1. Muscular Histology and Physiology

2. Photomicrograph of the capillary network surrounding skeletal muscle fibers

3. Microscopic anatomy of a skeletal muscle fiber
Nuclei
Fiber
(a)
Sarcolemma
Mitochondrion
Myofibril
(b)
Dark
A band
Light
I band
Nucleus
Z disc
H zone
Z disc
Thin (actin) filament
Thick (myosin)
filament
(c)

4. Composition of thick and thin filaments
Thick filament
Thin filament
Tail
Heads
Flexible hinge region
(a)
Myosin molecule
(d)
Longitudinal section of filaments within
one sarcomere of a myofibril
Thin filament (actin)
Myosin heads
Thick filament (myosin)
Myosin head
(b)
Portion of a thick filament
Troponin complex
Tropomyosin
Actin
(c)
Portion of a thin filament
(e)
Transmission electron micrograph of part
of a sarcomere

5. Microscopic anatomy of a skeletal muscle fiber
Z disc
H zone
Z disc
Thin (actin) filament
Thick (myosin)
filament
(c)
I band
A band
I band
M line
Sarcomere
M line
Z disc
Z disc
Thin (actin) filament
Elastic (titin)
filaments
Thick (myosin)
filament
(d)
I band
thin filaments
only
H zone
thick filaments
only
M line
thick filaments linked
by accessory proteins
Outer edge of
A band
thick and thin
filaments overlap
(e)

6. I band A band I band Z disc H zone Z disc M line Part of a skeletal
Relationship of the sarcoplasmic reticulum and T tubules to myofibrils of skeletal muscle
I band
A band
I band
Z disc
H zone
Z disc M
line
Part of a skeletal
muscle fiber (cell)
Sarcolemma
Triad
Mitochondrion
Myofibrils
Myofibril
Tubules of
sarcoplasmic
reticulum
Sarcolemma
Terminal cisterna
of the sarcoplasmic
reticulum
T tubule

7. Sliding filament model of contractionZ Z H 1 I A I Z Z A 3 Z Z A 2

8. Connective tissue sheaths of skeletal muscle
Epimysium
Tendon
Muscle fiber
in middle of
a fascicle
Epimysium
Endomysium
(between
fibers)
Endomysium
(b)
Perimysium
Blood vessel
Bone
Muscle fiber
(cell)
(a)
Perimysium
Blood
vessel
Endomysium
Fascicle
(wrapped by
perimysium)

9. Figure 4.30

10. The neuromuscular junction
Myelinated axon
of motor neuron
Action
potential
Axon terminal at
neuromuscular junction
Sarcolemma
of the
muscle fiber
Nucleus
(a)
Axon terminal
Axon terminal of
a motor neuron
Fusing synaptic
vesicle
Mitochondrion
Ca2+
Synaptic
vesicle
ACh molecules
Synaptic cleft
Acetic acid
T tubule
Junctional
folds of the
sarcolemma
at motor end
plate
Synaptic
cleft
Choline
Acetylcholinesterase K+
Na+
Part of a
myofibril
Binding of Ach
to receptor opens
Na+/K+ channel
(c)
(b)

11. Figure 9.7a: The neuromuscular junction, p. 290.
Myelinated axon
of motor neuron
Action
potential
Axon terminal at
neuromuscular junction
Sarcolemma
of the
muscle fiber
Nucleus
(a)

12. The neuromuscular junction
Axon terminal of
a motor neuron
Mitochondrion
Ca2+
Synaptic
vesicle
Synaptic cleft
T tubule
Junctional
folds of the
sarcolemma
at motor end
plate
Part of a
myofibril
(b)

13. Muscle Contraction Physiology

14. The neuromuscular junction
Axon terminal
Fusing synaptic
vesicle
ACh molecules
Acetic acid
Choline
Synaptic
cleft
Acetylcholinesterase K+
Na+
Binding of Ach
to receptor opens
Na+/K+ channel
(c)

15. An action potential in a skeletal muscle fiber
Electrical conditions of a resting (polarized) sarcolemma.
The outside face is positive, while the inside face is negative.
The predominant extracellular ion is sodium (Na+); the
predominant intracellular ion is potassium (K+). The sarcolemma
is relatively impermeable to both ions.
[K+]
[Na+]
(a)
(b)
Step 1: Depolarization and generation of the action potential.
Production of an end plate potential at the motor end plate causes
adjacent areas of the sarcolemma to become permeable to sodium
(voltage-gated sodium channels open). As sodium ions diffuse rapidly
into the cell, the resting potential is decreased (i.e., depolarization
occurs). If the stimulus is strong enough, an action potential is
initiated.
Na+
Stimulus
(b)
(c)
Step 2: Propagation of the action potential.
The positive charge inside the initial patch of sarcolemma
changes the permeability of an adjacent patch, opening voltage-
gated Na+ channels there. Consequently the membrane potential
in that region decreases and depolarization occurs there as well.
Thus, the action potential travels rapidly over the entire
sarcolemma.
(c)
(d)
Step 3: Repolarization.
Immediately after the depolarization wave passes, the
sarcolemma's permeability changes once again: Na+ channels
close and K+ channels open, allowing K+ to diffuse from the cell.
This restores the electrical conditions of the resting (polarized)
state. Repolarization occurs in the same direction as
depolarization, and must occur before the muscle fiber can be
stimulated again. The ionic concentrations of the resting state
are restored later by the sodium-potassium pump K+
(d)

16. Membrane potential (mV) Relative membrane permeability
Action potential scan showing changing sarcolemma permeability to Na+ and K+ ions
Na+ channels
close
Action potential
+30
K+ channels
open
Membrane potential (mV)
Relative membrane permeability
Na+
channels
open
Threshold
–55
–70 1 2 3 4
Time (ms)

17. Excitation-contraction coupling
Neurotransmitter released
diffuses across the synaptic
cleft and attaches to ACh
Axon terminal
Synaptic
cleft
Synaptic vesicle
Sarcolemma
T tubule 1
Net entry of Na+ initiates
an action potential which
is propagated along the
sarcolemma and down
the T tubules.
ACh
ACh
ACh
Ca2+
Ca2+
SR tubules (cut) SR 2
Action potential
in T tubule activates
voltage-sensitive
receptors, which in
turn trigger Ca2+
release from terminal
cisternae of SR
into cytosol.
Ca2+
Ca2+
ADP Pi
Ca2+
Ca2+
Ca2+
Ca2+ 6
Tropomyosin blockage
restored, blocking myosin
binding sites onactin;
contraction ends and
muscle fiber relaxes. 3
Calcium ions bind to troponin;
troponin changes shape, removing
the blocking action of tropomyosin;
actin active sites exposed.
Ca2+ 5
Removal of Ca2+ by active transport
into the SR after the action
potential ends.
Ca2+ 4
Contraction; myosin heads alternately attach to
actin and detach, pulling the actin filaments toward
the center of the sarcomere; release of energy by
ATP hydrolysis powers the cycling process.

18. Role of ionic calcium in the contraction mechanism
Overview
Actin
Troponin
Myosin
head
Tropomyosin
Plane of (a)
Plane of (d)
Additional
calcium
ions
bind
to TnC
TnT
Myosin
binding
site
Tropomyosin
TnC
Tnl
Myosin
binding
sites
Actin
+ Ca2+
Actin
Additional
calcium
ions
bind
Troponin
complex
Myosin
head
Myosin
head
(a)
(b)
(c)
(d)

19. The cross bridge cycle
Myosin head
(high-energy
configuration)
ADP Pi 1
Myosin head attaches to the actin
myofilament, forming a cross bridge.
Thin filament
ADP
ATP
hydrolysis
ADP
Thick filament Pi 2
Inorganic phosphate (Pi) generated in theprevious
contraction cycle is released, initiating
the power (working) stroke. The myosin head
pivots and bends as it pulls on the actin filament,
sliding it toward the M line. Then ADP is released. 4
As ATP is split into ADP and Pi, the myosin
head is energized (cocked into the high-energy
conformation).
ATP
Myosin head
(low-energy
configuration)
ATP 3
As new ATP attaches to the myosin head, the link between
Myosin and actin weakens, and the cross bridge detaches.

20. neuromuscular junctions Nerve
, p. 296.
Spinal cord
Motor
unit 1
Motor
unit 2
Axon terminals at
neuromuscular junctions
Nerve
Motor neuron
cell body
Motor neuron
axon
Muscle
Muscle fibers
Muscle
fibers
Branching axon
to motor unit
(a)
(b)

21. maximum tension Percentage of maximum tension Percentage of
The muscle twitch
Latent period
Latent
period
Period of
contraction
Period of
relaxation
Extraocular muscle (lateral rectus)
Gastrocnemius
Soleus
maximum tension
Percentage of
maximum tension
Percentage of 20 40 60 80
100
120
140 40 80
120
160
200
Single
stimulus
Single
stimulus
Time (ms)
Time (ms)
(a)
(b)

22. Methods of regenerating ATP during muscle activity
Glucose (from
glycogen breakdown or
delivered from blood)
Glucose (from
glycogen breakdown or
delivered from blood) CP
ADP O2
Glycolysis
in cytosol
Pyruvic acid
Fatty
acids O2 O2
Aerobic respiration
in mitochondria
Amino
acids
Creatine
ATP 2
ATP
Pyruvic acid
net gain O2 38
ATP
CO2
Released
to blood
Lactic acid
H2O
net gain per glucose
(a) Direct phosphorylation
[coupled reaction of creatine
phosphate (CP) and ADP]
(b) Anaerobic mechanism (glycolysis
and lactic acid formation)
(c) Aerobic mechanism (aerobic cellular
respiration)
Energy source: CP
Energy source: glucose
Energy source: glucose; pyruvic acid; free
fatty acids from adipose tissue; amino acids
from protein catabolism
Oxygen use: None
Products: 1 ATP per CP, creatine
Duration of energy provision: 15s
Oxygen use: None
Products: 2 ATP per glucose, lactic acid
Duration of energy provision: 30–60 s.
Oxygen use: Required
Products: 38 ATP per glucose, CO2, H2O
Duration of energy provision: Hours

23. Large number of muscle fibers activated Large muscle fibers
Factors influencing force, velocity, and duration of skeletal muscle contraction
Large number
of muscle
fibers activated
Large
muscle
fibers
Asynchronous
tetanic
contractions
Muscle and
sarcomere
length slightly
over 100% of
resting length
Predominance
of fast glycolytic
(fatigable) fibers
Small load
Predominance
of slow oxidative
(fatigue-resistant)
fibers
(a)
Increased
contractile
force
(b)
Increased
contractile
velocity
(c)
Increased
contractile
duration

24. Influence of load on contraction velocity and duration
Light load
Velocity of shortening
Distance shortened
Intermediate load
Heavy load 20 40 60 80
100
120
Time (ms)
Increasing load
Single action
potential initiated
(b)
(a)

25. Innervation of smooth muscle
Mucosa
Smooth muscle cell
Varicosities
Autonomic
nerve
fiber
Submucosa
Serosa
Muscularis
externa
Varicosity
Mitochondrion
Synaptic vesicles

26. Sequence of events in excitation-contraction coupling of smooth muscle
Ca2+
Extracellular fluid
Plasma membrane
Cytoplasm 1
Calcium ions (Ca2+) enter
the cytosol from the ECF
or from the scant SR.
Ca2+ 2
Ca2+ binds to and
activates calmodulin.
Sarcoplasmic reticulum
Ca2+
Inactive
calmodulin
Activated
calmodulin 3
Activated calmodulin activates
the myosin light chain kinase
enzymes.
Inactive
kinase
Activated
kinase
ATP 4
The activated kinase
enzyme catalyzes transfer
of phosphate to myosin
heads, activating the
myosin head ATPases.
ADP Pi Pi
Activated
(phosphorylated)
myosin molecule
Inactive myosin
molecule
Thin myofilament Pi 5
Phosphorylated myosin
heads form cross bridges
with actin of the thin
filaments and shortening
occurs.
Thick filament Pi 6
Cross bridge activity ends
when phosphate is removed
from the myosin heads by
phosphorylase enzymes and
intracellular Ca2+ levels fall.