Download Notes: How Muscles Work

The Muscular System
Chapter 7
There are four characteristics associated
with muscle tissue:
 Excitability
- Tissue can receive & respond to stimulation
 Contractility
- Tissue can shorten & thicken
 Extensibility
- Tissue can lengthen
 Elasticity
- After contracting or lengthening, tissue
always wants to return to its resting state
The characteristics of muscle tissue enable it to
perform some important functions, including:
 Movement – both voluntary & involuntary
 Maintaining posture
 Supporting soft tissues within body cavities
 Guarding entrances & exits of the body
 Maintaining body temperature
Types of muscle tissue:
Skeletal muscle tissue
• Associated with & attached to the skeleton
• Under our conscious (voluntary) control
• Microscopically the tissue appears striated
• Cells are long, cylindrical & multinucleate
-c
•Rapid onset, rapid fatigue
Cardiac muscle tissue
• Makes up myocardium of heart
• Unconsciously (involuntarily) controlled
• Microscopically appears striated
• Cells are short, branching & have a single nucleus
• Cells connect to each other at intercalated discs
•Slower onset, fatigue resistant, can’t tetanize
Smooth (visceral) muscle tissue
• Makes up walls of organs & blood vessels
• Tissue is non-striated & involuntary
• Cells are short, spindle-shaped & have a single
nucleus
• Tissue is extremely extensible, while still retaining
ability to contract
•Slow onset, fatigue resistant
Anatomy of a Skeletal Muscle
Entire muscle is surrounded by epimysium
(fibrous ct)—at the end forms a tendon
Contains blood vessels and nerves
 Made up of fascicles (bundles of muscle
fibers) surrounded by perimysium
 Fascicles made up of muscle fibers
surrounded by endomysium
 Fibers are the cells-made of myofibrils

Sarcolemma—muscle cell membrane
 Sarcoplasm—cytoplasm-many
mitochondria, many nuclei

Myofibrils are surrounded by sarcoplasmic
reticulum which stores Ca needed for
contraction
 Myofibrils are bundles of thick filaments
(myosin) and thin filaments (actin)

 Repeating
units of these filaments form a
sarcomere
 Interactions between the myosin and actin
filaments produce contraction
Organization of Skeletal Muscles
Anatomy of skeletal muscles
epimysium
tendon
perimysium
Muscle
Fascicle
Surrounded by
perimysium
Skeletal
muscle
Surrounded by
epimysium
endomysium
Skeletal
muscle
fiber (cell)
Surrounded by
endomysium
Play IP Anatomy of Skeletal muscles (IP p. 4-6)
Microanatomy of a Muscle Fiber
Microanatomy of a Muscle Fiber (Cell)
transverse
(T) tubules
sarcoplasmic
reticulum
sarcolemma
terminal
cisternae
mitochondria
myoglobin
thick myofilament
thin
myofilament
myofibril
nuclei
triad
Muscle fiber
sarcomere
Z-line
myofibril
Thin filaments
Thick filaments
Thin myofilament
Myosin molecule of
thick myofilament
Myofilaments of sarcomere
Z line
Z line
Thin
myofilaments
M line
Thick myofilaments
Muscle contraction
Under control of nervous system
 Nerves and skeletal muscle fiber connect
at neuromuscular junctions
 Neuron branches out and ends in
expanded knobs-synaptic knobs which
contain a neurotransmitter Acetylcholine
(Ach) that changes the sarcolemma and
triggers contraction

Neuromuscular junction
telodendria
Synaptic
terminal
(end bulb)
Synaptic
vessicles
containing
Ach
Synaptic cleft
Neuromuscular
junction
Motor end plate
of sarcolemma
Muscle contraction
1. electrical impulse from brain
 2. release of Ach
 3. triggers Ca ions to be released from SR
into sarcoplasm
 4. linkages (cross bridges) form between
the actin and myosin filaments –requires
ATP
 5. actin filaments slide inward along
myosin filaments
 6.muscle fiber shortens (contraction)

Sliding Filament Theory
• Myosin heads attach to actin molecules (at binding (active) site)
• Myosin “pulls” on actin, causing thin myofilaments to slide
across thick myofilaments, towards the center of the sarcomere
• Sarcomere shortens, I bands get smaller, H zone gets smaller, &
zone of overlap increases
relaxation
1. cholinesterase is secreted and causes
ACh to decompose
 2. Ca are pumped back into SR
 3. linkages between actin and myosin
broken
 4. actin and myosin slide apart
 5. muscle relaxes

Muscle mechanics
All or none response
 A muscle fiber contracts or doesn’t
 The amount of tension produced by a
whole muscle is determined by the
frequency of stimulation and the # of fibers
stimulated


Twitch—single stimulus contraction
relaxation sequence
 Latent
period-getting ready
 Contraction-tension rises to a peak
 Relaxation-tension falls to resting lines
contraction
latent
relaxation
Summation-(sustained contraction)-stimuli
arrive before relaxation complete
 Complete tetanus-(sustained powerful
contraction)-frequency of stimulation so
high-relaxation eliminated
 Motor unit- all muscle fibers controlled by a
single neuron (finer control, fewer muscle
fibers)

 The size of the motor unit determines how fine the control of
movement can be –
small motor units  precise control (e.g. eye muscles
large motor units gross control (e.g. leg muscles)
 Recruitment is the
ability to activate more
motor units as more
force (tension) needs to
be generated
 There are always some motor
units active, even when at rest.
This creates a resting tension
known as muscle tone, which
helps stabilize bones & joints, &
prevents atrophy
PLAY
Play IP Contraction of motor units p. 3-7
Recruitment- increased tension produced
by increase in the number of motor units
 muscle tone-resting tension
 Isotonic contraction-increased tension to
move resistance (lifting, walking, running)
 Isometric contraction-resistance doesn’t
move (pushing against wall, maintaining
posture)


Muscle fatigue-muscles cannot contract
due to:
 Exhaustion
of ATP
 Damage to SR
 Decrease in oxygen
 Decreased blood flow
Recovery period-return to preexertion
levels
 Oxygen debt-breathing rate increases until
homeostasis is reached (preexertion level)
 Hypertrophy

 Increased
muscle size due to increased
numbers of mitochondria, myofibrils, and
glycogen reserves
 Due to repeated exhaustive stimulation

Atrophy
 Muscle
not stimulated on a regular basis
 Loss of muscle tone and mass
Muscle performance







Types of Fibers
1. fast- contract .01 seconds or less, large, powerful
contractions, fatigue rapidly, “white color”
2. Slow- ½ size of fast, takes 3 times longer to contract,
increased endurance, increased blood flow, red pigment
(myoglobin) carries oxygen darker in color
3. intermediate- pale, more capillaries than fast fibers,
resistant to fatigue
Humans are a mixture of types.
Fast & intermediate in eyes & hand
Slow in legs
Physical Conditioning
Increased blood flow improves oxygen and
nutrient availability
 Anaerobic endurance-fast fibers, brief
intensive workouts that stimulate
hypertrophy
 Aerobic endurance-sustained low level
workouts, jogging, distance swimming,
warm up to increase blood flow & treppe

Hormones for muscles

1. growth hormone & testosterone
 Increase
synthesis of proteins and
enlargement of muscles

2. thyroid hormone
 Increases

the rate of energy consumption
3. Adrenaline
 Stimulates
muscle metabolism and increases
the duration of stimulation and force of
contraction
Aging
Muscle fibers decrease in diameter due to
a decrease in myofibrils
 Decrease in ATP, strength and endurance
 Increased fibrous connective tissue-less
flexible
 Rapid fatigue, may overheat
 Decreased healing, increased scar tissue

Thin Myofilament
(myosin binding site)
Thick myofilament
(has ATP
& actin
binding
site)
*Play IP sliding filament theory p.5-14 for overview of thin &
thick filaments
Sarcomere
A band
Z line
Z line
H zone
I band
Thin
myofilaments
Zone of
overlap
Thick
myofilaments
M line
Zone of
overlap
• As sarcomeres shorten, myofibril shortens. As myofibrils shorten,
so does muscle fiber
• Once a muscle fiber begins to contract, it will contract maximally
• This is known as the “all or none” principle
Physiology of skeletal muscle contraction
• Skeletal muscles require stimulation from the nervous
system in order to contract
• Motor neurons are the cells that cause muscle fibers to
contract
cell body
dendrites
axon
(motor neuron)
telodendria
Synaptic terminals
(synaptic end bulbs)
Overview of Events at the neuromuscular junction
• An action potential (AP), an electrical impulse, travels down
the axon of the motor neuron to the end bulbs (synaptic
terminals)
•Release of Acetylcholine (Ach) into the synaptic cleft
• Ach diffuses across the synaptic cleft & binds to Ach receptors
on the motor end plate
• The binding of Ach to its receptors causes a new AP to be
generated along the muscle cell membrane
• Immediately after it binds to its receptors, Ach will be broken
down by Acetylcholinesterase (AchE) – an enzyme present in
the synaptic cleft
Action potential
Arrival of an action potential
at the synaptic terminal
Axon
Arriving action potential
Synaptic terminal
Sarcolemma
Vesicles
ACh
Synaptic
cleft
Sarcolemma of
motor end plate
AChE molecules
ACh
receptor
site
Muscle
fiber
• An action potential (AP), an electrical impulse, travels down the
axon of the motor neuron to the end bulbs (synaptic terminals)
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 7-4(b-c)
2 of 5
Action potential
Arrival of an action potential
at the synaptic terminal
Axon
Arriving action potential
Synaptic terminal
Sarcolemma
Vesicles
ACh
Synaptic
cleft
Sarcolemma of
motor end plate
AChE molecules
ACh
receptor
site
Muscle
fiber
Release of acetylcholine
Vesicles in the synaptic terminal fuse
with the neuronal membrane and dump
their contents into the synaptic cleft.
•Release of Acetylcholine (Ach) into the
synaptic cleft
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 7-4(b-c)
3 of 5
Action potential
Arrival of an action potential
at the synaptic terminal
Axon
Arriving action potential
Synaptic terminal
Sarcolemma
Vesicles
ACh
Synaptic
cleft
Sarcolemma of
motor end plate
AChE molecules
ACh
receptor
site
ACh binding at the
motor and plate
Release of acetylcholine
Vesicles in the synaptic terminal fuse
with the neuronal membrane and dump
their contents into the synaptic cleft.
Muscle
fiber
The binding of ACh to the receptors
increases the membrane permeability to
sodium ions. Sodium ions then rush
into the cell.
Na+
•Ach diffuses across
the synaptic cleft &
binds to Ach
receptors on the
motor end plate
Na+
Na+
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 7-4(b-c)
4 of 5
•The binding of Ach to its receptors
causes a new AP to be generated along
the muscle cell membrane
•Immediately after it binds to its receptors,
Ach will be broken down by
Acetylcholinesterase (AchE) – an enzyme
present in the synaptic cleft
Action potential
Arrival of an action potential
at the synaptic terminal
Axon
Arriving action potential
Synaptic terminal
Sarcolemma
Vesicles
ACh
Synaptic
cleft
Sarcolemma of
motor end plate
AChE molecules
ACh
receptor
site
ACh binding at the
motor and plate
Release of acetylcholine
Vesicles in the synaptic terminal fuse
with the neuronal membrane and dump
their contents into the synaptic cleft.
Muscle
fiber
The binding of ACh to the receptors
increases the membrane permeability to
sodium ions. Sodium ions then rush
into the cell.
Appearance of an action
potential in the sarcolemma
An action potential spreads across the
surface of the sarcolemma. While this
occurs, AChE removes the ACh.
Action
potential
Na+
Na+
Na+
 Play IP neuromuscular junction p. 14
Physiology of Skeletal Muscle Contraction
•Once an action potential (AP) is generated
at the motor end plate it will spread like an
electrical current along the sarcolemma of
the muscle fiber
• The AP will also spread into the T-tubules,
exciting the terminal cisternae of the
sarcoplasmic reticula
•This will cause Calcium (Ca+2 ) gates in the
SR to open, allowing Ca+2 to diffuse into the
sarcoplasm
•Calcium will bind to troponin (on the thin
myofilament), causing it to change its
shape. This then pulls tropomyosin away
from the active sites of actin molecules.
•The exposure of the active sites allow the
sliding of the filaments
Table 7-1
Physiology of skeletal muscle contraction – events
at the myofilaments
Resting sarcomere
ADP
+
P
Myosin head
Active-site exposure
ADP
+ P
Sarcoplasm
Troponin
Actin
ADP
+
Ca2+
Tropomyosin
Cross-bridge formation
Ca2+
Active site
ADP
P +
Myosin reactivation
P
Ca2+
ADP Ca2+
P +
ADP
P +
Cross bridge detachment
Pivoting of myosin head
ATP
ADP
+ P
ADP + P
Ca2+
Ca2+
Ca2+
ADP
P +
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Ca2+
Ca2+
ATP
Ca2+
ADP + P
Figure 7-5
1 of 7
Resting sarcomere
ADP
+
P
Myosin head
Active-site exposure
ADP
+ P
Sarcoplasm
Troponin
Ca2+
Tropomyosin
Actin
Active site
ADP
P +
Ca2+
ADP
P +
• Calcium (Ca+2 ) gates in the SR open, allowing Ca+2 to
diffuse into the sarcoplasm
• Calcium will bind to troponin (on the thin myofilament),
causing it to change its shape.
• This then pulls tropomyosin away from the active sites of
actin molecules.
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 7-5
3 of 7
Resting sarcomere
ADP
+
P
Myosin head
Active-site exposure
ADP
+ P
Sarcoplasm
Troponin
Actin
ADP
+
Ca2+
Tropomyosin
Cross-bridge formation
P
Ca2+
Active site
ADP
P +
Ca2+
ADP
ADP Ca2+
P +
P +
• Myosin heads are “energized” by the presence of ADP + PO43at the ATP binding site (energy is released as phosphate bond of
ATP breaks)
• Once the active sites are exposed, the energized myosin
heads hook into actin molecules forming cross-bridges
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 7-5
4 of 7
Resting sarcomere
ADP
+
P
Myosin head
Active-site exposure
ADP
+ P
Sarcoplasm
Troponin
Actin
ADP
+
Ca2+
Tropomyosin
Cross-bridge formation
P
Ca2+
Active site
ADP
P +
Ca2+
ADP Ca2+
P +
ADP
P +
Pivoting of myosin head
• Using the stored energy, the attached
myosin heads pivot toward the center of
the sarcomere
• The ADP & phosphate group are
released from the myosin head
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
ADP + P
Ca2+
Ca2+
ADP + P
Figure 7-5
5 of 7
Resting sarcomere
ADP
+
P
Myosin head
Active-site exposure
ADP
+ P
Sarcoplasm
Troponin
Actin
ADP
+
Ca2+
Tropomyosin
Cross-bridge formation
Ca2+
Active site
ADP
P +
• A new molecule of
ATP binds to the
myosin head, causing
the cross bridge to
detach from the actin
strand
Ca2+
ADP Ca2+
P +
ADP
P +
Cross bridge detachment
Pivoting of myosin head
ATP
ADP + P
Ca2+
Ca2+
Ca2+
• The myosin head will
get re-energized as the
ATP  ADP+P
P
ATP
Ca2+
ADP + P
• As long as the active sites are still exposed, the myosin head can bind
again to the next active site
Resting sarcomere
ADP
+
P
Myosin head
Active-site exposure
ADP
+ P
Sarcoplasm
Troponin
Actin
P
Ca2+
Active site
ADP
P +
Myosin reactivation
Ca2+
ADP Ca2+
P +
ADP
P +
Cross bridge detachment
Pivoting of myosin head
ATP
ADP
+ P
ADP + P
Ca2+
Ca2+
Ca2+
ADP
P +
PLAY
ADP
+
Ca2+
Tropomyosin
Cross-bridge formation
Ca2+
Ca2+
ATP
IP Sliding filament theory – p. 17-24 single cross bridge;
p. 27 multiple cross bridges
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Ca2+
ADP + P
Figure 7-5
7 of 7
Physiology of Skeletal Muscle Contraction
• If there are no longer APs generated on
the motor neuron, no more Ach will be
released
• AchE will remove Ach from the motor end
plate, and AP transmission on the muscle
fiber will end
• Ca+2 gates in the SR will close & Ca+2 will
be actively transported back into the SR
• With Ca+2 removed from the sarcoplasm
(& from troponin), tropomyosin will re-cover
the active sites of actin
• No more cross-bridge interactions can
form
• Thin myofilaments slide back to their
resting state
Table 7-1
Key Note
Skeletal muscle fibers shorten as thin
filaments interact with thick filaments and
sliding occurs. The trigger for contraction is
the calcium ions released by the SR when
the muscle fiber is stimulated by its motor
neuron. Contraction is an active process;
relaxation and the return to resting length is
entirely passive.
These physiological processes describe what
happen at the cellular level – how skeletal
muscle fibers contract
But what about at the organ level? How do
skeletal muscles (like your biceps brachii)
contract to create useful movement?
• Skeletal muscles are made up of thousands of muscle
fibers
• A single motor neuron may directly control a few fibers
within a muscle, or hundreds to thousands of muscle fibers
• All of the muscle fibers controlled by a single motor neuron
constitute a motor unit
When skeletal muscles contract, they may
produce two types of contractions:
 Isotonic contraction
 Isometric contraction
Isotonic contraction – as tension increases (more
motor units recruited), length of muscle changes
usually resulting in movement of a joint. The
tension (load) on a muscle stays constant (iso =
same, tonic = tension) during a movement.
(Example: lifting a baby, picking up object, walking,
etc. )
Isometric contraction – no change in length of
muscle even as tension increases. The length of a
muscle stays constant (iso = same, metric = length)
during a “contraction” (Example: holding a baby at
arms length, pushing against a closed door.)
Necessary in everyday life to counteract effects of
gravity (e.g. postural muscles keeping head up)
Anatomy of the Muscular System
•Origin
Muscle attachment that remains
fixed
•Insertion
Muscle attachment that moves
•Action
What joint movement a muscle
produces
i.e. flexion, extension, abduction,
etc.
• For muscles to create a movement,
they can only pull, not push
• Muscles in the body rarely work alone,
& are usually arranged in groups
surrounding a joint
• A muscle that contracts to create the
desired action is known as an agonist or
prime mover
• A muscle that helps the agonist is a
synergist
• A muscle that opposes the action of the
agonist, therefore undoing the desired
action is an antagonist
Skeletal muscle movements
Flexion/extension
Abduction/adduction
Rotation – left/right; internal(medial)/external(lateral)
pronation/supination
Elevation/depression
Protraction/retraction
Dorsiflexion/plantarflexion
Inversion/eversion
An
Overview
of the Major
Skeletal
Muscles
Figure 7-11(a)
An
Overview
of the Major
Skeletal
Muscles
Figure 7-11(b)
Anatomy of the Muscular System
Muscles of the Head and Neck
Figure 7-12(a)
Anatomy of the Muscular System
Muscles of the
Head and
Neck
Figure 7-12(b)
Anatomy of the Muscular System
Muscles of the Head and Neck
Figure 7-12(c)
Anatomy of the Muscular System
Muscles of the Anterior Neck
Figure 7-13
Anatomy of the Muscular System
Muscles of
the Spine
Figure 7-14
Anatomy of the Muscular System
Oblique and Rectus
Muscles and the
Diaphragm
Figure 7-15(a)
Anatomy of the Muscular System
Oblique and Rectus Muscles and
the Diaphragm
Figure 7-15(b)
Anatomy of the Muscular System
Oblique and Rectus Muscles and
the Diaphragm
Figure 7-15(c)
Anatomy of the Muscular System
Muscles of the Shoulder
Figure 7-17(a)
Anatomy of the Muscular System
Muscles of the Shoulder
Figure 7-17(b)
Anatomy of the Muscular System
Muscles that Move the Arm
Figure 7-18(a)
Anatomy of the Muscular System
Muscles that Move the Arm
Figure 7-18(b)
Anatomy of the Muscular System
Muscles That Move the Forearm and Wrist
Figure 7-19
Anatomy of the Muscular System
Muscles That Move the Thigh
Figure 7-20(a)
Anatomy of the Muscular System
Muscles That Move
the Thigh
Figure 7-20(b)
Anatomy of the Muscular System
Muscles That Move the Leg
Figure 7-21
Anatomy of the Muscular System
Muscles That Move the Foot and Toes
Figure 7-22(a)
Anatomy of the Muscular System
Muscles That Move
the Foot and Toes
Figure 7-22(b)
Anatomy of the Muscular System
Muscles That Move
the Foot and Toes
Figure 7-22(c)
Anatomy of the Muscular System
Muscles That
Move the Foot
and Toes
Figure 7-22(d)