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Anatomy and Physiology > A&P Chp. 9: Muscles and Muscle Tissue > Flashcards

A&P Chp. 9: Muscles and Muscle Tissue Flashcards

1
Q

Muscle Term Prefixes

A

Myo- Mys- Sarco-

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2
Q

Skeletal Muscle Tissue

A

Has obvious stripes called striations
Often activated by reflexes, but voluntary muscles
Only type subject to conscious control
Think skeletal, striated, voluntary

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3
Q

Cardiac Muscle Tissue

A

Only in heart
Striated, not voluntary
Can and does contract without being stimulated by the nervous system
Think cardiac, striated, and involuntary

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4
Q

Smooth Muscle Tissue

A

Found in walls of hollow visceral organs, such as the stomach urinary bladder, and respiratory passages
Forces fluids and other substances through internal body channels
No striations, involuntary
Visceral, nonstriated, involuntary

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5
Q

Special Characteristics of Muscle Tissue

A

Excitability (responsiveness): ability to receive and respond to a stimulus
Contractibility: ability to shorten forcibly when adequately stimulated
Extensibility: ability to extend or stretch
Elasticity: ability of a muscle cell to recoil and resume its resting length after stretching

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6
Q

Muscle Functions

A 
Producing Movement
Maintaining Posture and Body Position
Stabilizing Joints
Generating Heat
Protect fragile internal organs
Regulates passage of substances through internal body openings
Dilates and constricts the pupils of your eyes 
Forms the arrector pili muscles
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7
Q

Layers of Skeletal Muscle (deep to superficial)

A

Muscle fiber (cell): wrapped in endomysium
groups to form
Fasicles: wrapped in perimysium
groups to form
A single muscle: wrapped in epimysium
Forms connective tissue, deep fascia (diveded into muscle groups), superficial fascia/hypodermis, dermis, epidermis, air

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8
Q

Muscle Attachments

A

Insertion: movable bone
Origin: immovable or less movable bone
Direct/fleshy: epimysium of the muscle is fused to the periosteum of a bone or perichondrium of a cartilage
Indirect: the muscle’s connective tissue wrappings extend beyond the muscle either as a ropelike tendon or as a sheetlike aponeurosis

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9
Q

Four steps of Muscle Contraction

A
  1. Fiber must be activated, that is, stimulated by a nerve ending so that a change in membrane potential occurs.
  2. Generate an electrical current, called an action potential, in its sarcolemma.
  3. Action potential is automatically propagated along sarcolemma
  4. Intracellular calcium ion levels must rise briefly, providing the final trigger for contraction
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10
Q

Sarcolemma

A

The cell membrane of a muscle fiber

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11
Q

Sarcoplasm

A

the cytoplasm of a muscle fiber

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12
Q

Myofibrils

A

bundles of contractile protein filaments (myofilaments) arranged in parallel, fill most of the cytoplasm of each muscle fiber

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13
Q

Sarcomeres

A

the repeating unit of contraction in each myofibril

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14
Q

mitochondria

A

provide the ATP required for contraction

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15
Q

Sarcoplasmic Reticulum

A

smooth ER

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16
Q

Myofilaments

A

Thin filaments: actin (plus some tropomyosin and troponin)
Thick filaments: myosin
Elastic filaments: titin (connectin) attaches myosin to the Z discs (very high mol. wt.)

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17
Q

Striations/Sarcomeres

A

Z discs (lines): the boundary between sarcomeres; proteins anchor the thin filaments; bisects each I band
A (anisotropic) band: overlap of thick (myosin) filaments and thin filaments
I (isotropic) band: thin (actin) filaments only
H zone: thick filaments only
M line: proteins anchor the adjacent thick filaments

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18
Q

Myosin Protein

A

Each head (2 heads): Each head contains ATPase and an actin-binding site; breaks to produce energy; splitting ATP releases energy which causes the head to “rachet” and pull on actin fibers

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19
Q

Thin (Actin) Myofilaments

A

Two G actin strands are arranged into helical strands
Each G actin has a binding site for myosin
Two tropomyosin filaments spiral around the actin strands
Troponin regulatory proteins (“switch molecules”) may bind to actin and tropomyosin and have Ca2+ binding sites

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20
Q

Muscle Fiber Triads

A

Triads: 2 terminal cisternae + 1 T tubule
Sarcoplasmic Reticulum (SER): modified smooth ER, bag of calcium
Terminal cisternae: large flattened sarcs of the SER
Transverse T tubules: inward folding of the sarcolemma; extension of the cell membrane that continues through the cell incasing the myofibers

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21
Q

The Neuromuscular Junction

A

Axon terminal: end of the axon
Motor end plate: specialized region of the muscle cell plasma membrane adjacent to the axon terminal (folds are called junctional folds so surface area across from axon is highly increased; receptor plates to receive neurotransmitters)
Synapse: point of communication is a small gap
Synaptic Cleft: space between axon terminal and motor end plate
Synaptic vesicles: membrane-enclosed sacs in the axon terminals containing a neurotransmitter
Neurotransmitter: chemical messenger that travels across the synapse (acetylcholine ACh)

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22
Q

Acetylcholine ACh Receptors

A

integral membrane proteins which bind to the neurotransmitter acetylcholine ACh
Released through exocytosis
Triggered by Ca
Receptors are ligand-gated sodium channels (No Potassium moving)

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23
Q

Action Potential

A

large transient depolarization of the membrane potential

transmitted over the entire sarcolemma (and down the T tubules)

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24
Q

Generation of an Action Potential (Excitation)

A
  1. Binding of neurotransmitter (ACh) causes ligand-gated Na+ channels to open
  2. Opening of the Na+ channels depolarizes the sarcolemma (cell membrane)
  3. Initial depolarization causes adjacent voltage-gated Na+ channels to open; Na+ flows in, triggering an action potential
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25
Depolarization
Making the cell more positive or less negative
26
Repolarization
Returning to original polarization due to closing the voltage-gated Na+ channels and the opening of the voltage gated K+ channels
27
Refractory Period
time during membrane repolarization when the muscle fiber cannot respond to a new stimulus (few milliseconds)
28
All-or-None Response
once an action potential is initiated it results in a complete contraction of a muscle
29
The Power Stroke
1. Cross Bridge Attachment: myosin binds to actin 2. The Working Stroke: myosin changes shape (pulls actin toward it); releases ADP + Pi 3. Cross Bridge Detachment: myosin binds to new ATP; releases actin 4. "Cocking" of the myosin head: ATP hydrolyzed (split) to ADP + Pi; provides potential energy for the next stroke
30
The "Rachet Effect"
Repetition of Power Stroke resulting in shortening of sarcomeres and myofibrils until Ca2+ ions are removed from the sarcoplasm of the ATP supply is exhausted.
31
Excitation-Contraction Coupling
1. The action potential (excitation) travels over the sarcolemma, including T-Tubules 2. DHP receptors serve as voltage sensors on the T-Tubules and cause ryanodine receptors on the SR to open and release Ca2+ ions into the cytosol 3. Ca2+ binds to troponin, causing tropomyosin to move out of its blocking position 4. Myosin forms cross bridges to actin, the power stroke occurs, filaments slide, muscle shortens. 5. Calsequestrin and calmodulin help regulate Ca2+ levels inside muscle cells; Ca2+ pumps on the SR remove calcium ions from the sarcoplasm when the stimulus ends
32
Destruction of Acetylcholine
Acetylcholinesterase: an enzyme that rapidly breaks down acetylcholine is located in the neuromuscular junction; prevents continuous excitation (generation of more action potentials) Many drugs and diseases also interfere
33
Myasthenia gravis
loss of function at ACh receptors; skeletal muscle weakness; Ex: hard time keeping eyes open; possibly an autoimmune disease
34
Curare (poison arrow toxin)
binds irreversibly to and blocks the ACh receptors
35
Muscle Contraction (tug-of-war)
One power stroke shortens a muscle about 1% Normal muscle contraction shortens a muscle by about 35% The Cross Bridge (Rachet Effect) cycle repeats bringing Z lines together About half the myosin molecules are attached at any time Cross bridges are maintained until Ca2+ levels decrease
36
3 phases of a Myogram
1. Latent Period: delay between stimulus and response. excitation occurs 2. Contraction phase: tension or shortening occurs 3. Relaxation phase: relaxation or lengthening
37
3 Ways Contraction Force Can Be Altered
1. changing the frequency of stimulation (temporal summation) 2. changing the stimulus strength (recruitment) 3. changing the muscle's length
38
Rigor Mortis
Ca2+ ions leak from SR causing binding of actin and myosin and some contraction of the muscles Lasts less than 24 hours, then enzymatic tissue disintegration eliminates it in another 12 hours.
39
The Motor Unit
= Motor Neuron + Muscle Fibers to which it connects (synapses) Size: small" two muscle fibers/unit (larynx, eyes); large: hundreds to thousands of units (biceps, gastrocnemius, lower back muscles)
40
Temporal (Timing) Summation
contractions repeated before complete relaxation, leads to progressively stronger reactions. Treppe: the staircase look Unfused (incomplete) tetanus: frequency allows only incomplete relaxation. Fused(complete) tetanus: frequency of stimulation allows no relaxation.
41
The Size Principle
As stimulus intensity increases, motor units leads with larger fibers are recruited.
42
Stretch: Length-Tension Relationship
Stretch (sarcomere length) determines the number of cross bridges Extensive overlap of actin with myosin: less tension Optimal overlap of actin with myosin: most tension Reduced overlap of actin with myosin: less tension Optimal overlap: most cross bridges available for the power stroke and least structural interference
43
Contraction of a Skeletal Muscle
Isometric: muscle does not shorten, tension increases Isotonic: tension does not change, muscle length shortens
44
Multiple Motor Unit Summation (Recruitment)
The stimulation of more motor units leads to more forceful contraction. More neurons are being stimulated. More tension equals more force.
45
Muscle Tone
Regular small contractions caused by spinal reflexes
46
Muscle Metabolism
Energy availability Not much ATP is available at any given moment ATP is needed for cross bridges and Ca2+ removal Maintaining ATP levels is vital for continued activity 3 ways to replenish ATP
47
Direct Phosphorylation: Creatine Phosphate System
One of the three ways to replenish ATP CrP stored in cell Allows for rapid ATP replenishment 10-30 seconds worth of energy
48
Anaerobic Glycolysis: Lactic Acid System
``` One of the three ways to replenish ATP No O2 required Does not create much ATP Only useful for 30 seconds to 1 minute Produces lactic acid as a by-product Glycolysis turns to lactic acid which builds up causing muscle burning ```
49
Aerobic System
Uses oxygen from RBCs in the blood and the myoglobin storage depot (explains why muscles contain so many blood vessels) Uses many substrates such as carbs (glucose), lipids, and proteins Good for long term exercise May provide 90-100% of the needed ATP during these periods
50
Oxygen Deficit
The amount of O2 needed to get back to the pre-exercise state Circulating lactic acid is converted back to glucose by the liver o2, ATP CrP and glycogen levels, and a normal ph must be restored
51
Factors Affecting the Force of Contraction
1. Number of muscle fibers contracting (recruitment) 2. Size of the muscle: muscle cells get bigger (more myofibrils, more actin/myosin, more protein due to protein synthesis) 3. Frequency of stimulation 4. Degree of muscle stretch when the contraction begins
52
Muscle Fiber Type: Speed of Contraction
1. Slow oxidative fibers: contract slowly, have slow acting myosin ATPases, and are fatigue resistant; use anaerobic to make ATP 2. Fast oxidative fibers: contract quickly, have fast myosin ATPases, and have moderate resistance to fatigue; aerobic to make ATP 3. Fast glycolytic fibers: contract quickly, have fast mysocin ATPases, are easily fatigued; use glycolysis to make ATP
53
Peristalsis
alternating contractions and relaxations of smooth muscles that squeeze substances through the lumen of hollow organs; think digestion
54
Segmentation
contractions and relaxations of smooth muscles that mix substances in the lumen of hollow organs
55
Smooth Muscles
Contracts under the influence of autonomic nerves, hormones, and local factors. Some smooth muscles act as pacemakers and set the contractile pace for whole sheets of muscle and are self-excitatory and depolarize without external stimuli
56
Muscular Dystrophy
homeostatic imbalances group of inherited muscle-destroying diseases where muscles enlarge due to fat and connective tissue deposits, but muscle fibers atrophy
57
sarcopenia
muscle mass loss
58
Duchenne Muscular Dystrophy
Inherited lack of functional gene for formation of a protein, dystrophin, that helps maintain the integrity of the sarcolemma Cell membrane doesn't stay in tact, lost control of osmotic process, cell starts to die
59
Intercalated Discs
Desmosomes: connect cells | Gap Junctions: Electrical synapses; excitation spreads rapidly
60
Cardiac Muscle Tissue
Striated; unicellular; branched; intercalated discs
61
Smooth Muscle
No striations (no sarcomeres); uninucleate; spindle-shaped; involuntary; may have gap junctions

Anatomy and Physiology (6 decks)

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