle
cells.
Moreover, the contractile activity of smooth muscle is finely tuned by
intracellular signaling pathways involving calcium ions (Ca2+), cyclic nucleotides
(cAMP and cGMP), and protein kinases. Calcium ions play a central role in triggering
smooth muscle contraction by binding to calmodulin and activating myosin light chain
kinase, which phosphorylates myosin and initiates the cross-bridge cycling required for
muscle contraction.
In summary, smooth muscle represents a versatile and adaptable type of muscle
tissue that plays a vital role in regulating the function of hollow organs and tubular
structures throughout the body. Its unique morphology, organization, and regulatory
mechanisms enable smooth muscle to support essential physiological processes and
maintain homeostasis in diverse anatomical contexts. Continued research into the
molecular mechanisms underlying smooth muscle function holds promise for advancing
our understanding of normal physiology and developing new therapeutic approaches for
diseases and disorders involving smooth muscle dysfunction.
Cardiac muscle is found only in the heart. It looks striated, like skeletal muscle.
Unlike skeletal and smooth muscle, however, cardiac muscle can contract without
stimulation by signals from the nervous system. Special junctions between its cells allow
the contraction signals to pass between them so fast that for all intents and purposes the
cells contract as a single unit.
We do not have conscious control over contractions of cardiac muscle and smooth
muscle, so they are said to be “involuntary” muscles. We can control many of our
skeletal muscles, so they are “voluntary” muscles. Major skeletal muscles in the body.
Some are close to the surface, others deep in the body wall. Some, such as facial muscles,
attach to the skin. The trunk has muscles of the thorax (chest), spine, abdominal wall, and
pelvic cavity. And of course, other muscle groups attach to limb bones.
When we speak of the body’s muscular system, we’re talking about skeletal
muscle—the focus of the rest. Those movements range from delicate adjustments that
help you keep your balance to the cool moves you might execute on a dance floor. Our
skeletal muscles also help stabilize joints and generate body heat.
h. The Structure and Function of Skeletal Muscles
A skeletal muscle contains bundles of muscle fibers. Each fiber contains
threadlike myofibrils (myorefers to skeletal muscle). These structures contain the units
that contract a muscle fiber. There may be hundreds, even thousands, of fibers in a
muscle, all bundled together by connective tissue that extends past them to form tendons.
You may remember from that a tendon is a strap of dense connective tissue that attaches
a muscle to bone or to another muscle. Tendons make joints more stable by helping keep
the adjoining bones properly aligned. Tendons often rub against bones, but they slide
inside fluid-filled sacs that help reduce the friction. Each sac is called a bursa (plural:
bursae). In some cases a bursa is elongated into a tendon sheath that folds around a
tendon. Your knees, wrists, and finger joints all have tendon sheaths.
You have more than 600 skeletal muscles, and each one helps produce some kind
of body movement. In general, one end of a muscle, called the origin, is attached to a
bone that stays relatively motionless during a movement. The other end of the muscle,
called the insertion, is attached to the bone that moves the most. In effect, the skeleton
and the muscles attached to it are like a system of levers in which bones (rigid rods)
move near joints (fixed points). When a skeletal muscle contracts, it pulls on the bones it
attaches to. Because muscles attach very close to most joints, a muscle only has to
contract a short distance to produce a major movement.
Many skeletal muscles are arranged as pairs or groups. Some work in opposition
(that is, antagonistically) so that the action of one opposes or reverses the action of the
other. Antagonistic muscle pair, the biceps and triceps of the arm. Try extending your
right arm in front of you, then place your left hand over the biceps in the upper arm and
slowly “bend the elbow.” Can you feel the biceps contract? When the biceps relaxes and
its partner (the triceps) contracts, your arm straightens. This kind of coordinated action
comes partly from reciprocal innervation by nerves from the spinal cord. When one
muscle group is stimulated, no signals are sent to the opposing group, so it does not
contract.
Synergistic muscles play a crucial role in coordinating and optimizing movement
within the human body, working in tandem with primary muscles to enhance efficiency,
stability, and overall performance. These muscles contribute to the complex interplay of
forces and actions required for a wide range of activities, from basic everyday
movements to athletic endeavors and specialized tasks.
In the context of musculoskeletal function, synergistic muscles function in a
supportive capacity, assisting primary muscles in generating force, controlling
movement, and maintaining joint stability. While primary muscles are primarily
responsible for producing the desired movement or action, synergistic muscles work in
concert to provide additional support, fine-tune motor control, and distribute load more
evenly across joints and tissues.
The concept of muscle synergy extends beyond simple stabilization or support
and encompasses a spectrum of interactions and coordination patterns among multiple
muscles acting together to achieve a common goal. Synergistic muscles may act
simultaneously or sequentially, depending on the specific requirements of the movement
or task at hand.
For example, in the case of making a fist while keeping the wrist straight,
synergistic muscles play a critical role in stabilizing the wrist joint to maintain its position
and integrity while the primary muscles in the hand exert force to close the fingers.
Muscles such as the flexor carpi radialis, flexor carpi ulnaris, and extensor digitorum
work synergistically to stabilize the wrist and provide a stable base of support for the
actions of the finger flexors and extensors.
Furthermore, the coordination of synergistic muscle activity is highly adaptable
and responsive to changes in movement patterns, environmental conditions, and task
demands. Through proprioceptive feedback mechanisms and neural control mechanisms,
the nervous system orchestrates the activation and modulation of synergistic muscle
activity to optimize movement efficiency, minimize energy expenditure, and protect
against injury.
In addition to their role in movement coordination and joint stabilization,
synergistic muscles contribute to postural control, balance, and proprioception, helping to
maintain proper alignment and alignment of the body's segments during static and
dynamic activities. By working in synergy with primary muscles and other synergists,
these muscles contribute to the overall quality and effectiveness of movement patterns
and enhance functional performance in various activities of daily living, sports, and
occupational tasks.
Understanding the roles and interactions of synergistic muscles is essential for
rehabilitation, sports performance training, and movement optimization in clinical and
athletic settings. By targeting synergistic muscle groups through specific exercises,
corrective techniques, and neuromuscular training strategies, individuals can improve
movement efficiency, reduce the risk of injury, and enhance overall physical function and
performance.
Your body has two basic types of skeletal muscle. “Slow” or “red” muscle
appears crimson because its fibers are packed with myoglobin, a reddish protein that
binds oxygen for the cell’s use in making ATP. Red muscle also is served by larger
numbers of the tiny blood vessels called capillaries. (Red muscle is the dark meat in
chicken and turkey.) Red muscle contracts fairly slowly, but because its fibers are so well
equipped to make lots of ATP, the contractions can be sustained for a long time. For
example, some muscles of the back and legs—called postural muscles because they aid
body support—must contract for long periods when a person is standing. They have a
high proportion of red muscle fibers. By contrast, the muscles of your hand have fewer
capillaries and relatively more “fast” or “white” muscle fibers, in which there are fewer
mitochondria and less myoglobin. Fast muscle can contract rapidly and powerfully for
short periods, but it can’t sustain contractions for long periods. This is why you get
writer’s cramp if you write longhand for an extended period.
When an athlete trains rigorously, one goal is to increase the relative size and
contractile strength of fast or slow fibers in muscles. The type of sport determines which
type of fiber is targeted. A sprinter will benefit from larger, stronger fast muscle fibers in
the thighs, while a distance swimmer will train to increase the number of mitochondria in
the shoulder muscle fibers.
i. How Muscles Contract
Skeletal muscle contraction is a complex physiological process orchestrated by
the intricate interactions of molecular components within muscle fibers. Understanding
the structural and functional characteristics of skeletal muscle at the cellular level
provides insights into the mechanisms underlying muscle contraction and the generation
of force.
At the microscopic level, skeletal muscle fibers are composed of myofibrils,
which are elongated structures that run parallel to the length of the muscle fiber.
Myofibrils contain repeating units of contractile proteins called sarcomeres, which are the
fundamental functional units responsible for muscle contraction.
Each sarcomere is bounded by Z-lines (also known as Z-discs), which serve as
anchor points for the thin filaments of actin. Within the sarcomere, actin and myosin
filaments overlap to form a highly organized lattice-like structure. Myosin filaments,
composed of the protein myosin, extend from the center of the sarcomere toward the
edges, while actin filaments, composed of the protein actin, span the space between the
Z-lines.
During muscle contraction, the interaction between actin and myosin filaments
within the sarcomere drives the sliding filament theory, which describes the mechanism
by which sarcomeres shorten and muscle fibers contract. This process involves the cyclic
binding and hydrolysis of adenosine triphosphate (ATP) by myosin heads, which
generates the force necessary for muscle contraction.
When a muscle is stimulated to contract, calcium ions (Ca2+) are released from
the sarcoplasmic reticulum, a specialized organelle within muscle cells. These calcium
ions bind to troponin molecules associated with actin filaments, causing a conformational
change that exposes binding sites on the actin filaments.
Subsequently, myosin heads bind to the exposed binding sites on actin, forming
cross-bridges between actin and myosin filaments. ATP is then hydrolyzed by the myosin
heads, providing energy for the myosin heads to undergo a conformational change and
pull the actin filaments toward the center of the sarcomere.
As myosin heads detach from actin, ATP is required to reset the myosin heads to
their original position, allowing for another cycle of cross-bridge formation and
contraction to occur. This repeated cycling of cross-bridge formation and detachment
results in the sliding of actin filaments past myosin filaments, leading to sarcomere
shortening and muscle fiber contraction.
The coordinated contraction of sarcomeres within muscle fibers generates tension
and force, which can be transmitted through connective tissue structures to produce
movement at the level of whole muscles. The magnitude and duration of muscle
contraction are regulated by neural input, hormonal factors, and metabolic processes,
which modulate the release of calcium ions and the activity of contractile proteins within
muscle cells.
In summary, sarcomeres serve as the basic contractile units of skeletal muscle,
where the interaction between actin and myosin filaments drives the process of muscle
contraction. Understanding the molecular mechanisms underlying sarcomere function
provides valuable insights into the physiology of skeletal muscle and the generation of
force during movement and physical activity.
Bundles of fibers in a skeletal muscle run parallel along the muscle’s length.
Looking a bit deeper, each of the myofibrils in a muscle fiber is divided into bands. The
bands appear as an alternating light–dark pattern when they are stained and viewed under
a microscope. Bands in neighboring myofibrils line up closely, which is why a skeletal
muscle fiber looks striped. The dark bands are called Z lines. They mark the ends of each
sarcomere.
The intricate architecture of the sarcomere, the functional unit of skeletal muscle,
comprises a complex arrangement of thick and thin filaments organized in a highly
ordered lattice-like structure. These filaments play essential roles in the process of muscle
contraction, where the sliding of actin and myosin filaments past each other generates
force and shortens the sarcomere.
Within the sarcomere, thick filaments composed primarily of the protein myosin
extend from the center of the sarcomere towards the edges, while thin filaments
composed predominantly of the protein actin span the space between the Z-lines, which
serve as anchor points at either end of the sarcomere. The overlapping arrangement of
thick and thin filaments forms the basis for the sliding filament theory of muscle
contraction, which describes how muscle fibers contract by the interaction of actin and
myosin filaments.
At the molecular level, the thin filaments are composed of globular actin (G-actin)
molecules that polymerize to form long, filamentous strands called F-actin. Each F-actin
strand resembles two twisted strands of beads, with the individual actin molecules
serving as the "beads" or subunits along the filament. These actin filaments extend from
the Z-line towards the center of the sarcomere, where they partially overlap with the thick
myosin filaments.
The binding sites for myosin are located on the actin filaments, specifically on the
globular actin molecules within the F-actin strand. During muscle contraction, myosin
heads on the thick filaments undergo a cyclic interaction with actin molecules, forming
cross-bridges that pull the actin filaments towards the center of the sarcomere.
The Z-lines, composed of proteins such as alpha-actinin, serve as anchoring
points for the thin filaments and help maintain the structural integrity of the sarcomere
during contraction. Other structural proteins, such as tropomyosin and troponin, are
associated with the actin filaments and play critical roles in regulating muscle contraction
by controlling access to the myosin binding sites on actin.
The coordinated cycling of cross-bridge formation and detachment between actin
and myosin filaments, coupled with the release and reuptake of calcium ions from the
sarcoplasmic reticulum, drives the process of muscle contraction and relaxation. This
dynamic interplay of molecular events within the sarcomere enables skeletal muscle to
generate force, produce movement, and maintain posture in response to neural and
hormonal signals.
In summary, the sarcomere represents a marvel of molecular architecture and
biomechanics, where the interaction of thick and thin filaments orchestrates the complex
process of muscle contraction. Understanding the structural organization and functional
properties of sarcomeres provides insights into the mechanisms underlying muscle
function and dysfunction, with implications for health, exercise physiology, and
therapeutic interventions for musculoskeletal disorders.
Each thick filament is made of molecules of the protein myosin. A myosin
molecule has a tail and a double head. In a thick filament many of them are bundled
together so that all the heads stick out, away from the sarcomere’s center. Muscle
bundles, muscle fibers, myofibrils, and their filaments all run in the same direction. This
alignment focuses the force of a contracting muscle. All sarcomeres in all fibers of a
muscle work together and pull a bone in the same direction.
A sliding filament mechanism explains how interactions between thick and thin
filaments allow muscle fibers to contract. In a contraction, all the myosin filaments stay
in place. They use short “power strokes” to slide the sets of actin Each power stroke is
driven by energy from ATP. Each myosin head repeatedly “grabs” binding sites on a
nearby actin filament. The head is an ATPase, a type of enzyme. It binds ATP and
catalyzes a phosphate group transfer that powers the reaction.
A rise in the concentration of calcium ions causes the myosin head to attach to the
actin. This link tilts the myosin head and pulls the actin filament toward the sarcomere’s
center. Next, with the help of energy from ATP, the myosin head’s grip on actin is
broken and the head returns to its starting position. Each time a sarcomere contracts,
hundreds of myosin heads make a series of short strokes down the length of actin
filaments.
When someone dies, her or his body cells stop making ATP. In muscles this
means that the myosin cross bridges with actin can’t break apart after a power stroke. As
a result skeletal muscles “lock up,” a stiffening called rigor mortis (“stiffness of death”).
Rigor mortis lasts for 24 to 60 hours, or until the natural decomposition of dead tissues
gets under way. Understanding rigor mortis helps crime investigators determine when a
suspicious death occurred.
j. How the Nervous System Controls Muscle Contraction
The role of the nervous system in controlling skeletal muscle contraction is
essential for the coordination and execution of voluntary movements as well as
maintaining posture and stability. This intricate process involves the transmission of
signals from the central nervous system (CNS), specifically the brain and spinal cord, to
individual muscle fibers via specialized nerve cells known as motor neurons.
Motor neurons serve as the conduits through which commands from the CNS are
relayed to muscles, facilitating the initiation, modulation, and termination of muscle
contraction. These specialized neurons have cell bodies located within the spinal cord
(for somatic motor neurons) or the brainstem (for cranial motor neurons), with long
axonal projections that extend to innervate skeletal muscle fibers at neuromuscular
junctions.
At the neuromuscular junction, the terminal end of a motor neuron forms synaptic
connections with the sarcolemma (cell membrane) of a muscle fiber. This synaptic
connection consists of a small gap called the synaptic cleft, across which
neurotransmitters are released from synaptic vesicles in response to an action potential
(electrical signal) traveling along the motor neuron.
When an action potential reaches the synaptic terminal of a motor neuron, it
triggers the release of the neurotransmitter acetylcholine (ACh) into the synaptic cleft.
Acetylcholine diffuses across the synaptic cleft and binds to receptors on the sarcolemma
of the muscle fiber, leading to depolarization of the muscle cell membrane and initiation
of an action potential in the muscle fiber.
The action potential propagates along the sarcolemma and into the interior of the
muscle fiber via specialized structures known as transverse (T) tubules. This
depolarization of the muscle cell membrane triggers the release of calcium ions (Ca2+)
from the sarcoplasmic reticulum, a specialized organelle within the muscle fiber.
The released calcium ions bind to regulatory proteins within the sarcomere,
leading to a conformational change that exposes binding sites on the actin filaments. This
allows the myosin heads of thick filaments to interact with actin, forming cross-bridges
and initiating the sliding filament mechanism of muscle contraction.
The entire process of excitation-contraction coupling, from the arrival of the
action potential at the neuromuscular junction to the initiation of muscle contraction,
occurs within milliseconds and is tightly regulated to ensure precise control over muscle
activity. Once the action potential ceases, acetylcholine is rapidly degraded by the
enzyme acetylcholinesterase, terminating its action at the neuromuscular junction and
allowing the muscle fiber to relax.
In addition to initiating muscle contraction, motor neurons also play a role in
modulating the intensity and duration of muscle activity through graded recruitment of
motor units and the regulation of firing frequency. By varying the number and frequency
of action potentials sent to muscle fibers, the nervous system can fine-tune muscle force
production and adjust to changing movement demands.
Furthermore, the nervous system coordinates the activity of multiple muscles
acting together to produce coordinated movements and maintain postural stability. This
coordination is achieved through complex neural circuits and feedback mechanisms
involving sensory input from proprioceptors (receptors that detect muscle length and
tension) and higher brain centers involved in motor control and integration.
In summary, the nervous system exerts precise control over skeletal muscle
contraction by transmitting signals from the CNS to individual muscle fibers via motor
neurons. This neural control allows for the precise regulation of muscle activity, enabling
the execution of voluntary movements, maintenance of posture, and adaptation to
changing environmental demands. Understanding the mechanisms of neural control of
muscle contraction provides insights into the coordination and integration of motor
function and has implications for rehabilitation, sports performance, and the treatment of
neuromuscular disorders.
When nerve impulses arrive at a muscle fiber, they quickly spread. Eventually
they reach small extensions of the cell’s plasma membrane. These “T tubules” connect
with a membrane system that laces around the fiber’s myofibrils. The system, called the
sarcoplasmic reticulum (SR), is a version of the endoplasmic reticulum described. SR
takes up and releases calcium ions (Ca11). An incoming nerve impulse triggers the
release of calcium ions from the SR. The ions diffuse into myofibrils, and when they
reach actin filaments the stage is set for contraction.
Two proteins on the surface of actin filaments have important roles in muscle
contraction. One of them, called troponin (tropo- means “turn or change”), has a rounded
shape. It attaches to the actin filament and also to the second protein, called tropomyosin
(“myosin changer”), which winds along the actin filament. Importantly, in a resting
muscle fiber troponin covers up the sites where myosin can link up with actin. This
changes when incoming calcium binds to troponin. Then the troponin moves, twisting
tropomyosin away from the actin binding sites. Myosin now can attach to the sites, and
muscle contraction can occur.
When nerve impulses stop, calcium is actively transported back into the SR.
Tropomyosin covers the binding sites on actin again, myosin can’t bind to actin, and the
muscle fiber relaxes. Notice the importance of calcium in these events. Its central role in
muscle contraction is one reason why mechanisms of homeostasis that maintain proper
blood levels of calcium are so important.
A motor neuron has long extensions called axons that carry nerve impulses. The
nerve impulses that stimulate a skeletal muscle fiber arrive at neuromuscular junctions.
These are places where the branched endings of axons come close to muscle fiber
membranes. Between the neuron endings and each muscle cell is a gap called a synapse.
A type of chemical messenger, a neurotransmitter called ACh (for acetylcholine), carries
the signals from a motor neuron across the gap.
The signaling between a neuron and a muscle cell takes place in steps. As these
steps take place, calcium ions from the extracellular fluid flow inside the axon endings,
and vesicles in each ending release ACh. If enough ACh binds to receptors on the muscle
cell membrane, the events that cause the muscle cell to contract may get under way. ACh
can excite or inhibit muscle and gland cells, as well as some cells in the brain and spinal
cord.
Each year in the United States about 2 million people have injections of Botox to
smooth out facial wrinkles. Made by the bacterium Clostridium botulinum, Botox blocks
the release of ACh, so the muscle contractions that produce wrinkles stop for a while.
The muscle-relaxing effect lasts four to six months and can have side effects, such as
droopy eyelids. Botox also is used to treat disorders. For example, it may relieve
abnormal muscle contractions that trouble stroke patients. Only a physician can legally
prescribe Botox.
k. Ways Muscle Cells Get Energy
A resting muscle fiber has a small amount of stored ATP and much more of a
substance called creatine phosphate. This substance is generated in the fiber from natural
stores of the amino acid creatine. When the fiber is stimulated to contract, a fast reaction
transfers phosphate from creatine phosphate to ADP, to form more ATP. This reaction
can fuel contractions until a slower ATP-forming pathway, such as aerobic cellular
respiration.
Normally, most of the ATP for muscle contraction comes from the oxygen-using
reactions of cellular respiration. If you exercise hard, however, your respiratory and
circulatory systems may not be able to deliver enough oxygen for aerobic cellular
respiration in some muscles. Then, glycolysis (which does not use oxygen) will
contribute more of the ATP being formed. Muscle cells rely on glycolysis until there is
too little stored glycogen to provide glucose or until muscle fatigue sets in. This is a state
in which a muscle can no longer contract. One cause of fatigue may be an oxygen debt
that results when muscles need more ATP than aerobic cellular respiration can deliver.
They then switch to glycolysis, which produces lactic acid. Along with the already low
ATP supply, the rising acidity hampers the contraction of muscle cells. It also causes the
“burn” you might feel while working out. Deep, rapid breathing helps repay the oxygen
debt.
A motor neuron supplies a number of fibers in a muscle. The motor neuron and
the muscle fibers it synapses with form a motor unit. The number of fibers in a motor unit
depends on how precise the muscle control must be. For instance, motor units in the
bulky, powerful thigh muscles may include hundreds of thousands of fibers. In contrast,
we need much more precise control over the tiny muscles that move the eye. In these
muscles, motor units have only a few hundred muscle fibers.
A muscle contraction may last a long time or only a few thousandths of a second.
When a motor neuron fires, all the fibers in its motor unit contract briefly. This response
is a muscle twitch. If a new nerve impulse arrives before a twitch ends, the muscle
twitches again. Repeated stimulation of a motor unit in a short period of time makes all
the twitches run together. The result is a sustained contraction called tetanus. Our
muscles normally contract in this way, which generates three or four times the force of a
single twitch.
A skeletal muscle contains a large number of muscle fibers, but not all of them
contract at the same time. If a muscle is contracting only weakly—say, as your forearm
muscles do when you pick up a pencil—it is because the nervous system is activating
only a few of the muscle’s motor units. In stronger contractions (when you heft a stack of
books) more motor units are stimulated. Even when a muscle is relaxed, however, some
of its motor units are contracted. This steady, lowlevel contracted state is called muscle
tone. It helps maintain muscles in general good health and is important in stabilizing the
skeleton’s movable joints.
