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Unit 2 Muscular System

The document outlines the characteristics and functions of muscle tissue, including excitability, contractility, extensibility, and elasticity. It describes the three types of muscle tissue: skeletal, cardiac, and smooth, along with their unique properties and structures. Additionally, it details the physiology of muscle contraction, including the sliding filament theory, the role of ATP, and the neuromuscular junction's function in muscle activation.

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0% found this document useful (0 votes)
3 views53 pages

Unit 2 Muscular System

The document outlines the characteristics and functions of muscle tissue, including excitability, contractility, extensibility, and elasticity. It describes the three types of muscle tissue: skeletal, cardiac, and smooth, along with their unique properties and structures. Additionally, it details the physiology of muscle contraction, including the sliding filament theory, the role of ATP, and the neuromuscular junction's function in muscle activation.

Uploaded by

sahimbagban6
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

The Muscular System

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

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

Surrounded by
endomysium
Microanatomy of a Muscle Fiber (cell)
Structure of Skeletal Muscle:
Connective Tissue Covering
◼ Epimysium
 Surrounds entire muscle
◼ Perimysium
 Surrounds bundles of muscle fibers
◼ Fascicles
◼ Endomysium
 Surrounds individual muscle fibers
Structure of Skeletal Muscle:
Microstructure
◼ Sarcolemma
 Muscle cell membrane
◼ Myofibrils
 Threadlike strands within muscle fibers
 Actin (thin filament)
◼ Troponin
◼ Tropomyosin

 Myosin (thick filament)


Structure of Skeletal Muscle:
The Sarcomere
◼ Further divisions of myofibrils
 Z-line (Dark bands across a striated muscle fiber that mark
the junction of actin filaments)
 A-band (The region of a striated muscle sarcomere that
contains myosin thick filaments)
 I-band (The I bands contain only thin (actin) filaments)

 Within the sarcoplasm


 Sarcoplasmic reticulum
◼ Storage sites for calcium
 Transverse tubules
 Terminal cisternae
Sarcomere
A band
Z line Z line
H zone

I band Zone of Zone of


overlap M line overlap
Thin
myofilaments Thick
myofilaments
Microanatomy of a Muscle Fiber (Cell)

transverse
(T) tubules sarcoplasmic
reticulum sarcolemma
terminal
cisternae
myoglobin

mitochondria

thick myofilament
thin
myofilament

myofibril

triad
nuclei
Thin Myofilament

Z-line
(Z-disc)

(myosin binding site)


Thick myofilament

M-line

(has ATP
& actin
binding
site)

▪ Play IP sliding filament theory p.5-14 for overview of thin & thick filaments
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
Cross-Bridge Formation in
Muscle Contraction
Sliding Filament Theory
◼ Rest – uncharged ATP cross-bridge complex
◼ Excitation-coupling – charged ATP cross-bridge
complex, “turned on”
◼ Contraction – actomyosin – ATP > ADP & Pi +
energy
◼ Recharging – reload cross-bridge with ATP
◼ Relaxation – cross-bridges “turned off”
Muscle Function
◼ All or none law – fiber contracts
completely or not at all
◼ Muscle strength gradation
 Multiple motor unit summation – more motor
units per unit of time
 Wave summation – vary frequency of
contraction of individual motor units
Energy for Muscle Contraction
◼ ATP is required for muscle contraction
 Myosin ATPase breaks down ATP as fiber
contracts
◼ Sources of ATP
 Phosphocreatine (PC)
 Glycolysis
 Oxidative phosphorylation
Sources of ATP for Muscle Contraction
Properties of Muscle Fibers
◼ Biochemical properties
 Oxidativecapacity
 Type of ATPase

◼ Contractile properties
 Maximal force production
 Speed of contraction
 Muscle fiber efficiency
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

End bulbs contain


vesicles filled with
Acetylcholine (Ach)
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
their contents into the synaptic cleft.
•The AP causes the synaptic vesicles to
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
with the neuronal membrane and dump
their contents into the synaptic cleft.
increases the membrane permeability to
sodium ions. Sodium ions then rush
the synaptic cleft &
binds to ACh
into the cell.

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
•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
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 (myosin binding sites)
of actin molecules.
•The exposure of the active sites allow
myosin to bind to actin, and cause the
sliding of the filaments
Table 7-1
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 +

[Link] -
animation

[Link] –
animation with Taylor Swift song
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)

Play IP Contraction of motor units p. 3-7


▪ 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

Play IP Contraction of motor units p. 3-7


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 functional
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 at joints

Flexion/extension
Abduction/adduction
Rotation – left/right; internal(medial)/external(lateral)
pronation/supination
Elevation/depression
Protraction/retraction
Dorsiflexion/plantarflexion
Inversion/eversion
Naming of
skeletal
muscles
◼ An Overview
of the Major
Skeletal
Muscles

Figure 7-11(a)
◼ An Overview
of the Major
Skeletal
Muscles

Figure 7-11(b)

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