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9
Skeletal Muscle
Tissue
PowerPoint® Lecture Presentations prepared by
Alexander G. Cheroske
Mesa Community College at Red Mountain
© 2011 Pearson Education, Inc.
Section 1: Functional Anatomy of Skeletal
Muscle Tissue
• Learning Outcomes
• 9.1 Describe the organization of skeletal muscle at the
tissue level.
• 9.2 Identify the structural components of a sarcomere.
• 9.3 Describe the structural components of a thin
filament and a thick filament.
• 9.4 Identify the components of the neuromuscular
junction, and summarize the events involved in the
neural control of skeletal muscles.
• 9.5 Describe the role of ATP in a muscle contraction,
and explain the steps involved in the contraction of
a skeletal muscle fiber.
© 2011 Pearson Education, Inc.
Section 1: Functional Anatomy of Skeletal
Muscle Tissue
• Muscle tissue
• One of the four primary tissue types
• Consists chiefly of muscle cells specialized for
contraction
• Three types
1. Cardiac
•
In heart propelling blood through blood vessels
2. Smooth
•
Move fluids and solids along digestive tract
•
Regulate diameters of small arteries
•
Other functions
© 2011 Pearson Education, Inc.
Section 1: Functional Anatomy of Skeletal
Muscle Tissue
• Muscle tissue (continued)
• Three types (continued)
3. Skeletal
•
Move body by pulling on bones
•
Each cell is a single muscle fiber
•
Each muscle is an organ
•
© 2011 Pearson Education, Inc.
Primarily muscle cells plus connective tissues, nerves,
and blood vessels
Skeletal Muscle Tissue
Skeletal muscle tissue contractions
move the body by pulling on bones
of the skeleton, making it possible
for us to walk, dance, bite an apple,
or play the ukulele.
Cardiac Muscle Tissue
Cardiac muscle tissue contractions
in the heart propel blood through
the blood vessels.
Smooth Muscle Tissue
Smooth muscle tissue contractions
move fluids and solids along the
digestive tract and regulate the
diameters of small arteries, among
other functions.
Figure 9 Section 1
© 2011 Pearson Education, Inc.
Section 1: Functional Anatomy of Skeletal
Muscle Tissue
• Skeletal muscle tissue functions
• Produce skeletal movements
• Pull tendons and move bones
• Maintain posture and body position
• Skeletal muscle tension maintains body posture
• Support soft tissues
• Support weight of visceral organs and shield internal
tissues from injury
© 2011 Pearson Education, Inc.
Section 1: Functional Anatomy of Skeletal
Muscle Tissue
• Skeletal muscle tissue functions (continued)
• Guard entrances and exits
• Openings of digestive and urinary tracts encircled by
skeletal muscle (sphincters)
• Provide voluntary control of swallowing, defecation,
and urination
• Maintain body temperature
• Some energy used for muscle contraction is released
as heat
• Provide nutrient reserves
• Amino acids from muscle fibers can be released into
circulation and used to produce glucose and energy
© 2011 Pearson Education, Inc.
Module 9.1: Skeletal muscle anatomy
• Skeletal muscle
• Complex organ containing:
• Skeletal muscle fibers (contraction)
• Connective tissues (harness contractile forces)
• Blood vessels (nourish muscle fibers)
• Nerves (control contractions)
© 2011 Pearson Education, Inc.
Module 9.1: Skeletal muscle anatomy
• Skeletal muscle connective tissues
• Tendon
• Bundle of collagen fibers that attach muscle to bone
• Collagen fibers extend into bone matrix providing firm
attachment
• Also occurs as a sheet (= aponeurosis)
• Epimysium (epi-, on + mys, muscle)
• Dense layer of collagen fibers surrounding entire muscle
• Separates muscle from surrounding tissues and organs
• Connected to deep fascia
© 2011 Pearson Education, Inc.
Module 9.1: Skeletal muscle anatomy
• Skeletal muscle connective tissues (continued)
• Perimysium (peri-, around)
• Fibrous layer that divides muscle into compartments
or bundles of cells (= fascicles)
• Contains collagen and elastin fibers, blood vessels,
and nerves
• Endomysium (endo-, inside)
• Surrounds individual muscle cells or fibers
• Loosely interconnects adjacent muscle fibers
• Contains capillaries, myosatellite (stem) cells, and
axons of neurons that control muscle fibers
© 2011 Pearson Education, Inc.
Module 9.1: Skeletal muscle anatomy
Animation: Muscle Physiology: Muscle Layers
Animation: Anatomy of Skeletal Muscles
© 2011 Pearson Education, Inc.
Module 9.1: Skeletal muscle anatomy
• Skeletal muscle cell development
• Myoblasts (myo-, muscle + blastos, formative
cell) fuse, forming multinucleate cells
• Develop into skeletal muscle fibers
• Each skeletal muscle fiber nucleus represents a
myoblast
• Not all myoblasts fuse into developing muscle
fibers
• Some remain in endomysium and help muscle repair
© 2011 Pearson Education, Inc.
The development of a skeletal muscle
fiber from myoblast to maturity
Myoblasts
Muscle fibers develop through the
fusion of embryonic mesodermal
cells called myoblasts.
Myosatellite cell
Nuclei
Over time, most of the myoblasts fuse
together to form larger multinucleate cells.
However, a few myoblasts remain within the
tissue as myosatellite cells, even in adults.
Immature
muscle fiber
Myosatellite cell
The multinucleate cells begin
differentiating into skeletal
muscle fibers as they enlarge and
begin producing the proteins
involved in muscle contraction.
Mature skeletal
muscle fiber
Up to 30 cm
in length
Figure 9.1
© 2011 Pearson Education, Inc.
4
–
5
Module 9.1: Skeletal muscle anatomy
• Mature muscle cell characteristics
• Very large cells
• Can have diameter of 100 µm and length of 30
cm (12 in.)
• Each contains hundreds of nuclei just internal
to plasma membrane (sarcolemma) (sarkos,
flesh + lemma, husk)
• Genes in nuclei control production of enzymes
and structural proteins for contraction
• Many nuclei = many genes = faster production
• Cytoplasm = sarcoplasm
© 2011 Pearson Education, Inc.
A mature skeletal muscle fiber
Myosatellite cell
Mature skeletal
muscle fiber
Up to 30 cm
in length
Myofibrils
Sarcoplasm
Nuclei
Mitochondria
Sarcolemma
Figure 9.1
© 2011 Pearson Education, Inc.
5
–
6
Module 9.1 Review
a. Define tendon and aponeurosis.
b. Describe the connective tissue layers
associated with skeletal muscle tissue.
c. How would severing the tendon attached to a
muscle affect the muscle’s ability to move a
body part?
© 2011 Pearson Education, Inc.
Module 9.2: Skeletal muscle fiber anatomy
•
Myofibrils
•
Cylindrical structures 1–2 µm in diameter and as
long as muscle fiber
•
Hundreds to thousands comprise an individual
muscle cell
•
Each is banded and gives the skeletal muscle cells
their banded appearance
•
Made of protein filaments (= myofilaments)
•
Thin filaments (primarily actin)
•
Thick filaments (primarily myosin)
© 2011 Pearson Education, Inc.
The myofibril, the source of a muscle fiber’s striations
Myofibril
Nuclei
Sarcolemma
Sarcoplasm
Skeletal muscle fiber
Figure 9.2
© 2011 Pearson Education, Inc.
1
A section of a muscle fiber, revealing
its myofibrils, each of which is
composed of myofilaments
Sarcolemma
Myofibril
Thin filament
Thick filament
Mitochondria
Figure 9.2
© 2011 Pearson Education, Inc.
2
Module 9.2: Skeletal muscle fiber anatomy
•
Myofilament structure
•
Have repeating functional units called sarcomeres
(sarkos, flesh + meros, part)
•
Approximately 10,000 sarcomeres/myofibril
•
Each sarcomere has a 2-µm resting length
•
Zone of overlap
•
•
Thin and thick filaments interspersed
Z lines
•
Boundary of adjacent sarcomeres
•
Interconnect thin filaments from adjacent sarcomeres
•
Consist of proteins (actinins)
© 2011 Pearson Education, Inc.
Module 9.2: Skeletal muscle fiber anatomy
•
Myofilament structure (continued)
•
A band
•
•
Dense sarcomere region containing thick filaments
I band
•
Contains thin filaments (no thick)
•
Extends from A band of one sarcomere to the next A band
•
M line
•
•
Connects central portion of each thick filament
H band
•
Lighter region around M line
•
Contains only thick filaments (no thin)
© 2011 Pearson Education, Inc.
Sarcomeres, the repeating
functional units of myofilaments
Arrangement
of filaments in
zone of overlap
A band
I band
Myofibril
M line
Z line
Sarcomere
H band
Figure 9.2
© 2011 Pearson Education, Inc.
3
Module 9.2: Skeletal muscle fiber anatomy
•
Specialized parts of skeletal muscle cells
•
Sarcolemma
•
Separates sarcoplasm from interstitial fluid
•
Maintains distribution of positive and negative
charges on either side
•
= Transmembrane potential
•
All cells have a characteristic transmembrane potential
•
Large changes in skeletal muscle transmembrane
potential lead to contraction
•
© 2011 Pearson Education, Inc.
Are transmitted along entire muscle cell surface
Module 9.2: Skeletal muscle fiber anatomy
•
Specialized parts of skeletal muscle cells
(continued)
•
Transverse tubules (T tubules)
•
Narrow tubes from sarcolemma extending into
sarcoplasm
•
Transmembrane potential changes travel along
T tubules to cell interior
•
Encircle each sarcomere
© 2011 Pearson Education, Inc.
Module 9.2: Skeletal muscle fiber anatomy
•
Specialized parts of skeletal muscle cells
(continued)
•
Sarcoplasmic reticulum (SR)
•
Similar to smooth endoplasmic reticulum of
other cells
•
Forms tubular network around each myofibril
•
On either side of T tubule, forms expanded chambers
(terminal cisternae)
•
T tubule + terminal cisternae = triad
© 2011 Pearson Education, Inc.
The transverse tubules and the sarcoplasmic reticulum
Transverse tubules (T tubules)
T tubule encircling sarcomere
at zone of overlap
Sarcolemma
Transverse tubule
Terminal cisternae
Position of M line
Triad
Figure 9.2
© 2011 Pearson Education, Inc.
4
Module 9.2: Skeletal muscle fiber anatomy
•
Specialized parts of skeletal muscle cells
(continued)
•
Sarcoplasmic reticulum (SR) (continued)
•
Contains pumps moving calcium from sarcoplasm
to SR
•
SR calcium occurs as free ions and bound to proteins
•
SR calcium concentrations can be 40,000× that of
sarcoplasm
•
Muscle contraction begins with SR calcium release
© 2011 Pearson Education, Inc.
Sarcoplasmic reticulum (SR)
Ca2+
Gated calcium
channel (closed)
Sarcoplasm
Calcium ion
pump
The membrane of the sarcoplasmic reticulum, which contains calcium ion pumps
Figure 9.2
© 2011 Pearson Education, Inc.
5
Module 9.2 Review
a. Define transverse tubules.
b. Describe the structural components of a
sarcomere.
c. Where would you expect the greatest
concentration of Ca2+ to be in a resting
skeletal muscle?
© 2011 Pearson Education, Inc.
Module 9.3: Thick and thin filaments
•
Thin filaments
•
Attached to Z lines with actinin
•
5–6 µm in diameter, 1 µm in length
•
Primarily actin
•
Individual G-actin molecules (with active site for
binding myosin) link together to form F-actin
(filamentous)
•
F-actin strand held together with nebulin
© 2011 Pearson Education, Inc.
Module 9.3: Thick and thin filaments
•
Thin filaments (continued)
•
Also contain two regulatory proteins
1.
2.
Tropomyosin
•
Covers G-actin active sites and prevents actin–myosin interaction
•
Attached to troponin
Troponin
•
Consists of three subunits
1.
Binds to tropomyosin (forms complex)
2.
Binds to G-actin (maintains position on actin)
3.
Binds two calcium ions (for activation during contraction)
Animation: Muscle Physiology: Troponin
© 2011 Pearson Education, Inc.
A longitudinal section of a sarcomere
Myofibril
Z line
Thin filament
Thick filament
Actinin
The structure of thin filaments
Z line
The attachment of thin filaments to
the Z line at either end of a sarcomere
Active site
F-actin
Troponin
Nebulin
G-actin
Tropomyosin
A thin filament, which is primarily composed of
actin associated with other interacting proteins
© 2011 Pearson Education, Inc.
Figure 9.3
1
Module 9.3: Thick and thin filaments
•
Thick filaments
•
10–12 nm in diameter and 1.6 µm long
•
Have core of titin
•
•
Connect to Z lines
•
Are elastic and recoil after stretching
Contain ~300 myosin molecules
© 2011 Pearson Education, Inc.
Module 9.3: Thick and thin filaments
•
Thick filaments (continued)
•
Myosin molecule
•
Has long tail bound to other myosin molecules
•
Has two globular subunits (= free head)
•
•
Forms cross-bridges with actin during contraction
Connection between head and tail allows a hinge-like
(pivot) motion
Animation: Muscle Physiology: Myosin Parts
Animation: Muscle Physiology: Muscle Proteins
© 2011 Pearson Education, Inc.
Module 9.3: Thick and thin filaments
•
Sliding filament theory
•
When muscles contract, thin filaments slide past thick
filaments, and
1.
H bands and I bands get smaller
2.
Zones of overlap get larger
3.
Z lines approach each other
4.
A bands remain constant
•
Sliding occurs in all sarcomeres of a myofibril
•
 Myofibril gets shorter
•
 Muscle cell gets shorter
Animation: Muscle Physiology: Sarcromeres
© 2011 Pearson Education, Inc.
The sliding filament theory
I band
Z line
A band
H band
Sarcomere at rest
Z line
I band
A band
Z line
H band
Z line
Sarcomere contraction and filament sliding
Figure 9.3
© 2011 Pearson Education, Inc.
3
Figure 9.3
© 2011 Pearson Education, Inc.
4
Module 9.3 Review
a. Describe the components of thin filaments
and thick filaments.
b. What gives skeletal muscle its striated
appearance?
c. Briefly describe the sliding filament theory.
© 2011 Pearson Education, Inc.
Module 9.4: Neuromuscular junction
•
Neuromuscular junction (NMJ)
•
Intercellular connection between motor neuron and
skeletal muscle fiber
•
Muscle fiber contracts only under control from the
NMJ
•
Only one NMJ per muscle fiber
•
Although one motor neuron axon may branch to control
multiple muscle cells
A&P Flix: Events at the Neuromuscular Junction
© 2011 Pearson Education, Inc.
Motor end
plate
Synaptic terminal
Sarcoplasmic
reticulum
Myofibril
Motor neuron
Axon
Path of electrical
impulse (action
potential)
Neuromuscular
junction
Myofibril
Motor end plate
The structural relationship between a skeletal
muscle fiber and its lone neuromuscular junction
© 2011 Pearson Education, Inc.
Figure 9.4
1
Module 9.4: Neuromuscular junction
•
Neuromuscular junction (NMJ) (continued)
•
Consists of:
1.
Synaptic terminal of neuron
•
Has vesicles filled with neurotransmitter
(acetylcholine [ACh])
•
2.
3.
Changes permeability of sarcolemma
Motor end plate of muscle fiber
•
Has junctional folds (creases)
•
Contains acetylcholinesterase (AChE), an enzyme
that breaks down ACh
Synaptic cleft (space between neuron and muscle fiber)
•
Also contains AChE
© 2011 Pearson Education, Inc.
Synaptic cleft
Vesicles
containing
ACh (red)
Motor end plate
AChE
Junctional fold
The locations of ACh and AChE in
a resting neuro-muscular junction
Figure 9.4
© 2011 Pearson Education, Inc.
2
Module 9.4: Neuromuscular junction
•
Activities at the neuromuscular junction
1. Electrical impulse (action potential) at the synaptic
terminal causes vesicles of ACh to fuse with neuron
plasma membrane
•
= Exocytosis of ACh
2. ACh diffuses across synaptic cleft and binds to
receptors in motor end plate
•
ACh binding allows Na+ to diffuse into the cell
3. Sarcolemma generates action potential
•
AChE inactivates receptors by quickly removing ACh
from synaptic cleft
© 2011 Pearson Education, Inc.
Arriving action
potential
Junctional
fold
The arrival of an action potential,
the stimulus for ACh release
Figure 9.4
© 2011 Pearson Education, Inc.
3
Sarcolemma of
motor end plate
Exocytosis of ACh into the synaptic
cleft in response to arriving action
potential
Figure 9.4
© 2011 Pearson Education, Inc.
4
Na+
Na+
ACh
receptor site
Na+
Diffusion of ACh molecules and
their binding to receptors on the
motor end plate
Figure 9.4
© 2011 Pearson Education, Inc.
5
Action
potential
AChE
Generation of an action potential by
the sudden inrush of sodium ions,
and the removal of ACh by AChE
Figure 9.4
© 2011 Pearson Education, Inc.
6
Module 9.4: Neuromuscular junction
•
Action potential in the muscle cell
•
Action potential (AP) generated at motor end plate
sweeps across sarcolemma
•
Effect is almost immediate since AP is an electrical event
•
Event is brief since ACh has been removed and no other
stimulus occurs until another AP at motor end plate
•
Action potential sweeps down T tubules and causes
calcium to be released from SR to sarcomeres causing
muscle contraction
•
= Excitation-contraction coupling
Animation: Muscle Fiber Contraction
© 2011 Pearson Education, Inc.
Figure 9.4
© 2011 Pearson Education, Inc.
7
T tubule
Sarcoplasm
Ca2+
Sarcoplasmic
reticulum (SR)
Ca2+
Excitation-contraction coupling,
the dumping of calcium ions onto
sarcomeres as a result of the
movement of an action potential
down the T tubule
Figure 9.4
© 2011 Pearson Education, Inc.
8
Module 9.4 Review
a. Describe the neuromuscular junction.
b. How would a drug that blocks acetylcholine
release affect muscle contraction?
c. Predict what would happen if there were no
AChE in the synaptic cleft.
© 2011 Pearson Education, Inc.
Module 9.5: Muscle fiber contraction cycle
•
Resting sarcomere
Each myosin head is already “energized” and
“cocked” (heads pointing away from M line)
•
•
Energy supplied by breakdown of ATP by myosin
•
Myosin acting as an ATPase
•
Breakdown products (ADP and P) still attached to
myosin head
© 2011 Pearson Education, Inc.
Resting Sarcomere
Contraction Cycle Begins
Myosin head
Troponin
Tropomyosin
Actin
Figure 9.5
© 2011 Pearson Education, Inc.
1
Module 9.5: Muscle fiber contraction cycle
•
Steps of muscle fiber contraction cycle
1. Contraction cycle begins
• Arrival of calcium ions at zone of overlap
2. Active-site exposure
• Calcium binds to troponin
•
•
Weakens bond between actin and troponin–
tropomyosin complex
Troponin changes position, exposing active sites
on actin
3. Cross-bridge formation
• Myosin heads bind to exposed active sites on actin
forming cross-bridges
© 2011 Pearson Education, Inc.
Module 9.5: Muscle fiber contraction cycle
•
Steps of muscle fiber contraction cycle (continued)
4.
Myosin head pivoting
•
Stored energy within myosin head releases and head pivots
toward M line
•
•
5.
= Power stroke
ADP and P are released from myosin head
Cross-bridge detachment
•
Attachment of new ATP causes release of myosin from actin
•
6.
Exposes active site again for formation of another cross-bridge
Myosin reactivation
•
New ATP broken down and head “recocks”
© 2011 Pearson Education, Inc.
Module 9.5: Muscle fiber contraction cycle
A&P Flix: The Cross Bridge Cycle
Animation: Muscle Physiology: Intracellular Calcium
Proteins
© 2011 Pearson Education, Inc.
Module 9.5: Muscle fiber contraction cycle
•
Contracted sarcomere
•
Entire cycle repeated as long as Ca2+ concentrations remain
high and ATP is available
•
•
Calcium levels remain high as long as action potentials
continue down T tubules
Once stimulus is removed
•
SR calcium channels close
•
Calcium pumps move Ca2+ from sarcoplasm into terminal
cisternae
•
Troponin–tropomyosin complex moves to cover active sites,
preventing further cross-bridge formation
Animation: Muscle Physiology: Muscle Cycles of
Attachment and Detachment
© 2011 Pearson Education, Inc.
Module 9.5 Review
a. What molecule supplies the energy for a
muscle contraction?
b. List the interrelated steps that occur once the
contraction cycle has begun.
c. What triggers myosin reactivation?
© 2011 Pearson Education, Inc.
Section 2: Functional Properties of Skeletal
Muscle Tissue
• Learning Outcomes
• 9.6 Describe the mechanism responsible for tension
production in a muscle fiber, and discuss the
factors that determine the peak tension
developed during a contraction.
• 9.7 Discuss the factors that affect peak tension
production during the contraction of an entire
skeletal muscle, and explain the significance of
the motor unit in this process.
• 9.8 Compare the different types of muscle
contractions.
© 2011 Pearson Education, Inc.
Section 2: Functional Properties of Skeletal
Muscle Tissue
• Learning Outcomes
• 9.9
Describe the mechanisms by which muscle
fibers obtain the energy to power contractions.
• 9.10 Describe the factors that contribute to muscle
fatigue, and discuss the stages and
mechanisms involved in the muscle’s
subsequent recovery.
• 9.11 Relate the types of muscle fibers to muscle
performance.
• 9.12 CLINICAL MODULE Explain the physiological
factors responsible for muscle hypertrophy,
atrophy, and paralysis.
© 2011 Pearson Education, Inc.
Section 2: Functional Properties of Skeletal
Muscle Tissue
• Review
• Neural control
• Skeletal muscle fibers contract when stimulated by
motor neuron at neuromuscular junction
• Stimulus is an action potential (AP) at synaptic terminal
• Excitation-contraction coupling
• AP causes release of ACh into synaptic cleft
• ACh binds to motor end plate receptors opening Na+
channels
• Leads to AP in sarcolemma
• AP travels along T tubules causing release of Ca2+
from terminal cisternae of SR
© 2011 Pearson Education, Inc.
Section 2: Functional Properties of Skeletal
Muscle Tissue
• Review (continued)
• Excitation-contraction coupling (continued)
• Contraction cycle begins and continues as long as
ATP is available and APs are still produced at motor
end plate
• Thick and thin filaments interact, shortening
sarcomeres/muscle fibers/muscle
• Contraction of entire muscle produces a pull or tension
© 2011 Pearson Education, Inc.
Module 9.6: Tension and muscle length
• Variance in tension that a muscle fiber produces
depends on resting length of sarcomere and
stimulation time
• Does not depend on number of sarcomeres contracted
• All sarcomeres are stimulated and contract together
• = Muscle fiber “on” (producing tension) or “off” (relaxed)
• Stretched or compressed compared to optimal resting
length, produces less tension
• Normal sarcomere length range is 75%–130% of
optimal
• Muscle arrangement, connective tissues, and bones
usually prevent too much stretching or compression
© 2011 Pearson Education, Inc.
Module 9.6: Tension and muscle length
• Tension within optimal sarcomere lengths
• Maximum number of cross-bridges can form
• Produces greatest tension
• Tension at increased (stretched) sarcomere lengths
• Reduction in tension due to reduction in size of zone
of overlap and number of cross-bridges
• At extreme lengths, no zone of overlap exists and no
tension can be generated
• Normally prevented by titin filaments (tie thick filaments to Z
lines) and connective tissues
© 2011 Pearson Education, Inc.
Module 9.6: Tension and muscle length
• Tension at decreased (compressed) sarcomere
lengths
• Reduces tension as sarcomeres have little area to
shorten before thin filaments collide with or
overlap with thin filaments from opposite side
• When sarcomeres are fully compressed (thick
filaments contacting Z lines), no tension can be
produced
© 2011 Pearson Education, Inc.
Tension production
falls to zero when
the thick filaments
are jammed against
the Z lines and the
sarcomere cannot
shorten further.
Tension (percent of maximum)
A decrease in the resting
sarcomere length reduces
tension because stimulated
sarcomeres cannot shorten
very much before the thin
filaments extend across the
center of the sarcomere and
collide with or overlap the thin
filaments of the opposite side.
Sarcomeres produce tension
most efficiently within an
optimal range of lengths. When
resting sarcomere length is
within this range, the maximum
number of cross-bridges can
form, producing the greatest
tension.
An increase in sarcomere length
reduces the tension produced by
reducing the size of the zone of overlap
and the number of potential
cross-bridge interactions.
Normal
range
Decreased length
Increased sarcomere length
When the zone of overlap is reduced to
zero, thin and thick filaments cannot
interact at all. The muscle fiber cannot
produce any active tension, and a
contraction cannot occur. Such
extreme stretching of a muscle fiber is
normally prevented by titin filaments
(which tie the thick filaments to the Z
lines) and by the surrounding
connective tissues.
Figure 9.6
© 2011 Pearson Education, Inc.
1
Module 9.6: Tension and muscle length
• Muscle twitch
• Single stimulus-contraction-relaxation sequence in a
muscle fiber
• Vary in duration depending on:
• Muscle type
• Muscle location
• Internal and external conditions
• Other factors
• Can be viewed on myograms (graph of tension
development in muscle fibers)
© 2011 Pearson Education, Inc.
A myogram, a graph of tension development in muscle fibers
Tension
Eye muscle Deep muscle
of the calf
Time (msec)
Stimulus
Figure 9.6
© 2011 Pearson Education, Inc.
2
Module 9.6: Tension and muscle length
• Twitch phases
• Latent period
• Action potential sweeps across sarcolemma
• SR releases calcium ions
• Contraction cycle has not begun (= no tension)
• Contraction phase
• Tension rises to peak
• Calcium binds to troponin allowing cross-bridge
formation between myosin head and active site on
actin
© 2011 Pearson Education, Inc.
Module 9.6: Tension and muscle length
• Twitch phases (continued)
• Relaxation phase
• Calcium levels fall
• Active sites covered by tropomyosin
• Number of cross-bridges decline with
detachment
© 2011 Pearson Education, Inc.
The phases of a 40-msec twitch in a muscle fiber from the
gastrocnemius muscle
Tension
Maximum tension development
Resting
phase Stimulus
Contraction
phase
Relaxation
phase
Time (msec)
The latent period
begins at stimulation
and typically lasts about
2 msec. During this
period, an action
potential sweeps across
the sarcolemma, and the
sarcoplasmic reticulum
releases calcium ions.
The muscle fiber does
not produce tension
during the latent period,
because the contraction
cycle has yet to begin.
© 2011 Pearson Education, Inc.
In the contraction
phase, tension rises to
a peak. As the tension
rises, calcium ions are
binding to troponin,
active sites on thin
filaments are being
exposed, and
cross-bridge
interactions are
occurring.
The relaxation phase
lasts about 25 msec.
During this period, calcium
levels are falling, active
sites are being covered by
tropomyosin, and the
number of active
cross-bridges is declining
as they detach. As a result,
tension returns to resting
levels.
Figure 9.6
3
Module 9.6 Review
a. Name a factor that affects the amount of tension
produced when a skeletal muscle contracts.
b. Explain two key concepts of the length–tension
relationship.
c. For each portion of a myogram tracing a twitch in
a stimulated gastrocnemius (calf) muscle fiber,
describe the events that occur within the muscle.
© 2011 Pearson Education, Inc.
Module 9.7: Developing peak tension
•
Two factors determine amount of tension
produced by a skeletal muscle
1. Amount of tension produced by each muscle
fiber
•
Dependent on stimulation frequency
2. Total number of muscle fibers stimulated
© 2011 Pearson Education, Inc.
Module 9.7: Developing peak tension
•
Effects of stimulation frequency on tension
•
Treppe (German for staircase)
•
Stimulation of skeletal muscle fiber immediately
after relaxation phase produces increasing
maximum tension
•
Continues for first 30–50 stimulations
•
Most skeletal muscles do not demonstrate
treppe
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Tension
Treppe
Maximum tension (in treppe)
KEY
= Stimulus
Time
Figure 9.7
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1
Module 9.7: Developing peak tension
•
Effects of stimulation frequency on tension
(continued)
•
Wave summation
•
Stimulation of skeletal muscle fiber before relaxation
phase completion produces increasing maximum
tension
•
•
= Addition of one twitch to another
Duration of twitch determines maximum time
available to produce wave summation
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Tension
Wave summation
KEY
= Stimulus
Time
Figure 9.7
© 2011 Pearson Education, Inc.
2
Module 9.7: Developing peak tension
•
Effects of stimulation frequency on tension
(continued)
•
Incomplete tetanus (tetanos, convulsive
tension)
•
•
Wave summation producing almost peak tension
Complete tetanus
•
Wave summation where stimulation frequency
eliminates relaxation phase and produces peak
tension
•
•
SR cannot reclaim Ca2+ making contraction continuous
Seldom occurs in normal functioning muscles
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Incomplete tetanus
Tension
Maximum tension (in tetanus)
KEY
= Stimulus
Time
Figure 9.7
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3
Tension
Complete tetanus
KEY
= Stimulus
Time
Figure 9.7
© 2011 Pearson Education, Inc.
4
Module 9.7: Developing peak tension
•
Effects of muscle fiber number on tension
•
Typical muscle has thousands of muscle fibers
•
Groups of muscle fibers controlled by one motor
neuron = motor unit
•
Size of motor unit varies with muscle control
•
•
Examples:
•
External eye muscle (fine control): 4–6 muscle cells
•
Leg muscle (gross control): 1000–2000 muscle cells
Muscle fibers of different motor units are
intermingled
© 2011 Pearson Education, Inc.
Module 9.7: Developing peak tension
•
Effects of muscle fiber number on tension
(continued)
•
Motor units
•
•
Recruitment
•
Movements begin with the smallest motor units
•
As movement continues, more and larger motor units are
stimulated to contribute producing greater tension
Asynchronous motor unit summation
•
Motor units activated on a rotating basis to maintain a
sustained contraction
© 2011 Pearson Education, Inc.
The structure of a motor unit, which consists of all the muscle fibers
controlled by a single motor neuron
Spinal cord
Cell bodies of
motor neurons
Axons
of motor
neurons
Motor
nerve
Intermingled muscle fibers from
different motor units
KEY
Motor unit 1
Motor unit 2
Motor unit 3
© 2011 Pearson Education, Inc.
Figure 9.7
5
Asynchronous motor unit summation
during a sustained contraction
Tension
Tension in tendon
Motor unit 1
Motor unit 2
Motor unit 3
Time
Figure 9.7
© 2011 Pearson Education, Inc.
6
Module 9.7: Developing peak tension
•
Effects of muscle fiber number on tension
(continued)
•
Motor units (continued)
•
Muscle tone
•
Variable number of motor units always active to produce
low level tension (not enough to produce movement)
•
Regulated at subconscious level
•
Activated muscle fibers use energy and therefore can
affect metabolism by a small amount
© 2011 Pearson Education, Inc.
Module 9.7 Review
a. Define motor unit.
b. Describe the relationship between the
number of fibers in a motor unit and the
precision of body movements.
c. Compare incomplete tetanus with wave
summation.
© 2011 Pearson Education, Inc.
Module 9.8: Isotonic and isometric contractions
•
Isotonic contraction (iso-, equal + tonos, tension)
•
Tension rises, until muscle length changes, then remains
constant
•
Examples: lifting an object, walking, running
•
Concentric contraction
•
Muscle tension overcomes load and muscle shortens
•
Speed of contraction inversely related to load
•
Eccentric contraction
•
When load is more than peak tension produced, muscle
lengthens
•
Rate of elongation varies with difference in load/tension
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A concentric isotonic contraction
Tendon
Muscle
contracts
(isotonic
contraction)
2 kg
2 kg
Figure 9.8
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1
Muscle tension and length changes during a
concentric isotonic contraction
Amount
of load
Muscle
tension
(kg)
Peak tension
production
Muscle
relaxes
Contraction
begins
Resting length
Muscle
length
(percent
of resting
length)
Time
Figure 9.8
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2
Speed of muscle contraction
The inverse relationship between speed of muscle
contraction and load on the muscle
Load (kg)
Figure 9.8
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3
An eccentric isotonic contraction
Support removed,
contraction begins
6 kg
6 kg
Figure 9.8
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4
Muscle tension and length changes during an eccentric
isotonic contraction
Muscle
tension
(kg)
Peak tension
production
Support removed,
contraction begins
Muscle
length
(percent
of resting
length)
When the eccentric
contraction ends,
the unopposed load
stretches the
muscle until either
the muscle tears, a
tendon breaks, or
the elastic recoil of
the skeletal muscle
is sufficient to
oppose the load.
Resting length
Time
Figure 9.8
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5
Module 9.8: Isotonic and isometric contractions
•
Isometric contraction (metric, measure)
•
Muscle length does not change and tension never
exceeds load
•
Contracting muscle bulges but not as much as
during isotonic contraction
•
•
Individual muscle fibers shorten only due to
connective tissues stretching
Example: postural muscle contractions
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An isometric contraction
Muscle
contracts
(isometric
contraction)
6 kg
6 kg
Figure 9.8
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6
Muscle tension and length dynamics
during an isometric contraction
Muscle
tension
(kg)
Peak tension
production
Contraction
begins
Resting length
Muscle
length
(percent
of resting
length)
Time
Figure 9.8
© 2011 Pearson Education, Inc.
6
Module 9.8 Review
a. Define isotonic contraction and isometric
contraction.
b. Can a skeletal muscle contract without
shortening? Why or why not?
c. Explain the relationship between load and
speed of muscle contraction.
© 2011 Pearson Education, Inc.
Module 9.9: ATP production in muscles
•
Three sources of ATP in muscles
1. Glycolysis (anaerobic: does not require oxygen)
•
Occurs in sarcoplasm
•
Produces 2 ATP and 2 pyruvate molecules for
each glucose
2. Aerobic metabolism
•
Provides 95% of ATP demands of resting muscle
cell
•
Occurs in mitochondria
•
•
Primarily through electron transport chain activity
Produces 17 ATP for each pyruvate
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The sites and processes of ATP production in cells
CYTOPLASM
Glucose
Glycolysis
Pyruvate
MITOCHONDRION
ADP +
phosphate
Citric acid
cycle
Aerobic metabolism
Electron
transport
system
MATRIX
Figure 9.9
© 2011 Pearson Education, Inc.
1
Module 9.9: ATP production in muscles
•
Three sources of ATP in muscles (continued)
3. Creatine phosphate (CP)
•
Creatine assembled from amino acids
•
Facilitates regeneration of ATP
•
ADP + CP  ATP + C
© 2011 Pearson Education, Inc.
Figure 9.9
© 2011 Pearson Education, Inc.
2
Module 9.9: ATP production in muscles
•
•
Muscles store few high-energy molecules
•
ATP
•
CP
Most energy stored as glycogen
•
May account for 1.5% of total muscle weight
•
Enables extended periods of muscle
contractions
© 2011 Pearson Education, Inc.
Module 9.9: ATP production in muscles
•
ATP demand and production at different activity
levels
•
At rest
•
Demand for ATP is low
•
Surplus ATP produced by mitochondria
•
•
Used to build up CP and glycogen reserves
At moderate activity levels
•
Demand for ATP increases
•
ATP production by mitochondria (aerobic
metabolism) meets demand
© 2011 Pearson Education, Inc.
Module 9.9: ATP production in muscles
•
ATP demand and production at different activity
levels (continued)
•
At peak activity levels
•
Mitochondria can provide only ~1/3 ATP demand
•
Glycolysis provides most ATP
•
Excess pyruvate converts to lactic acid (dissociates into
lactate and H+)
•
Decreases intracellular pH
•
Can affect enzymatic activities and cause fatigue
© 2011 Pearson Education, Inc.
Module 9.9 Review
a. Identify three sources of energy utilized by
muscle fibers.
b. How do muscle cells continuously synthesize
ATP?
c. Under what conditions do muscle fibers
produce lactic acid?
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Module 9.10: Muscle fatigue and recovery
•
Fatigue
•
When a muscle can no longer perform at the
required activity level
•
Decline in pH is a major factor
•
Decreases calcium/troponin binding
•
Alters enzyme activities
© 2011 Pearson Education, Inc.
Module 9.10: Muscle fatigue and recovery
•
Under conditions of insufficient oxygen
•
Glycolysis quickly produces ATP
•
Lowers pH due to lactic acid buildup
•
Faster ATP production than aerobic metabolism
•
•
Less efficient than aerobic metabolism
•
•
Only until glycogen reserves are depleted (1–2 min)
Only 4%–6% of energy captured from conversion of
glucose to pyruvate
Elevates body temperature
•
Triggers increased sweating
© 2011 Pearson Education, Inc.
Glycolysis, which enables a skeletal muscle to continue contracting
even when insufficient oxygen is available
OXYGEN INSUFFICIENT
Glycogen
Glucose
Glycolysis
(anaerobic)
Pyruvate
Lactate
MITOCHONDRION
Citric acid
cycle
Electron
transport
system
CYTOPLASM
Figure 9.10
© 2011 Pearson Education, Inc.
1
Module 9.10: Muscle fatigue and recovery
•
Under conditions of available oxygen
•
During recovery period, intracellular conditions return to
normal (can take hours to days)
•
Oxygen available in abundance
•
ATP production primarily through aerobic metabolism
•
More efficient than glycolysis
•
•
Heat produced
•
•
Fiber captures ~42% of energy released
~85% of heat needed for normal body temperature
Lactate converted back to pyruvate
•
Pyruvate can be used to generate ATP by mitochondria or used
to aid synthesis of glucose and glycogen reserves
© 2011 Pearson Education, Inc.
Aerobic metabolism, which is much more efficient than glycolysis
OXYGEN AVAILABLE
Glycogen
Glucose
70% converted
back to glucose
Pyruvate
30% broken
down for energy
MITOCHONDRION
Citric acid
cycle
Lactate
Electron
transport
system
CYTOPLASM
Figure 9.10
© 2011 Pearson Education, Inc.
2
Module 9.10: Muscle fatigue and recovery
•
Lactate cycling
•
During peak activity
•
Lactate produced by muscle fibers diffuses into
blood
•
Liver begins process of
•
Lactate  pyruvate  glucose
•
30% of pyruvate converted to ATP by mitochondria
•
70% of pyruvate converted to glucose
•
Ultimately, glucose is released into blood by liver
and returns to muscle cells
•
= Cori cycle
© 2011 Pearson Education, Inc.
Module 9.10: Muscle fatigue and recovery
•
Lactate cycling (continued)
•
During recovery period
•
Liver continues converting lactate to glucose and
returning to cells via blood
•
Glucose absorbed by skeletal muscle fibers and
replenishes glycogen reserves
•
From producing ATP in muscle cells and liver,
body oxygen demand is high
•
Oxygen debt (excess postexercise oxygen
consumption: EPOC)
•
© 2011 Pearson Education, Inc.
Amount of oxygen needed to return to pre-exertion
conditions
The production of lactate during peak activity, its conversion to glucose in the liver, and the rebuilding of
glycogen reserves in the muscles during recovery
Recovery
Peak Activity
Much of the large amounts of lactate
produced during peak exertion diffuses
out of the muscle fibers and into the
bloodstream. The liver absorbs this lactate
and begins converting it into pyruvate.
This process continues after exertion has ended, because lactate
levels within muscle fibers remain relatively high, and lactate
continues to diffuse into the bloodstream. After the absorbed
lactate is converted to pyruvate in the liver, roughly 30 percent of
the new pyruvate molecules are broken down in the
mitochondria, providing the ATP needed to convert the remaining
70 percent of pyruvate
molecules into
glucose. The
20–30%
glucose molecules
LIVER
are then released
into the circulation,
where they are
absorbed by skeletal
muscle fibers and used
to rebuild their glycogen
reserves.
70–80%
Glucose
Pyruvate
Lactate
Lactate
MUSCLE
Pyruvate
Glucose
Glucose
Glycogen reserves in muscle
Figure 9.10
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3
Module 9.10 Review
a. Define oxygen debt (excess postexercise
oxygen consumption).
b. What two processes are crucial in repaying a
muscle’s oxygen debt during the recovery
period?
c. After strenuous exercise, what causes the
“burning” sensation in skeletal muscles?
© 2011 Pearson Education, Inc.
Module 9.11: Skeletal muscle fiber types
• Three major types of skeletal muscle fibers
1. Fast fibers
•
Reach peak tensions in <0.01 sec
•
Large in diameter
•
Have densely packed myofibrils, large glycogen
reserves, few mitochondria
•
Powerful
•
Fatigue rapidly since most ATP produced
anaerobically
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Fast fibers in cross section
LM x 171
Figure 9.11
© 2011 Pearson Education, Inc.
1
Module 9.11: Skeletal muscle fiber types
• Three major types of skeletal muscle fibers
(continued)
2. Slow fibers
•
Half diameter of fast fibers
•
Take 3× as long to contract compared to fast fibers
•
Can maintain longer sustained contractions
•
Primarily use aerobic metabolism for ATP production
•
•
Increased oxygen reserves due to:
•
Extensive capillary network
•
Myoglobin pigment (stores O2 like hemoglobin)
Are dark red
© 2011 Pearson Education, Inc.
Slow fibers in cross section
LM x 171
Figure 9.11
© 2011 Pearson Education, Inc.
2
Module 9.11: Skeletal muscle fiber types
• Three major types of skeletal muscle fibers
(continued)
3. Intermediate fibers
•
More closely resemble fast fibers
•
Contain little myoglobin
•
Relatively pale
•
But more capillaries and more fatigue resistant
© 2011 Pearson Education, Inc.
Fast (W) and slow (R) fibers
in longitudinal section
TEM x 783
Figure 9.11
© 2011 Pearson Education, Inc.
3
Figure 9.11
© 2011 Pearson Education, Inc.
4
Module 9.11: Skeletal muscle fiber types
• Most muscles have a mixture of fiber types
• Percentages of each type vary
• According to muscle function
• Back and calf muscles dominated by slow fibers
• Eye or hand may have no slow fibers
• According to genetics
• Percentage of fast to slow inherited
• According to physical training
• Percentage of intermediate to fast can be modified
with athletic training
© 2011 Pearson Education, Inc.
Module 9.11 Review
a. Identify the three types of skeletal muscle
fibers.
b. Why would a sprinter experience muscle
fatigue before a marathon runner would?
c. Which type of muscle fiber would you expect to
predominate in the large leg muscles of
someone who excels at endurance activities,
such as cycling or long-distance running?
© 2011 Pearson Education, Inc.
CLINICAL MODULE 9.12: Factors and clinical
conditions affecting muscles
• Hypertrophy
• Increase in muscle size due to:
• Increase in myofilaments
• Increase in myofibril size
• Increase in mitochondria
• More glycogen and glycolytic enzymes
• As a result of repeated exhaustive stimulation
• Can be promoted by administration of steroid
hormones
© 2011 Pearson Education, Inc.
CLINICAL MODULE 9.12: Factors and clinical
conditions affecting muscles
• Atrophy
• Decrease in muscle size, tone, and power
• As a result of decreased stimulation such as
during:
• Paralysis by spinal injury
• Damage to nervous system
• Having body part in cast after bone fracture
• Initially reversible, but after prolonged disuse,
muscle fibers can die and not be replaced
© 2011 Pearson Education, Inc.
CLINICAL MODULE 9.12: Factors and clinical
conditions affecting muscles
• Clinical conditions
• Polio
• Virus attacks motor neurons of brain and spinal cord
causing paralysis (lost of voluntary movement)
• Tetanus
• Toxin from bacteria (Clostridium tetani) that suppresses
the mechanism inhibiting motor neuron activity
• Thrives in low-oxygen areas like deep punctured tissues
• Results in sustained, powerful contractions of affected
muscles
• Severe tetanus can have 40%–60% mortality
• Deaths rare due to immunization in U.S.
© 2011 Pearson Education, Inc.
CLINICAL MODULE 9.12: Factors and clinical
conditions affecting muscles
• Clinical conditions (continued)
• Botulism
• Toxin from bacteria (Clostridium botulinum) that
blocks ACh release at neuromuscular junctions
• Acquired through bacteria-contaminated food
• Myasthenia gravis
• Loss of ACh receptors at neuromuscular junctions
• Results in progressive weakness
© 2011 Pearson Education, Inc.
CLINICAL MODULE 9.12: Factors and clinical
conditions affecting muscles
• Clinical conditions (continued)
• Rigor mortis
• Generalized muscle contraction shortly after death
(2–7 hours)
• Begins with small muscles of face, neck, and arms
• Due to depletion of ATP, leaving myosin crossbridges attached to actin
• Ends 1–6 days later as muscular tissue
decomposes
© 2011 Pearson Education, Inc.
Four clinical conditions that
affect skeletal muscles
Polio: a virus affects motor neurons in the
spinal cord and brain, causing muscle
atrophy and paralysis
Tetanus: the bacterium Clostridium tetani releases a
powerful toxin that suppresses the mechanism that
inhibits motor neuron activity, causing sustained,
powerful contraction of skeletal muscles throughout
the body
Botulism: ingestion of a toxin produced by the bacterium
Clostridium botulinum paralyzes skeletal muscles by preventing
ACh release at neuromuscular junctions
Myasthenia gravis: loss of ACh receptors at the neuromuscular
junctions results in progressive muscular weakness
Figure 9.12
© 2011 Pearson Education, Inc.
3
CLINICAL MODULE 9.12 Review
a. Define muscle hypertrophy and muscle atrophy.
b. Six weeks after Fred broke his leg the cast is
removed, and as he steps down from the exam
table, his leg gives way and he falls. Propose a
logical explanation.
c. Explain how the flexibility or rigidity of a dead
body can provide a clue about a murder victim’s
time of death.
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