HUMAN ANATOMY &

PHYSIOLOGY I

The Muscular System

DR WAN SAFWANI WAN KAMARUL ZAMAN

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
• Cardiac
• Smooth (Visceral)
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

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
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
Anatomy of skeletal muscles

epimysium
tendon perimysium

Muscle
Fascicle

Surrounded by
perimysium

Skeletal endomysium
muscle
Skeletal
Surrounded by muscle
epimysium fiber (cell)

Surrounded by
endomysium
Microanatomy of a Muscle Fiber (cell)
Microanatomy of a Muscle Fiber (Cell)

transverse
(T) tubules sarcoplasmic
reticulum sarcolemma
terminal
cisternae
myoglobin

mitochondria

thick myofilament
thin
myofilament

myofibril

triad
nuclei
Muscle fiber

sarcomere
Z-line

myofibril

Thin filaments Thick filaments

Myosin molecule of
Thin myofilament thick myofilament
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 Zone of Zone of

overlap M line overlap
Thin
myofilaments Thick
myofilaments
 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
•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
Synaptic terminals
axon (synaptic end bulbs)
telodendria
axon hillock

(motor neuron)
 Neuromuscular junction

telodendria

Synaptic
terminal
(end bulb)
Synaptic
vessicles
containing
Ach

Synaptic cleft
Neuromuscular
junction
Motor end plate
of sarcolemma
 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)
•The AP causes the synaptic vesicles to fuse with the end bulb
membrane, resulting in the 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 AChE molecules
cleft ACh
receptor
Sarcolemma of site Muscle
motor end plate fiber

• An action potential (AP), an electrical impulse, travels down the

axon of the motor neuron to the end bulbs (synaptic terminals)

Figure 7-4(b-c)
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings 2 of 5
 Action potential
Arrival of an action potential
at the synaptic terminal Axon
Arriving action potential Synaptic terminal
Sarcolemma

Vesicles

ACh
Synaptic AChE molecules
cleft ACh
receptor
Sarcolemma of site Muscle
motor end plate fiber

Release of acetylcholine

Vesicles in the synaptic terminal fuse

with the neuronal membrane and dump

•The AP causes the synaptic vesicles to

their contents into the synaptic cleft.

fuse with the end bulb membrane, resulting

in the release of Acetylcholine (Ach) into
the synaptic cleft

Figure 7-4(b-c)
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings 3 of 5
 Action potential
Arrival of an action potential
at the synaptic terminal Axon
Arriving action potential Synaptic terminal
Sarcolemma

Vesicles

ACh
Synaptic AChE molecules
cleft ACh
receptor
Sarcolemma of site Muscle
motor end plate fiber

ACh binding at the

Release of acetylcholine motor and plate •Ach diffuses across
Vesicles in the synaptic terminal fuse The binding of ACh to the receptors increases
with the neuronal membrane and dump
their contents into the synaptic cleft.
the membrane permeability to sodium ions.
Sodium ions then rush into the cell. the synaptic cleft &
binds to Ach
receptors on the
motor end plate
Na+

Na+
Na+

Figure 7-4(b-c)
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings 4 of 5
 •Thebinding 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

 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

•Thiswill 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-
Physiology of skeletal muscle contraction – events at the
myofilaments
Resting sarcomere Active-site exposure

ADP ADP
+ Myosin head Sarcoplasm
P + P
Troponin
Ca2+

Ca2+
Tropomyosin Actin Active site
ADP ADP

P + 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.
Figure 7-5
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings 3 of 7
Physiology of skeletal muscle contraction – events at the
myofilaments
Resting sarcomere Active-site exposure Cross-bridge formation

ADP ADP
+ Myosin head Sarcoplasm
P + P
ADP
Troponin +
P
Ca2+ Ca2+

Ca2+ ADP Ca2+

Tropomyosin Actin Active site P +
ADP ADP

P + P +

• Myosin heads are “energized” by the presence of ADP + PO43-

at 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

Figure 7-5
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings 4 of 7
Physiology of skeletal muscle contraction – events at the
myofilaments
Resting sarcomere Active-site exposure Cross-bridge formation

ADP ADP
+ Myosin head Sarcoplasm
P + P
ADP
Troponin +
P
Ca2+ Ca2+

Ca2+ ADP Ca2+

Tropomyosin Actin Active site P +
ADP ADP

P + P +

Pivoting of myosin head

• Using the stored energy, the attached
myosin heads pivot toward the center of ADP + P

the sarcomere Ca2+

Ca2+

• The ADP & phosphate group are ADP + P

released from the myosin head

Figure 7-5
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings 5 of 7
 Physiology of skeletal muscle contraction – events at the
myofilaments
Resting sarcomere Active-site exposure Cross-bridge formation

ADP ADP
+ Myosin head Sarcoplasm
P + P
ADP
Troponin +
P
Ca2+ Ca2+

Ca2+ ADP Ca2+

Tropomyosin Actin Active site P +
ADP ADP

P + P +

• A new molecule of
Cross bridge detachment Pivoting of myosin head
ATP binds to the
myosin head, causing ATP
the cross bridge to ADP + P

detach from the actin Ca2+

Ca2+
strand
Ca2+ Ca2+

• The myosin head will ATP ADP + P

get re-energized as the

ATP  ADP+P

• As long as the active sites are still exposed, the myosin head can bind
again to the next active site
Physiology of skeletal muscle contraction – events at the
myofilaments
Resting sarcomere Active-site exposure Cross-bridge formation

ADP ADP
+ Myosin head Sarcoplasm
P + P
ADP
Troponin +
P
Ca2+ Ca2+

Ca2+ ADP Ca2+

Tropomyosin Actin Active site P +
ADP ADP

P + P +

Myosin reactivation Cross bridge detachment Pivoting of myosin head

ADP ATP ADP + P

+ P

Ca2+ Ca2+
Ca2+

Ca2+ Ca2+ Ca2+

ADP
ATP ADP + P
P +
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
Skeletal muscle fibers shorten as thick
filaments interact with thin filaments (“cross
bridge”) and sliding occurs (“power stroke”).
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
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

 Hypertrophy – “stressing” a muscle (i.e. exercise) causes

more myofilaments/myofibrils to be produced within muscle
fibers; allows for more “cross bridges” resulting in more force
(strength) as well as larger size
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
MUSCLE TWITCH

3- Muscle contraction: Mechanical events

 1 stimulation  1 twitch

 Muscle twitch: 3 phases:

- latent phase
- contraction phase
- relaxation phase

☻ do not confuse the AP

and the twitch!!!
Figure 12.16
Events during the twitch
 Latent phase: Stimulus to
beginning contraction: AP to
myosin binding to actin active site
 Contraction phase: beginning to
end of muscle tension  myosin
heads slide along the actin
filaments
 Relaxation phase: peak tension
to no tension  Ca++ ions
moved back into the cisternae,
tropomyosin moves back over
actin, myosin head release actin
and the filaments move back into
resting position
Figure 12.18
Isometric/isotonic contractions

 Isometric: muscle
contraction without
movement  no
muscle shortening

 Isotonic: muscle
contraction with
movement  muscle
shortens
Effect of consecutive stimuli: Treppe

 Treppe: gradual increase in

contraction intensity during
sequential stimulation

 Might be due to calcium ions

accumulating in the cytoplasm
with each stimulation

Figure 12.15
Summation and tetanus
 Summation: Rapid sequence of stimuli muscle
twitches fuse into each other, each subsequent one
being stronger that its precedent (due to Ca++?)
 Tetanus: very rapid sequence of stimuli: no relaxation

Figure 12.17
Recruitment

 An increase in force is
made possible by recruiting
more motor units
 Muscles have various sizes
of motor units  allows
them to adjust the size of
the effort to be made
 Activating motor units
alternatively allows the
muscle to sustain
contraction with minimal
fatigue

Figure 12.19
IV- Muscle metabolism
 Muscle fibers use ATP (only
first few seconds) for
contraction
 ATP must then be generated
by the muscle cell:
- from creatine phosphate, first
- from glucose and glycogen
- from fatty-acids

ATP formation from the above

compound is possible if
oxygen is present (oxidative
phosphorylation: 36 ATP per
glucose)
Oxygen is delivered to the muscle
by myoglobin, a molecule with
high affinity to oxygen and
related to hemoglobin
If the effort is strong and
sustained, the muscle
might not have enough
oxygen delivered to it by
myoglobin  anaerobic
glycolysis with only 2 ATP
formed per glucose and
synthesis of lactic acid

Consequence of anaerobic
metabolism?

Figure 12.11
Muscle fatigue
 Muscle fatigue: a decline in the
ability of the muscle to sustain
the strength of contraction
 Causes:
- rapid build-up of lactic acid
- decrease in oxygen supply
- decrease in energy supply
(glucose, glycogen, fatty-acids)
- Decreased neurotransmitter at
the synapse
- psychological causes
Effects of exercise on the muscle

 Aerobic exercises: long

sustained exercises  promote
increased oxidative capacity of
the muscle fiber  increased
blood vessel supply, increased
mitochondria

 High intensity, short burst

exercise: increased glycolytic
activity  increased synthesis of
glycolytic enzymes, increased
synthesis of myofibrils (increased
muscle size)
Basis for classification of
skeletal muscle
 Velocity of contraction: slow vs fast
 Energy source: oxidative vs glycolytic
Oxydative Glycolytic
Primary energy through Primary energy through
oxidative anaerobic glycolysis
phosphorylation  Fewer mitochondria
 Many mitochondria  Many glycolytic enzymes

 Myoglobin (red)  High glycogen stores

 Small diameter  Use little oxygen—

anaerobic
 Resistant to fatigue
 Large diameter
 Quick to fatigue
 Read Chapter 9 & see also table 9.3
(Marieb) on comparison of skeletal,
cardiac & smooth muscle.
Anatomy of the Muscular System

•Origin/Number of origin
Muscle attachment that remains
fixed e.g. biceps, triceps
•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
 NAMING OF SKELETAL MUCLES

 Number of origins – e.g., biceps (two

origins) and triceps (three origins)
 Location of attachments – named
according to point of origin or insertion
 Action – e.g., flexor or extensor, as in
the names of muscles that flex or
extend, respectively
FASCICLE ARRANGEMENT
 Convergent – fascicles converge
from a broad origin to a single
tendon insertion (e.g., pectoralis
major)
 Circular – fascicles are arranged in
concentric rings (e.g., orbicularis
oris)
 Parallel – fascicles run parallel to
the long axis of the muscle (e.g.,
sartorius)
 Fusiform – spindle-shaped
muscles (e.g., biceps brachii)
appear to be the same or similar
to parallel
 Pennate – short fascicles that
attach obliquely to a central
tendon running the length of the
muscle (e.g., rectus femoris)
 BASIC PRINCIPLES OF LEVER

Depending on relative position of 3 elements – fulcrum, load & effort:

1) Effort farther than load from fulcrum = mechanical advantage

2) Effort nearer to fulcrum than to load = mechanical disadvantage

Site of muscle insertion relative to fulcrum/joint

-Small difference in site can produce big differences in amount of force
a muscle must generate to move a load or resistance.
CLASSES OF LEVER

Important: Which of these is

at mechanical advantage &
disadvantage?
 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)