Chapter 10

Muscle Tissue

Lecture Presentation by
Lee Ann Frederick
University of Texas at Arlington

© 2015 Pearson Education, Inc.

 Outline
• Skeletal Muscles Structure
• Mechanisms of Contraction
• Contractions of Skeletal Muscle
• Motor Unit
• Energy Requirements of Skeletal Muscle
• Types of skeletal muscle
• Neural Control of Skeletal Muscles
• Bone
• Clinical application
Skeletal Muscles
 Introduction
• Muscle cells represent one of the four
basic tissue types of the human body.

• The collective skeletal muscles of the

body make up a substantial proportion
of total body weight, about 40% of
males and about 32% of females.

• Muscle tissues serve a range of

functions.
 4 Properties of Muscle
1. Contractility
Ability of a muscle to shorten with force

2. Excitability
Capacity of muscle to respond to a stimulus

3. Extensibility
Muscle can be stretched to its normal resting length
and beyond to a limited degree

4. Elasticity
Ability of muscle to recoil to original resting length
after stretched
 Classification of muscle

1. “Voluntary” muscles: the actions can be directed by our thoughts via

nervous system (skeletal muscles);

2. “Involuntary” muscles: the actions are not under conscious control.

Their functions are directed by the autonomic nervous system (cardiac
and smooth muscles);
 Classification of 3 Muscle Tissue Types
1. Skeletal
– Attached to bones
– Nuclei multiple and peripherally
located
– Striated, Voluntary and involuntary
(reflexes)

2. Smooth
– Walls of hollow organs, blood vessels,
eye, glands, skin
– Single nucleus centrally located
– Not striated, involuntary, gap
junctions in visceral smooth

3. Cardiac
– Heart
– Single nucleus centrally located
– Striations, involuntary, intercalated
disks
 Comparison of Skeletal, Cardiac, and Smooth
Muscle Tissues.

Sarcomeres are contractile units of skeletal muscle consisting of components between 2 Z discs
SR = Sarcoplasmic Reticulum (membrane bound structures found in muscle that stores Ca2+)
 Skeletal Muscle Structure
• Most distinctive feature of skeletal muscle is its striations and
multinucleate
 Skeletal Muscle Action
• When a muscle contracts, it
shortens.
– This places tension on
tendons connecting it to a
bone.
– This moves the bone at a
joint.
– The bone that moves is
attached at the muscle
insertion (distal to body).
– The muscle is attached to
a bone that does not
move at the muscle origin
(closer to body).
 Skeletal Muscles
• Flexor muscles decrease the angle
between two bones at a joint.

• Extensor muscles increase the angle

between two bones at a joint.
– The main muscle responsible for movement in
a given direction is the agonist (i.e. the
muscle that is contracting).
– Flexors and extensors that work together are
antagonists.
 Skeletal Muscle Structure
• Muscle fibers are
muscle cells

– Ensheathed by thin
connective tissue
layer called
endomysium

• Plasma membrane is
called sarcolemma

• Muscle fibers are

similar to other cells
except are
multinucleate and
striated

Sarcolemma =fine transparent tubular sheath which envelops the fibres of skeletal muscles.
1. Definitions of sarcolemma = the plasma membrane of the muscle fibre.
2. Definition of sarcomere = the smallest basic unit of the muscle
3. Definition of myofibril = long, cylindrical structures which contains the
thick and thin filaments. One myofibril contains 10,000 sarcomeres.
4. Muscle fibers = muscle cells
Mechanisms of Contraction
 Structure of Muscle Fiber
• Each fiber is packed with myofibrils
– Myofibrils are 1 in diameter and extend length of fiber
• Packed with myofilaments
– Myofilaments are composed of thick and thin filaments that give
rise to bands which underlie striations
 Structure of Myofibril
• A band is dark,
corresponds to the length of
thick filaments (mostly
myosin)
– Light area at center of A band
is H zone
• = area where actin and
myosin don’t overlap

• I band is light, corresponds

to the distance between A
bands, contain thin
filaments (mostly actin)
• At center of I band is Z
line/disc where actins attach
 Sarcomeres
• Sarcomeres are contractile units of skeletal muscle consisting of
components between 2 Z discs

• M lines are structural proteins that anchor myosin during contraction

• Titin is elastic protein attaching myosin to Z disc that contributes to elastic

recoil of muscle
How Fiber Contracts
 Sliding Filament Theory of Contraction
• During contraction:

• Two A bands (containing

shorten
actin) move closer together, Do not shorten

each do not shorten shorten

• I bands shorten because

they define distance between
A bands of successive
sarcomeres

• H bands (containing myosin)

shorten

• Muscle contraction occurs

because
• thin filaments slide over and
between thick filaments →
center: Shortening distance
Distance Shorten from Z to Z
from Z disc to Z disc
 Sliding Filament Theory of Contraction
• During contraction:

• Two A bands (containing

actin) move closer together,
each do not shorten

• I bands shorten because

they define distance between
A bands of successive
sarcomeres

• H bands (containing myosin)

shorten

• Muscle contraction occurs

because thin filaments slide
over and between thick
Distance Shorten Distance Shorten
filaments towards center: from Z to Z from Z to Z
Shortening distance from Z
disc to Z disc Bands ‘HI’ shorten
Cross Bridge
Cross Bridge
NOTE: In the video, you will see ADP release first then power stroke, in ppt you will read power stroke first then ADP release.
Either is fine. In the video you will hear “Step 2,the power stroke, ADP is released AND the activated myosin head pivots, sliding
the thin myofilament toward the centre of the sarcomere.” This indicates that BOTH ADP release and myosin head moving.
 Control of Contraction
• Control of cross bridge attachment to actin is via troponin-tropomyosin system

– Serves as a switch for muscle contraction and relaxation

– The filament tropomyosin lies in grove between double row of G-actins (that
make up actin thin filament)

– Troponin complex is attached to tropomyosin at intervals of every 7 actins

• In relaxed muscle, tropomyosin blocks binding sites on actin so crossbridges can’t

occur
– This occurs when Ca2+ levels are low

• Contraction can occur only when binding sites

are exposed
SUMMARY OF SLIDING FILAMENT THEORY

1) A myofiber, together with all its myofibrils, shortens by movement of the

insertion toward the origin of the muscle.

2) Shortening of the myofibrils is caused by shortening of the sarcomeres-the

distance between Z lines (or discs) is reduced.

3) Shortening of the sarcomeres is accomplished by sliding of the

myofilaments—the length of each filament remains the same during
contraction.

4) Sliding of the filaments is produced by asynchronous power strokes of

myosin cross bridges, which pull the thin filaments (actin) over the thick
filaments (myosin).

5) The A bands remain the same length during contraction, but are pulled
toward the origin of the muscle.

6) Adjacent A bands are pulled closer together as the I bands between them
shorten.

7) The H bands shorten during contraction as the thin filaments on the sides
of the sarcomeres are pulled toward the middle.
 Excitation-Contraction Coupling
Neuromuscular Junction (NMJ)
• Includes the single synaptic
ending of the motor
neuron innervating each
muscle fiber and
underlying specializations
of sarcolemma

• Place on sarcolemma
where NMJ occurs is the
motor end plate
 1 2
The cytoplasm of the axon The stimulus for ACh release
terminal contains vesicles filled is the arrival of an electrical
with molecules of acetylcholine, impulse, or action potential,
or ACh. Acetylcholine is a at the axon terminal. An action
neurotransmitter, a chemical potential is a sudden change in
released by a neuron to change the membrane potential that
the permeability or other travels along the length of the
properties of another cell’s plasma axon.
membrane. The synaptic cleft and
the motor end plate contain
molecules of the enzyme
acetylcholinesterase (AChE),
Arriving action
which breaks down ACh.
Vesicles ACh potential

The synaptic cleft is a

narrow space that separates
the axon terminal of the
neuron from the opposing
motor end plate.
Junctional AChE
fold of
motor end plate
3 4 5
When the action potential ACh molecules diffuse across the The sudden inrush of sodium ions
reaches the neuron’s axon synaptic cleft and blind to ACh results in the generation of an
terminal, permeability receptors on the surface of the action potential in the sarcolemma.
changes in its membrane motor end plate. ACh binding ACh is removed from the
trigger the exocytosis of ACh alters the membrane’s permeabil- synaptic cleft in two ways. ACh
into the synaptic cleft. ity to sodium ions. Because the either diffuses away from the
Exocytosis occurs as vesicles extracellular fluid contains a high synapse, or it is broken down by
fuse with the neuron’s plasma concentration of sodium ions, AChE into acetic acid and choline.
membrane. and sodium ion concentration This removal inactivates the ACh
inside the cell is very low, sodium receptor sites. The muscle fiber
ions rush into the cytosol. pictured above indicates the
Motor propagation of the action
end plate potential along the sarcolemma.

Na+ Action
potential

Na+
Na+ Break down AChE
ACh
of ACh
receptor site
 Excitation-Contraction Coupling
• Skeletal muscle
sarcolemma is
excitable
– Conducts Action
Potentials

• Release of ACh at
NMJ causes large
depolarizing end-
plate potentials and
APs in muscle

• APs race over

sarcolemma and
down into muscle
via T tubules
 Excitation-Contraction Coupling
• T tubules are extensions of
sarcolemma

• Ca2+ channels in SR 4 are

mechanically linked to
channels in T tubules 3

• APs in T tubules cause V-

gated channels to change
shape and Ca2+ release
channels to release Ca2+
– Called electromechanical
release
– channels are 10X larger
than nerve V-gated
channels
Excitation-Contraction Coupling
Relationship of the Action Potential

Relationship of the action potential, the

increase in intracellular [Ca2+ ], and muscle
contraction in skeletal muscle.
© 2015 Pearson Education, Inc.
 Muscle Relaxation

• Action potentials cease.

• Ca2+-ATPase pumps move Ca2+ back into SR.

• No more Ca2+ is available to bind to troponin C, so

no more cross bridges are formed.
 Motor Unit
a. One motor
neuron branches
to innervate a
variable # of
muscle fibers

b. A single motor
unit: includes a
branched motor
axon and the all
muscle fibers it
innervates
 Motor Unit
• When one motor neuron is activated, all muscle fibers in its
motor unit contract

• Number of muscle fibers in motor unit varies according to degree

of fine control capability of the muscle

• Contraction strength comes from motor unit recruitment.

– Finer muscle control requires smaller motor units (fewer muscle
fibers).
• The eye muscles may have ~20 muscle fibers/motor units.
• Larger, stronger muscles may have motor units with thousands of
muscle fibers.
• Control and strength are trade-offs.
Energy Requirements of
Skeletal Muscles
 Where Muscles Get Their Energy
• At rest and for mild exercise:
from fatty acids

• For moderate exercise:

equally from fatty acids and
glycogen stores

• For heavy exercise: mostly

from glycogen stores and
blood glucose.
We use fats first because it contains
more energy and is readily available in
muscles and blood.
 Where Muscles Get Their Energy
As exercise intensity and duration Glucose uptake in leg muscle during
increase, GLUT4 channels are exercise with a cycle ergometer.
inserted into the sarcolemma to
allow more glucose into cells.

Note that the uptake of blood glucose increases with the intensity of the
exercise (measured in Watts) and with the exercise time.
The increased uptake is largely due to the ability of muscle contraction to
increase the amount of GLUT4 carriers in the sarcolemma.
 Maximal Oxygen Uptake/Consumption
• Also called aerobic capacity, or VO2 max

• Determines whether a given exercise intensity is light,

moderate, or heavy for a given person

• Determined by a person’s age, sex, size, and athletic training

– Greater for males and younger people
– Ranges from 12 ml O2/minute/kg body weight to 84 ml
O2/minute/kg body weight
 Lactate Threshold (LT)
• Also called anaerobic threshold

• Another way to determine exercise intensity for a given

person

• % of maximal oxygen uptake at which a rise in blood

lactate levels occurs

• Occurs at about 50−70% VO2 max (e.g. when you

achieve 80% heart rate or 70% maximum O2 intake,
that’s when lactate will start to increase).

• Potential causes of lactate threshold.

➢ Low muscle oxygen.
➢ Accelerated glycolysis. LT (if you exercise
➢ Recruitment of fast-twitch fibres (fast fatigue muscles) below the LT level, any
➢ Reduced rate of lactate removal lactate produced by
muscles is removed by
• Significance: body). If you keep
The lactate threshold has practical uses such as exercising, eventually
1) in performance prediction and lactate builds up where
2) as a marker of training. it can’t be broken down
 Oxygen Debt

When exercise stops, rate of oxygen uptake does not

immediately return to pre-exercise levels in order to pay the
oxygen debt.
In other words, breathing rate continues after exercise to repay this debt.

Oxygen debt accumulates during exercise because:

1. When oxygen is withdrawn from hemoglobin and myoglobin
(myoglobin = O2 storage molecule, gives fibers its red color)
2. And because of O2 is needed for metabolism of lactic acid
produced by anaerobic respiration
Types of Skeletal Muscle
 Slow- and Fast-Twitch Fibers
• Skeletal muscle fibers can be divided on basis of contraction
speed (time to reach max tension) and resistance to fatigue:
1. Slow-twitch, slow fatigue (Type I fibers) e.g. soleus muscle
2. Fast-twitch, fast fatigue (Type IIA and IIX fibers) e.g. eye muscle

a=fast twitch (extraocular), b=gastrocnemius muscle, and c=slow-twitch soleus

 Type I Fibers (slow twitch) e.g. soleus
• Type I fibers also called red slow
oxidative fibers (e.g. soleus muscle)

• Adapted to contract slowly without

fatigue
– Mostly aerobic respiration
– Rich capillary supply,
– Many mitochondria, and aerobic enzymes
– Lots of myoglobin (O2 storage molecule)
• Gives fibers red color
• Have small motor neurons with small
motor units
 Type II Fibers (fast twitch)
1. Type IIX fibers (or white fast glycolytic fibers)
(e.g. eye muscles)
• Contracts fast
• Uses anaerobic metabolism
– Has large stores of glycogen, few capillaries and mitochondria, little
myoglobin

2. Type II A fibers (or red fast oxidative fibres)

(e.g. gastrocnemius muscle)
• Contracts fast
• Uses aerobic metabolism
• Intermediate to Type I and Type IIX
• Have large motor neurons with large motor units
Table 10-2 Properties of Skeletal Muscle Fiber Types.

Type II X
 Muscle Fatigue

Reduced ability to generate force due to:

– Accumulation of extracellular K+, reducing

membrane potential
• Short duration
– Depletion of stored glycogen
– Reduced SR calcium release
 Muscle Fatigue

1. Lactic acid accumulation and lower pH

2. Increased concentration of PO4 due to phosphocreatine
breakdown
3. Less ATP (slightly lower than when muscle was at rest)
4. Buildup of ADP
5. Fatigue of upper motor neurons, called central fatigue
(=Mental fatigue that develops during prolonged exercise
and is attributed to impaired function of the central
nervous system)
 Adaptation to Endurance
Exercise Training
Effects of Endurance Training on Skeletal Muscles
1. Improved ability to obtain ATP from oxidative phosphorylation
2. Increased size and number of mitochondria
3. Less lactic acid produced per given amount of exercise
4. Increased myoglobin content
5. Increased intramuscular triglyceride content
6. Increased lipoprotein lipase (enzyme needed to utilize lipids)
7. Increased proportion of energy derived from fat; less from carbohydrates
8. Lower rate of glycogen depletion during exercise
9. Improved efficiency in extracting oxygen from blood
10. Decreased number of type IIX (fast glycolytic) fibers; increased number
of type IIA (fast oxidative) fibers
Adaptation to Strength Training
• Hypertrophy: Type II muscle fibers become thicker due
to increased amount of actin and myosin (more
sarcomeres).

– Thicker fibers may split into two fibers, which can also
increase in size.

– Requires the addition of three more proteins that

serve as muscle fiber scaffolding:
1) Titin (protein attaching myosin to Z disc )
2) Nebulin (protein associated with actin)
3) Obscurin (protein that surround Z discs)
 Muscle Repair

• Skeletal muscles have stem cells called

satellite cells located near muscle fibers.

• These can fuse to damaged muscle cells and

repair them or fuse to each other to form new
muscle fibers.

• Myostatin is a paracrine regulator that inhibits

satellite cells.
 Muscle Decline with Aging
• Reduced muscle mass (usually type II fibers)
– Can be helped with strength training

• Reduction in capillary blood supply

– Can be helped with endurance training

• Fewer satellite cells

• Increased myostatin production (paracrine

regulator that inhibits satellite cells)
Neural Control of Skeletal
Muscles
 Neural Control of Skeletal Muscles
Motor neuron cell bodies are in ventral horn of
spinal cord; axons leave in ventral root

Ventral horn

These are called lower motor neurons and the final common
pathway

Activity influenced by
1) Sensory information from muscles and tendons,
2) Upper motor neuron (brain) which facilitates and
inhibits activity
 Sensory Feedback

To control skeletal muscle movements, NS must receive

continuous sensory feedback from:

1. Golgi tendon organs: respond to tension a

muscle puts on a tendon

2. Muscle spindle apparatus: respond to muscle

length
– Muscles that require more control have more spindles.
– Stretching a muscle causes spindles to stretch.
 Muscle Spindle Apparatus
• Contains thin muscle
cells called intrafusal
fibers
• Two types:
– Nuclear bag fibers
– Nuclear chain fibers

• Two types of sensory

cells wrap around the
fibers:
– Primary (annulospiral)
– Secondary (flower-
spray) stimulated if
sustained stretch.
When a muscle stretches → spindles stretch → both
– Both activated if the primary (1st) and secondary sensory endings.
sudden stretch
 Monosynaptic-Stretch Reflex
• Consists of only 1 synapse
within CNS

• Striking patellar ligament

passively stretches spindles
activating annulospiral
sensory neurons

• Which synapse on alphas

causing them to stimulate
extrafusals

• Produces knee-jerk reflex

 Golgi Tendon Organ Reflex
• Involves 2 synapses in the
CNS (=disynaptic reflex)

• Sensory axons from Golgi

tendon organ synapse on
interneurons
– Which make inhibitory
synapses on motor
neurons
Golgi tendon organs continuously monitors tension.
• Prevents excessive muscle
This inhibitory reflex helps prevent dangerous tension
contraction or passive
on a tendon from excessive muscle contraction.
muscle stretching
If you add more tension on a tendon or if a muscle is
stretched extensively, it will actually relax as a result
of the Golgi tendon organs.
Huntington's disease
i) Degeneration of the caudate nucleus
ii) Produces involuntary movements called
chorea=a hyperkinetic disorder
iii) Random, quick, uncontrolled, jerky
movements

Parkinson’s Disease
i) Degeneration of dopaminergic neurons from
the substantia nigra to the caudate nucleus (small
nucleus in the midbrain),
ii) Rigidity, Resting tremor, and difficulty in
initiating voluntary movements, slow movement.
iii) Treated with l-dopa (the precursor of
dopamine) or dopamine agonists.

However, l-dopa have side effects → dyskinesia

(an involuntary movements)
Bone
 Structural Features of Human Bone
• Two types of bone tissues:
➢ compact bone and spongy bone
➢ both present in a typical bone

• Compact bone:
➢ dense and solid
➢ basic functional unit: osteon (or called Haversian system)
➢ directional arrangement of osteons makes the bone strong

65
A Long Bone

66
Structure of Bone

67
 Structural Features of Human Bone (cont’d)
• Spongy bone:
➢ Less dense; an open network
➢ Characterized by the presence of bone plates, called
trabeculae
➢ No blood vessel and osteon
➢ Osteocytes get the nutrients via diffusion from canaliculi
of compact bone
➢ Functions:
▪ to withstand stresses from many directions
▪ to reduce weight of skeleton  easier for muscular
movement
▪ to supports the cells in bone marrow 68
Functions of Different Bone Cells (A Brief Summary)

69
 Remodeling of Bone
• The organic and mineral components of bone matrix are
continuously being recycled and renewed (remodeling)
• Throughout life
• Balanced activities involve osteocytes, osteoblasts and
osteoclasts
(Each year, 1/5 of adult skeleton is demolished and
rebuilt)
• Homeostasis of Ca2+ balance* Over balance of Ca2+
depends on hormonal actions: parathyroid hormone
(parathyroid gland) and calcitonin (thyroid gland)*,
calcitriol (kidney)

*(see hormone slides) 70