36
Musculoskeletal Systems
Chapter 36 Musculoskeletal Systems
Key Concepts
• 36.1 Cycles of Protein–Protein Interactions
Cause Muscles to Contract
• 36.2 The Characteristics of Muscle Cells
Determine Muscle Performance
• 36.3 Muscles Pull on Skeletal Elements to
Generate Force and Cause Movement
Chapter 36 Opening Question
How have musculoskeletal systems
evolved to maximize force generation and
do so at minimal metabolic cost?
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Three types of vertebrate muscle:
• Skeletal—voluntary movement, also
breathing
• Cardiac—beating of heart
• Smooth—involuntary, movement of
internal organs
All use same sliding filament contractile
mechanism.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Skeletal muscle (striated):
Cells are called muscle fibers—are large
and multinucleate
Form from fusion of embryonic myoblasts
One muscle consists of many muscle fibers
bundled together by connective tissue.
Figure 36.1 The Structure of Skeletal Muscle (Part 1)
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Muscle contraction due to interaction of
contractile proteins:
• Actin—thin filaments
• Myosin—thick filaments
Each muscle fiber has several myofibrils—
bundles of actin and myosin filament.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Each myofibril consists of sarcomeres—
repeating units of overlapping actin and
myosin filaments.
Each sarcomere is bounded by Z lines,
which anchor actin.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Other parts of sarcomere:
A band in center—contains myosin
H zone and I band—no overlap of actin and
myosin
M band within H zone—contains proteins
Figure 36.1 The Structure of Skeletal Muscle (Part 2)
Figure 36.1 The Structure of Skeletal Muscle (Part 3)
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Titin—the largest protein in the body, runs
the full length of the sarcomere.
Bundles of myosin filaments are held in the
center of the sarcomeres by titin.
When muscle contracts, sarcomeres
shorten and band pattern changes.
Figure 36.2 Sliding Filaments
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
The sliding filament contractile model of
muscle contraction depends on structure
of actin and myosin:
• Myosin molecule has two polypeptide
chains coiled together, ending in a globular
head
• Myosin filament is many molecules in
parallel
• Actin filament is actin monomers in a long,
twisted chain
Figure 36.3 Actin and Myosin Filaments Overlap in Myofibrils
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Muscle cells are excitable—membranes
can conduct action potentials.
Muscle contraction is initiated by action
potentials from a motor neuron at the
neuromuscular junction.
A motor unit—all the muscle fibers
activated by one motor neuron.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
One muscle may have many motor units.
To increase strength of muscle
contraction—increase rate of firing of
motor neuron or recruit more motor
neurons to fire (more motor units
activated).
Figure 36.4 The Neuromuscular Junction
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Action potentials in muscle fiber also travel
deep within the cell.
T tubules (transverse tubules) descend into
the sarcoplasm (muscle fiber cytoplasm).
T tubules run close to the sarcoplasmic
reticulum—a closed compartment that
surrounds every myofibril.
Figure 36.5 T Tubules Spread Action Potentials into the Fiber
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Two proteins span space between T tubules
and sarcoplasmic reticulum and are
physically connected.
The dihydropyridine (DHP) receptor on the
T tubule membrane is voltage-sensitive.
The ryanodine receptor in the sarcoplasmic
reticulum membrane is a Ca2+ channel.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
When an action potential reaches the DHP
receptor it changes conformation.
Ryanodine receptor then allows Ca2+ to
leave the sarcoplasmic reticulum.
Ca2+ ions diffuse into the sarcoplasm and
trigger interaction of actin and myosin and
sliding of filaments.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
• Actin filament is actin monomers in a long,
twisted molecule
• Tropomyosin twists around actin;
troponin attached at intervals
• Myosin heads can bind specific sites on
actin molecules to form cross bridges.
Myosin changes conformation, causes
actin filament to slide.
Figure 36.6 Release of Ca2+ from the Sarcoplasmic Reticulum Triggers Muscle Contraction
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Cardiac muscle is also striated—cells are
smaller than skeletal muscle and have one
nucleus (uninucleate).
Cardiac muscle cells also branch and
interdigitate—can withstand high
pressures.
Intercalated discs provide mechanical
adhesions between cells and contain gap
junctions.
In-Text Art, Ch. 36, p. 718 (1)
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Pacemaker and conducting cells initiate and
coordinate heart contractions.
Heartbeat is myogenic—generated by the
heart muscle itself.
Autonomic nervous system modifies the rate
of pacemaker cells but is not necessary for
their function.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Excitation and contraction of cardiac muscle
differs from skeletal muscle:
• T tubules are larger
• DHP proteins in T tubules are Ca2+
channels and are not connected to the
ryanodine receptors
Ryanodine receptors are ion-gated Ca2+
channels, sensitive to Ca2+.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
In cardiac cells, action potential spreads
through T tubules, opens voltage-gated
Ca2+ channels and Ca2+ flows into
sarcoplasm.
• Increase in Ca2+ opens the Ca2+ channels
in sarcoplasmic reticulum—large increase
in Ca2+ in sarcoplasm initiates fiber
contraction
Ca2+-induced Ca2+ release
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Smooth muscle—in most internal organs,
under autonomic nervous system control.
Smooth muscle cells are arranged in
sheets—have electrical contact via gap
junctions.
Action potential in one cell can spread to all
others in the sheet.
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Plasma membrane of smooth muscle cells
is sensitive to stretch.
Stretched cells depolarize and fire action
potentials, which start contraction.
Important for digestion.
In-Text Art, Ch. 36, p. 718 (2)
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Neural influences on smooth muscle come
from autonomic nervous system.
Acetylcholine in digestive tract causes
depolarization and action potentials,
causing contraction.
Norepinephrine causes the same cells to
hyperpolarize, leading to fewer
contractions.
Figure 36.7 Neurotransmitters and Stretch Alter the Potential of Smooth Muscle Cells (Part 1)
Figure 36.7 Neurotransmitters and Stretch Alter the Potential of Smooth Muscle Cells (Part 2)
Concept 36.1 Cycles of Protein–Protein Interactions Cause
Muscles to Contract
Smooth muscle contraction:
• Ca2+ influx to sarcoplasm stimulated by
stretching, action potentials, or hormones
• Ca2+ binds with calmodulin—activates
myosin kinase, which phosphorylates
myosin heads; can then bind and release
actin
Figure 36.8 The Role of Ca2+ in Smooth Muscle Contraction
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
In skeletal muscle—minimum unit of
contraction is a twitch.
Twitch measured in terms of tension, or
force it generates.
A single action potential generates a single
twitch. Force generated depends on how
many fibers are in the motor unit.
Figure 36.9 Twitches and Tetanus
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
Tension generated by entire muscle
depends on:
• Number of motor units activated
• Frequency at which motor units are firing
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
Single twitch—if action potentials are close
together in time, the twitches are summed,
tension increases.
Twitches sum because Ca2+ pumps can not
clear Ca2+ from sarcoplasm before next
action potential arrives.
Tetanus—action potentials are so frequent
there is always Ca2+ in the sarcoplasm.
Figure 36.9 Twitches and Tetanus
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
How long muscle fiber can sustain tetanic
contraction depends on ATP supply.
ATP is needed to break the actin–myosin
bonds, and “re-cock” the myosin heads.
To maintain contraction, actin–myosin
bonds have to keep cycling.
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
A low level of tension is maintained by some
muscles.
Muscle tone—a small but changing number
of motor units are contracting.
Muscle tone is constantly being adjusted by
the nervous system.
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
Type of muscle fiber determines endurance
and strength.
Skeletal muscle fibers can express genes
for different variants of myosin with
different ATPase activity.
Faster or slower ATPase activity determines
different muscle characteristics.
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
Slow-twitch fibers (oxidative or red
muscle).
Contain myoglobin, oxygen binding protein,
and many mitochondria; well-supplied with
blood vessels.
Maximum tension develops slowly but is
highly resistant to fatigue.
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
Slow-twitch fibers have reserves of
glycogen and fat—can produce ATP as
long as oxygen is available.
Muscles with high proportion of slow-twitch
fibers are good for aerobic work (e.g., long
distance running, cycling, swimming, etc.).
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
Fast-twitch fibers (glycolytic or white
muscle).
Fewer mitochondria, fewer blood vessels,
little or no myoglobin.
Develop greater maximum tension faster,
but fatigue more quickly.
Cannot replenish ATP for prolonged
contraction.
Figure 36.10 Slow- and Fast-twitch Muscle Fibers (Part 1)
Figure 36.10 Slow- and Fast-twitch Muscle Fibers (Part 2)
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
Muscles have three systems for supplying
ATP for contractions:
• Immediate system uses preformed ATP
and creatine phosphate
• Glycolytic system metabolizes
carbohydrates to lactic acid and pyruvate
• Oxidative system metabolizes
carbohydrates or fats to H2O and CO2
Figure 36.11 Supplying Fuel for High Performance
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
ATP is present in small amounts.
Muscles contain creatine phosphate (CP),
which stores energy in a phosphate bond
that can be transferred to ADP.
CP + ADP→ creatine + ATP
The immediate system enables fast-twitch
muscles to generate force quickly but is
exhausted within seconds.
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
The glycolytic system enzymes are in the
sarcoplasm—ATP generated is then
rapidly available to myosin.
Glycolysis alone is not very efficient—lactic
acid accumulates.
Immediate and glycolytic systems provide
energy for less than one minute.
Concept 36.2 The Characteristics of Muscle Cells Determine
Muscle Performance
Oxidative metabolism produces large
amounts of ATP but takes place in the
mitochondria.
ATP must diffuse from the mitochondria to
the myosin—rate is slower than other two
systems.
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Skeletal systems are the rigid supports
against which muscles can pull.
Three types of skeletal systems in
animals—hydrostatic, exoskeletons, and
endoskeletons.
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Hydrostatic skeleton consists of a volume
of fluid enclosed in a body cavity
surrounded by muscle.
When muscles oriented in one direction
contract, the fluid-filled body cavity bulges
out in the opposite direction.
Figure 36.12 A Hydrostatic Skeleton
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Exoskeleton consists of a hardened outer
surface to which muscles attach.
Contractions of the muscles cause
segments of the exoskeleton to move.
The complex arthropod exoskeleton (or
cuticle) covers all outer surfaces and
contains stiffening materials except at
joints.
For growth to occur, the animal must molt.
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Endoskeleton of vertebrates is an internal
scaffold.
An advantage is that growth can occur
without shedding the skeleton.
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Human skeleton has 206 bones and can be
divided:
• Axial skeleton includes skull, vertebral
column, sternum, and ribs
• Appendicular skeleton includes pectoral
and pelvic girdles, bones of the arms, legs,
hands, and feet
Figure 36.13 The Human Endoskeleton
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Vertebrate endoskeleton consists of two
kinds of connective tissue—cartilage and
bone.
These are produced by two kinds of
connective tissue cells.
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
• Cartilage cells produce a tough, rubbery
extracellular matrix of polysaccharides and
protein, mostly collagen
• Cartilage, the matrix, is found on bone
surfaces in joints, also in ears, nose, and
larynx
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Bone is an extracellular matrix of insoluble
calcium phosphate crystals—constantly
being replaced and remodeled by living
bone cells.
Osteoblasts make new bone matrix. When
they become enclosed in bone they are
called osteocytes.
Osteoclasts are cells that reabsorb bone.
Figure 36.14 Bone Is Living Tissue
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Two types of bone development:
Membranous bone forms on a scaffold of
connective tissue (e.g., outer bones of
skull).
Cartilage bone is first cartilaginous, then
ossifies or hardens (e.g., bones of limbs).
Growth can occur throughout the
ossification process.
Figure 36.15 The Growth of Long Bones
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Bone structure varies:
• Compact—solid and hard
• Cancellous—with numerous cavities,
appears spongy, is lightweight but strong
Most bones have both types.
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Joints are where bones come together.
Different types of joints allow motion in
different directions.
Muscles can exert force in only one
direction—work in antagonistic pairs.
• Flexor—the muscle that bends or flexes
the joint
• Extensor—the muscle the straightens or
extends the joint
Figure 36.16 Types of Joints
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
• Ligaments are bands of connective tissue
that hold bones together at joints
• Tendons are connective tissue straps that
join muscle to bone
Figure 36.17 Joints, Ligaments, and Tendons
Concept 36.3 Muscles Pull on Skeletal Elements to Generate
Force and Cause Movement
Bones are a system of levers moved by
muscles.
Levers have an effort arm and a load arm that
work around a fulcrum (pivot).
The length ratio of the two arms determine the
force that can be exerted.
Figure 36.18 Bones and Joints Work Like Systems of Levers
Answer to Opening Question
The ratio of leg length to body mass is large in
the frog—the increased leverage is good for
propelling a small mass a great distance.
Other adaptations include long tendons
working with small muscles in the camel,
and elasticity of tendons in the kangaroo.
All increase the efficiency of locomotion.
Figure 36.19 Champion Jumpers