1. Muscles 12

2. The Three Types of Muscle
Cylindrical shaped, multinuclei, straited, voluntary, fibers of different speeds
Branched, uni-/binuclei, involuntary, striated, rhythmic contractions
Spindled shaped, one nucleus, involuntary, non-straited, internal organs
Figure 12-1a

3. Muscles: Summary

4. Skeletal Muscle
Usually attached to bones by tendons- sometimes attached directly to bone (pectoralis major)
Origin: closest to the trunk- usually does not move a joint when contracts.
Insertion: more distal- moves joint when contracts
Flexor: brings bones together- decreases angle at joint
Extensor: bones move away- increases angle at joint
Antagonistic muscle groups: flexor-extensor pairs- antagonistic muscles are usually in opposite sides.

5. Anatomy Summary: Skeletal Muscle
Figure 12-3a (1 of 2)

6. Anatomy Review: Muscle Fiber Structure

7. Ultrastructure of Muscle
Figure 12-3b

8. Anatomy Summary: Skeletal Muscle
Figure 12-3a (2 of 2)

9. Ultrastructure of Muscle
Myosin are motor proteins. 250 myosins join to form the thick filaments. The thin filament is made up of a string of actin with tropomyosin and tropnin attached. Titin and nebulin anchor and stabilize.
Figure 12-3e

10. Ultrastructure of Muscle
Actin and myosin form crossbridges
Myofibril
A band
Z disk
I band
M line
H zone
Sarcomere
Thin filaments
Tropomyosin
Troponin
Actin chain
G-actin molecule
Myosin tail
Myosin
heads
Myosin molecule
(c)
(d)
(e)
Thick filaments
Hinge
region
(f)
Titin
Nebulin
Figure 12-3c–f

11. Summary of Muscle Contraction
Muscle tension: force created by muscle
Load: weight that opposes contraction
Contraction: creation of tension in muscle
Relaxation: release of tension
Figure 12-7

12. Neuromuscular Junction: Overview
Terminal boutons- insulate the site of the neuromuscular juction and secrete supportive growth factors
Synaptic cleft- space between the axon terminal and the sarcolemma
Acetylcholine- neurotransmitter released involves calcium and binds to nicotinic receptors
Motor end plate- folds on the sarcolemma of the muscle
On muscle cell surface
Nicotinic receptors

13. Anatomy of the Neuromuscular Junction
Figure (1 of 3)

14. Anatomy of the Neuromuscular Junction
Figure (2 of 3)

15. Anatomy of the Neuromuscular Junction
Figure (3 of 3)

16. Mechanism of Signal Conduction
Axon terminal (of presynaptic cell)
Action potential signals acetylcholine release
Motor end plate – series of folds in the plasma membrane of the postsynaptic cell
Two acetylcholine bind
Opens cation channel
Na+ influx – K+ efflux
Membrane depolarized
Stimulates fiber contraction as a result in increased intracellular calcium concentration

17. Events at the Neuromuscular Junction
Figure 11-13a

18. T-tubules and the Sarcoplasmic Reticulum
Figure 12-4

19. Excitation-Contraction Coupling
Muscle fiber
Motor end plate
ACh
Axon terminal of
somatic motor neuron
Sarcoplasmic reticulum
Actin
Troponin
Tropomyosin
Myosin
head
Z disk
Myosin thick filament
M line
T-tubule
DHP
receptor
Ca2+
Somatic motor neuron
releases ACh at neuro-
muscular junction.
(a) 1
Figure 12-11a, step 1

20. Excitation-Contraction Coupling
Muscle fiber
Motor end plate
ACh
Axon terminal of
somatic motor neuron
Sarcoplasmic reticulum
Actin
Troponin
Tropomyosin
Myosin
head
Z disk
Myosin thick filament
M line
T-tubule
DHP
receptor
Ca2+
Somatic motor neuron
releases ACh at neuro-
muscular junction.
Net entry of Na+ through ACh
receptor-channel initiates
a muscle action potential.
Na+ K+
(a)
potential 1
Action 2
Action potential
Figure 12-11a, steps 1–2

21. Excitation-Contraction Coupling
M line
Ca2+
Distance actin moves
released
Myosin thick filament
(b)
Action potential in
t-tubule alters
conformation of
DHP receptor.
DHP receptor opens Ca2+
release channels in
sarcoplasmic reticulum
and Ca2+ enters cytoplasm.
Ca2+ binds to troponin,
allowing strong actin-
myosin binding.
Myosin heads execute
power stroke.
Actin filament slides
toward center of
sarcomere. 3 4 5 6 7
PLAY
Animation: Muscular System: The Neuromuscular Junction
Figure 12-11b

22. Changes in Sarcomere Length during Contraction
PLAY
Animation: Muscular System: Sliding Filament Theory
Figure 12-8

23. Regulatory Role of Tropomyosin and Troponin
In the relaxed state the myosin head is at 90o but it is unbound to actin because the binding sites on actin are blocked.
Figure 12-10a

24. Regulatory Role of Tropomyosin and Troponin**Pi
ADP
G-actin moves
Cytosolic Ca2+
Tropomyosin shifts,
exposing binding
site on G-actin TN
Power stroke
Initiation of contraction
Ca2+ levels increase
in cytosol.
Ca2+ binds to
troponin.
Troponin-Ca2+
complex pulls
tropomyosin
away from G-actin
binding site.
Myosin binds
to actin and
completes power
stroke.
Actin filament
moves.
(b) 1 2 3 4 5
Figure 12-10b

25. The Molecular Basis of Contraction
ATP
binding
site
Myosin
sites
Tight binding in the rigor
state. The crossbridge is
at a 45° angle relative to
the filaments.
filament 45
G-actin molecule
ATP binds to its binding site
on the myosin. Myosin then
dissociates from actin. 1 2 3 4
Figure 12-9, steps 1–2

26. The Molecular Basis of Contraction
The ATPase activity of myosin
hydrolyzes the ATP. ADP and
Pi remain bound to myosin.
The myosin head swings over
and binds weakly to a new
actin molecule. The cross-
bridge is now at 90º relative to
the filaments. Pi
ADP
90° 1 2 3 4
Figure 12-9, steps 3–4

27. The Molecular Basis of Contraction
At the end of the power stroke,
the myosin head releases ADP
and resumes the tightly bound
rigor state.
ADP
Release of Pi initiates the power
stroke. The myosin head rotates
on its hinge, pushing the actin
filament past it. Pi
Actin filament
moves toward M line. 1 2 3 4 5 6
Figure 12-9, steps 5–6

28. The Molecular Basis of Contraction
At the end of the power stroke,
the myosin head releases ADP
and resumes the tightly bound
rigor state.
ATP
binding
site
ADP
Tight binding in the rigor
state. The crossbridge is
at a 45° angle relative to
the filaments.
Myosin filament
45°
G-actin molecule
ATP binds to its binding site
on the myosin. Myosin then
dissociates from actin.
The ATPase activity of myosin
hydrolyzes the ATP. ADP and
Pi remain bound to myosin.
The myosin head swings over and
binds weakly to a new actin molecule.
The crossbridge is now at 90º relative
to the filaments. Pi
90°
Release of Pi initiates the power
stroke. The myosin head rotates
on its hinge, pushing the actin
filament past it.
Actin filament
moves toward M line.
Contraction-
relaxation
Sliding
filament 1 2 3 4 5 6
Myosin
binding
sites
Figure 12-9

29. Muscle Fatigue: Multiple Causes
Extended submaximal exercise
Depletion of glycogen stores
Short-duration maximal exertion
Increased levels of inorganic phosphate
May slow Pi release from myosin
Decrease calcium release
Potassium is another factor in fatigue

30. Length-Tension Relationships in Contracting Muscle
The strength of the contraction is related to the length before the muscle contracts. Very short fibers do not produce much tension because there is a lot of overlap not allowing for much sliding and not many new crossbridges. At optimum lenght there is an optimum number of cross-bridges to there is optimum tension. At a longer length there is less overlap and less ability to produce optimal force
Figure 12-16

31. Electrical and Mechanical Events in Muscle Contraction
A twitch is a single contraction-relaxation cycle
Figure 12-12

32. Summation of Contractions
Stimuli is too far apart and allows the muscle to relax and lose tension
If action potentials come in at a closer time they recruit more fibers and the additive effect results in increased muscle tension
Figure 12-17a

33. Summation of Contractions
The more stimulus the more fibers recruited until there is a maximum tension but is there is alot of time between the stimulus the muscle relaxes resulting in an unfused tetanus
Figure 12-17c

34. Summation of Contractions
Complete tetanus results when action potentials arrive close enough to not allow the muscle to relax. Maximum tension can only be sustained for a limited time because fatigue
Figure 12-17d

35. Motor Units: Fine motor movements have more innervations

36. Mechanics of Body Movement
Isotonic contractions create force and move load- creates force and moves a load.
Concentric action is a shortening action- contraction that flexes the joint while working against a load
Eccentric action is a lengthening action- contraction that extends the joint while resisting a load
Isometric contractions create force without moving a load- the muscle produces tension and contracts but does not move the joint.

37. Isotonic and Isometric Contractions
Figure 12-19

38. Muscle Contraction
Duration of muscle contraction of the three types of muscle- in smooth muscle contraction and relaxation happen slower and can be sustained for a longer time.
Figure 12-24

39. Smooth Muscle: Properties
Uses less energy- can maintain maximum tension while using only a small percentage of the total maximum cross bridge
Maintain force for long periods- allows organs to be tonically contracted and maintain tension for a long time (sphincter muscles)
Low oxygen consumption- allows for to maintain tension for a long time without fatiguing (bladder).

40. Smooth Muscle
Smooth muscle is not studied as much as skeletal muscle because
It has more variety- impossible to come up with a single muscle function model- special types for vascular, gastrointestinal, urinary, respiratory, reproductive, and ocular
Anatomy makes functional studies difficult- fibers within cells and muscle layers within organs run indifferent directions.
It is controlled by hormones, paracrines, and neurotransmitters
It has variable electrical properties- contraction is not triggered only action potential
Multiple pathways influence contraction and relaxation- acts as an integrating center to interpret mutiple excitatory and inhibitory signals that may arrive at the same time

41. Smooth Muscle Locations
IV. Smooth Muscle- A tissue formed by uninucleated spindle shaped cells found in six areas of the body: blood vessel walls, respiratory tract, digestive tubes, urinary organs, reproductive organs, and the eye.

42. Smooth Muscle layer orientations

43. Cellular details of smooth muscle

44. Muscle Disorders
Muscle cramp: sustained painful contraction – hyperexcitability of the motor unit, countered with stretching
Overuse – excessive use that causes tearing in the muscle structures (fibers, sheaths, tendon connection)
Disuse- loss of muscle activity causes muscle atrophy because of loss of blood flow, can recover is disuse is less than a year
Acquired disorders – infectious diseases and toxin poisoning that lead to muscle weakness or paralysis
Inherited disorders -
Duchenne’s muscular dystrophy – muscle degenrates from pelvis up, happens most often in women, people live to be 20-30, die of respiratory failure
Dystrophin –links actin to proteins in cell membrane
McArdle’s disease – limited exercise tolerance
Glycogen to glucose-6-phosphate – enzyme missing thus muscles do not have the energy source available.