This document provides an overview of muscular tissue and muscle contraction. It discusses the three main types of muscle tissue - skeletal, cardiac, and smooth muscle - and their structural characteristics. The sliding filament theory of muscle contraction is explained, involving the interaction of the thick and thin filaments during the cross-bridge cycling of actin and myosin. Calcium release from the sarcoplasmic reticulum in response to the muscle action potential triggers contraction by exposing myosin binding sites on actin. Relaxation occurs when calcium is sequestered back into the sarcoplasmic reticulum.
34. Sarcolemma Sarcoplasmic
reticulum (SR)
Transverse
tubule
Terminal
cistern of SR
Sarcoplasm
Membrane
protein
Nucleus
Z
disc
Dystrophin
Thin filamentThick filament
Sarcomere
SimplisHc
representaHon
of
a
muscle
fiber
Myofibril
= Ca2+
Key:
= Ca2+ release
channels
= Ca2+ active
transport pumps
Glycogen granulesMyoglobinMitochondrion
Z
disc
36. 36
NMJ
Axon
terminal
of
motor
neuron
SynapHc
end
bulb
Motor
end
plate
Synapse
SynapHc
cleW
37. Neuromuscular
juncHon
Axon collateral of
somatic motor neuron
Axon terminal
Synaptic end bulb
Neuromuscular
junction (NMJ)
Sarcolemma
Myofibril in
muscle fiber
Muscle fiber
38. 38
Muscle
ContracHon
Nerve
impulse
reaches
axon
terminal
at
NMJ
SynapHc
vesicles
à
ACh
into
cle
ACh
à
receptors
on
sarcolemma
(motor
end
plate)
Na+
channels
OPEN
Na+
“soaks”
into
muscle
fiber
39. Enlarged
view
of
the
neuromuscular
juncHon
Axon terminal
Nerve impulse
Synaptic vesicle
containing
acetylcholine
(ACh)
SYNAPTIC END
BULB
Synaptic cleft
(space)
Ca2+
Voltage-gated
Ca2+ channel
Sarcolemma
MOTOR END
PLATE
40. Binding
of
acetylcholine
to
ACh
receptors
in
the
motor
end
plate
ACh is released
from synaptic
vesicle
Synaptic cleft
(space)
ACh binds to ACh
receptor
Junctional fold
Synaptic end bulb
ACh is broken down
MOTOR END PLATE
Muscle action
potential is produced
Na+
Ca2+
1
2
4
3
41. Nerve impulse arrives at axon
terminal of motor neuron and
triggers release of
acetylcholine (ACh).
1
ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Acetylcholinesterase in
synaptic cleft destroys ACh
so another muscle action
potential does not arise
unless more ACh is released
from motor neuron.
ACh receptor
Synaptic
vesicle filled
with ACh
Muscle action
potential
Transverse tubule
Muscle AP traveling along
transverse tubule opens Ca2+
release channels in the
sarcoplasmic reticulum (SR)
membrane, which allows calcium
ions to flood into the sarcoplasm.
SR
Ca2+
Ca2+ binds to troponin on the thin filament,
exposing the binding sites for myosin.
Elevated Ca2+
Contraction: power strokes use
ATP; myosin heads bind to actin,
swivel, and release; thin filaments
are pulled toward center of
sarcomere.
Muscle relaxes.
Troponin–tropomyosin complex slides
back into position where it blocks the
myosin binding sites on actin.
Ca2+ active
transport pumps
Ca2+ release channels in
SR close and Ca2+
active transport pumps use
ATP to restore low level of
Ca2+ in sarcoplasm.
Ca2+
Nerve impulse
2
3
4
5
67
8
9
42. 42
Muscle
ContracHon
Muscle
acHon
potenHal
à
sarcolemma
&
T-‐
tubules
SR
à
Ca+2
into
sarcoplasm
Ca+2
binds
to
troponin
43. 43
Muscle
ContracHon
Tropomyosin
swivels
open
Exposes
myosin-‐
binding
sites
(on
acQn)
ContracHon
Cycle
begins
44. 44
ContracHon
Cycle
1.
ATP
hydrolysis
at
myosin
head
2.
Binding
of
myosin
heads
to
acHn
(crossbridges)
3.
ContracHon
=
power
stroke
4.
Detachment
of
myosin
heads
49. Myosin heads hydrolyze
ATP and become
reoriented and
energized
Myosin heads bind to
actin, forming cross-
bridges
As myosin heads bind
ATP, the cross-bridges
detach from actin
Myosin cross-bridges
rotate toward center of
sarcomere (power stroke)
ADP
ADP
ADP
P
P
ATP
ATP
Key:
= Ca2+
Contraction cycle continues
if ATP is available and Ca2+
level in sarcoplasm is high
1
2
3
4
55. 55
CreaHne
Phosphate
Made
from
excess
ATP
in
resQng
muscle
15
sec
=
maximum
contracQon
Short,
intense
bursts
of
energy
56. 56
Anaerobic
Glycolysis
Makes
ATP
from
glucose
breakdown
during
glycolysis
If
no
O2:
Pyruvic
acid
à
lacQc
acid
à
blood
2
min
=
maximum
contracQon
57. 57
Aerobic
Cellular
RespiraHon
Makes
ATP
from
glucose
breakdown
in
mitochondria
If
O2:
Pyruvic
acid
à
mitochondria
à
ATP
Several
minutes
to
hours
=
maximum
contracQon
58. 58
Muscle
FaHgue
Feeling
Qred
&
wanQng
to
stop
exercise
=
central
faHgue
Low
Ach
&
Ca+2
Low
creaQne
phosphate
Low
O2
or
glycogen
Oxygen
debt
(recovery
oxygen
uptake)
Build-‐up
of
lacQc
acid
59. 59
Motor
Units
One
motor
neuron
+
10-‐2000
muscle
fibers
(150
fibers
avg)
All
fibers
contract
in
unison
Strength
of
contracQon
depends
on:
the
size
of
a
motor
unit
&
the
#
of
fibers
ac4vated
at
a
give
4me
70. 70
Why
does
summaHon
&
tetanus
occur?
Ca+2
remains
in
sarcoplasm
ElasQc
components
(tendons,
CT)
remain
taut
Myotonic
goats!
71. 71
Motor
Unit
Recruitment
Large
motor
units
à
High
tension
(Strength)
Small
motor
units
à
Low
tension
(Precision)
Motor
units
in
whole
muscle
fire
asynchronously
Why?
72. 72
Muscle
Tone
Involuntary
contracQon
&
relaxaQon
of
small
#
of
motor
units
Alternate
in
constantly
shiing
pa4ern
No
movement
produced
(but
muscles
kept
firm)
FuncQons:
posture,
blood
pressure
75. 75
VariaHons
in
Skeletal
Muscle
Fibers
Differ
in
amount
of
myoglobin,
mitochondria,
capillaries
Red
muscle
(darker)
White
muscle
(lighter)
Range
of
contracQon
speeds
&
faQgue
resistance
76. 76
3
Types
of
Skeletal
Muscle
Fibers
Slow
OxidaHve
(SO)
Fast
OxidaHve
GlycolyHc
(FOG)
Fast
GlycolyHc
(FG)
77. Transverse
secHon
of
three
types
of
skeletal
muscle
fibers
Slow oxidative fiber
Fast glycolytic fiber
Fast oxidative–
glycolytic fiber
LM 440x
78. 78
Slow
OxidaHve
(SO)
Fibers
Smallest,
weakest,
slowest
(slow-‐twitch)
Red
muscle:
lots
of
mito,
myo,
&
blood
Aerobic
cellular
respiraQon
à
ATP
86. 86
Cardiac
Muscle
Tissue
Same
acQn
&
myosin
arrangement
as
skeletal
muscle
Autorhythmic
Longer
contracQons
(longer
Ca+2
delivery)
87. 87
Smooth
Muscle
Tissue
Small,
single,
nonstriated,
tapered,
involuntary
fibers
No
T
tubules
&
li4le
SR
Contains
acQn
&
myosin,
but
no
sarcomeres
Dense
bodies