1. Muscle Tissue
Chapter 9
Biology 2121

2. Muscle Functions (1). Maintaining posture (2). Stabilizing joints
(3). Generating heat
(4). Storing and Moving
Smooth muscle (peristalsis)

3. Functional Characteristics of Muscle
(1). Excitability and Irritability
(2). Contractility
Ability to shorten
(3). Extensibility
Ability to be stretched
(4). Elasticity
Ability to recoil and resume original shape

4. Skeletal Muscle Tissue
Function
Voluntary
Large Cells
10 to 100 um diameter
30 cm length
Multinucleated
Striated
Functional Syncyntium

5. Smooth Muscle Tissue Functions Locations Uninucleated Non-striated
Hollow organs
“Visceral”
Uninucleated
Spindle-shaped cells
Non-striated
Involuntary
Peristalsis

6. Cardiac Muscle Tissue Function – Location Involuntary Striated
Intercalated discs
Specialized gap junctions

7. Skeletal Muscle Gross Anatomy
(1). Each skeletal muscle is a discrete organ
(2). Each muscle is supplied with Nerve and Blood tissue.
(3). Organizational levels of skeletal muscles page 282

8. Organization Level – Muscles

9. Connective Tissue Sheaths
Endomysium
Areolar CT fibers
Perimysium
Dense irregular fiberous CT
Epimysium
Dense irregular CT
CT sheaths
Connective Tissue Sheaths

10. Attachments – Skeletal Muscle Attach to Bones
Tendons
Aponeurosis
Direct or Indirect Attachments

11. Fascia
Superficial- Hypodermis
Deep
Epimysium
Endomysium
Perimysium

12. Blood and Nerve Supply Veins Muscle Contraction Artery Arterioles
Somatic Motor Neurons
-part of Peripheral Nervous System motor division
Muscle Contraction
Artery
Arterioles
Capillaries
Venuoles
Blood Returns to the Heart
Veins

13. Microscopic Anatomy – Skeletal Muscle
(1). Skeletal Muscle fiber
Size: multiple nuclei; um diameter; some 30 cm long
Syncytium
Sarcolemma
Sarcoplasma
(2). Myofibrils
1-2 um diameter; mitochondria and other organelles; densely packed
Contractile elements: striations, sarcomeres, and myofilaments

14. Myofilaments - Striations
Sarcomeres
Area between two Z discs
Smallest contractile unit (functional unit)
Myofilaments - Striations
Thick: span the entire A band
myosin
Thin: across I band and partly across (A)
Actin

16. Muscle Proteins Titin,Nebulin,Myomesin Actin, Myosin
Structural
Contractile
Regulatory
Titin,Nebulin,Myomesin
Actin, Myosin
Tropomyosin, Troponin

17. Ultrastructure of Myofilaments
Myosin (protein)
Two globular heads
Tail two interwoven polypeptide chains (heavy)
Thin filaments (Actin protein)
Tropomyosin
Troponin: 3-polypeptides
TnI ; TnT ; TnC
Elastic filaments
Titin

18. Microscopic Structure- Actin and Myosin

19. Sarcoplasmic Reticulum regulates intracellular levels of calcium ions
T Tubules
Triads: terminal cisterna, T tubule, terminal cisterna
Triad Relationship –integral proteins
T tubule proteins
SR proteins (foot proteins)

20. How muscles contract Sliding Filament Model Exitation-Coupling
Link (ch.7-myofilament and sarcomere contraction)

21. Sliding Filament Model of Contraction
Relaxed
Fully Contracted

22. What Causes a Muscle Contraction to Occur?
Muscle Contractions – Nerve Stimulation
Neuromuscular Junction
Nerves contain Neurotransmitters
Muscle contraction – Acetylcholine (ACh)
NT bind to sarcolemma of muscle (Receptor Sites)
Causes a nerve impulse (Action Potential)
Stimulates the Sarcoplasmic Reticulum to release Ca++
Stimulates the muscles to contract

23. Neuromuscular Junction

24. Neuromuscular Junction - Steps
1. Nerve impulse reaches axonal end
2. Voltage-gated channels open- Ca 2+ ions flow in
3. Synaptic vesicles fuse with axonal membrane
4. NT (ACh) released via exocytosis
5. ACh diffuses across the synaptic cleft and fuses with sarcolemma ACh receptors
ACh is the NT
6. Causes an electrical event stimulates muscle contraction
Action Potential
7. ACh is degraded by acetylcholinerasterase
Link (ch. 7 neuromuscular junction)

25. Generation of an Action Potential
(a) Polarized membrane
-70 mV (resting membrane potential)
(+) outside; (-) inside
(b) Depolarization
(c) Propagation
(d) Repolarization

26. Generation of action potential across sarcolemma
1. SODIUM (OUTSIDE) MORE + ; POTASSIUM (INSIDE) MORE –
2. When ACh binds to receptors, ion channels open.
3. More Na goes into the cell than K moving out.
4. Cell becomes less negative. “Depolarized”
5. This begins the Action Potential
II. Steps in the Action Potential
1. Currents spread to adjacent areas along the membrane, become depolarized and gates open and Na diffuses in.
2. Propagation of AP: moves along the length of the Sarcolemma; gates continued to be opened and the AP spreads.
3. Repolarization: Follows behind the depolarization wave; Na gates close and K opens and K diffuses out rapidly down concentration gradient.
4. Refractory period: until repolarization is complete, muscle cannot be stimulated again; original membrane potential is restored.

27. Excitation-Contraction Coupling – Sequence of Events by which transmission of an Action Potential leads to sliding of the filaments (contraction)
Steps in Excitation and Contraction
1. AP propagates down sarcolemma to T tubules.
2. At the triad the AP causes the SR to release Ca ions into the sarcoplasm.
3. Some Ca binds to troponin and it changes shape and removes the blockade of tropomyosin.
4. Myosin heads attach and pull the thin filaments to center of sarcomere.
5. Ca disapates, and the AP is over; Ca moved back into the SR via Ca pump (ATP driven) (page 293)
6. When Ca drops very low the tropomyosin again blocks the myosin binding sites.

28. Excitation-Contraction Coupling
1. AP propagates along sarcolemma and down T-Tubule
2. AP transmission past triads --- terminal cisternae of SR --- releases calcium ions
Becomes available to the myofilaments
3. Calcium binds to troponin -- changes shape- removes blocking action of tropomyosin
4. If Ca levels (10-5 M) myosin heads attach and pull thin filaments toward center of sarcomere
Cross-bridge formation
5. Ca signal ends (30ms)-- Ca levels fall (ATP calcium pump-back into SR)
6. Tropomyosin blocks binding site ending cross-bridge activity

30. Role of Ionic Calcium in Contraction
1. Tropomyosin blocks binding site (low Ca levels)
2. As Ca levels rise, binds to TnC of troponin
3. Troponin undergoes a transformation change- moves tropomyosin away from binding site
4. Attachment of myosin head
Notes on the Slide
TnT, TnC and Tnl are regulatory proteins in troponin.
Ca binds to the TnC which makes the troponin change shape and allow for exposure of the binding sites.

31. Events in Muscle Fiber Contraction
1. Cross-bridge is formed
2. Power Stroke
3. Cross-bridge detachment
4. Cocking of myosin head
Rigor Mortis

32. Events in the Sliding of Thin Filaments During Contraction
Notes on this Slide
Formation of the Cross-Bridge
Heads are fully attached to the tropomyosin on actin
Power Stroke
Head pivots changing from high energy configuration to low energy config (bent); this pulls on the actin sliding it towards the center of the sarcomere.
ADP And Pi are released from the head
Detachment
ATP binds to head, myosin loosens hold on actin and CB detachment occurs
Cocking
ATPase hydrolyses ATP; energy is released and the head returns to pre-stroke cocked position. Ready for another CB formation.

33. Links for Action Potential and Coupling
Link (ch. 7 – action potential)
NHC (sliding filament)

34. Each axon divides and serves muscle fibers
Each muscle
is served by one motor nerve or neuron which contains axons of hundreds of motor neurons (may serve many muscle fibers or a few)
Cell body of neuron
Contained within the spinal cord ‘grey matter’
Each axon divides and serves muscle fibers
All muscle fibers contract when the motor neuron sends impulses
Muscle control – fine vs weight bearing

35. Graded Muscle responses
Myogram
Response of motor unit to a single action potential of its motor neuron is called a muscle twitch
Latent period
Contraction
Relaxation
Graded Muscle responses
Muscle Twitch
Myogram: Produced when a muscle is attached to an apparatus
Twitch: response of a motor unit to a single action potential; involves a contraction and relaxation.
3. Parts of a myogram
Latent period
Ms following stimulation; excitation and coupling is occuring but cannot see on the myogram
Contraction
CB are activated ms
Relaxation
Ca reenters the SR; CB broken
4. Graded Responses
Healthy muscle contractions are smooth unlike the muscle twitch
Graded responses are control mechanisms for smooth contractions
Changes in Stimulation Frequency
Two identical stimuli are applied to a muscle in succession, second twitch is always stronger (wave summation)
Occurs before the muscle has relaxed.
Why? More Ca is released, muscle tension during the second contraction caused more shortening than the first
Summation of contractions (refractory period is always honored)
Sustained stimulation at faster rates causes the summation to be greater, quivering (incomplete tetanus)
If all relaxation disappears complete tetanus occurs
Response to strong stimuli
Force of contraction is controlled by motor unit summation
Called recruitment (many muscle fibers are called into play)
First contraction occurs- threshold
Max stimulus- strongest stimulus that produces a contractile force.
Increasing the stimulus beyond this point will not make the muscle contract stronger.
Recruitment accounts for a smooth touch or pat and the same hand can deliever a blow.
Treppe
When the same stimulus is applied the contractions get more strong
Due to increase in Ca ions opening up more binding sites.
As the muscle works harder it produces heat which makes it more pliable.

36. Twitches and Wave Summations

37. Treppe: Initial contractions are not as strong as later contractions caused by the same amount of stimulus. Why? Increasing availability of Ca in the SR; Increasing Ca increase the number of troponin binding sites open; muscles warm up and liberate heat making them more pliable