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BMSC 207 > Muscles > Flashcards

Muscles Flashcards

1
Q

What is the primary function of all muscle?

A

The primary function of all muscle is to generate force and/or movement in response to a physiological stimulus.

• Body movement
• Maintenance of posture
• Respiration
• Production of body heat
• Communication
• Constriction of organs and vessels
• Heart beat

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2
Q

Where do the three types of muscle reside?

A

Skeletal – mostly attached to skeleton but also to other muscles

Smooth – walls of hollow organs, blood vessels

Cardiac- heart

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3
Q

What is the main function of the three muscle types? (“All develop force and shorten for…”)

A

Skeletal – movement, posture, heat production

Smooth – varies with structure involved

Cardiac – pumps blood out of heart

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4
Q

Where do the three types of muscles contraction initiate?

A

Skeletal – exclusively neural (neuromuscular transmission)

Smooth – myogenic (pacemaker), neural, stretch, hormonal, local mediators

Cardiac- myogenic (pacemaker)

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5
Q

What is the role of innervation of the three muscle types?

A

Skeletal – initiate contraction

Smooth – can initiate / modify contraction

Cardiac – modify conduction/contraction

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6
Q

What do the three types of muscle innervates and what level of control do they imploy?

A

Skeletal – somatic nerves, conscious / subconscious regulation

Smooth – autonomic nerves / involuntary

Cardiac – autonomic nerves / involuntary

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7
Q

Do the muscle cells of the three types of muscle electrically couple (gap junctions)? (All muscle cells respond as one)

A

Skeletal – NO

Smooth – Varies (unitary versus Multiunit)

Cardiac – YES (within each chamber)

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8
Q

What is the mechanism of contraction for the three types of muscle cells?

A

Skeletal – sliding-filament mechanism

Smooth – sliding filament mechanism

Cardiac - sliding filament mechanism

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9
Q

Are thick (myosin) and thin (actin) filaments present in each of the three muscle types?

A

Skeletal – YES

Smooth – YES

Cardiac – YES

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10
Q

Are Troponin and tropomyosin present in the three muscle types?

A

Skeletal – YES

Smooth – tropomyosin only

Cardiac- YES

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11
Q

Are T tubules present in each of the three muscle types?

A

Skeletal – YES

Smooth – NO

Cardiac – YES

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12
Q

In the three muscle types, is cross bridge cycling turned on by calcium?

A

Skeletal – YES (thin filament control)

Smooth – YES (thick filament control)

Cardiac- YES (thin filament control)

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13
Q

What is the source of cytosolic calcium in each of the three muscle types?

A

Skeletal – sarcoplasmic reticulum (SR)

Smooth – Extracellular fluid + SR (varies)

Cardiac – Extracellular fluid (10%) + SR (90%)

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14
Q

In the three muscle types, what is the nature of “calcium sensor” for contraction?

A

Skeletal – Troponin

Smooth – Calmodulin

Cardiac- Troponin

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15
Q

In the three muscle types, what activates cross bridge cycling?

A

Skeletal – Ca2+ binding to troponin / removal of interaction block between myosin and actin

Smooth – Ca2+ binding to calmodulin / Activation of myosin light chain kinase and phosphorylation of myosin light chain

Cardiac – Ca2+ binding to troponin / removal of interaction block between myosin and actin

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16
Q

In each of the three muscle types, what terminates contraction?

A

Skeletal – Breakdown of Acetylcholine / re-uptake of Ca in SR

Smooth – Decrease sarcoplasmic Ca / Myosin light chain phosphatase

Cardiac- Repolarization / Decrease sarcoplasmic Ca

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17
Q

In each of the three muscle types, what type of metabolism is present?

A

Skeletal – oxidative / glycolytic

Smooth – dominantly glycolytic

Cardiac – Dominantly oxidative

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18
Q

In each of the three muscle types, what regulates force?

A

Skeletal – Frequency of stimulation and motor unit summation

Smooth – Balance of Myosin light chain kinase and phosphatase activity

Cardiac- Regulation of calcium entry

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19
Q

In each of the three muscle types, what is the contraction speed/energy usage?

A

Skeletal – FAST / 20% BMR (rest)

Smooth – SLOW / 1-2% BMR (economical)

Cardiac – INTERMEDIATE / 10% BMR

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20
Q

What is the striation on the three muscle types?

A

Skeletal: striated

Smooth: smooth

Cardiac: Striated

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21
Q

What is the fiber arrangement of the three muscle types?

A

Skeletal: Sarcomere

Smooth: No Sarcomere

Cardiac: Sarcomere

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22
Q

What is the nucleation of the three muscle types?

A

Skeletal: Multinucleate

Smooth: Uninucleate

Cardiac: Uninucleate

23
Q

What is origin, insertion, antagonistic muscle groups, flexor, extensor vocabulary in skeletal muscle?

A

• Origin: closest to the trunk or to more stationary bone
• Insertion: more distal or more mobile attachment
• Antagonistic muscle groups: flexor-extensor pairs
• Flexor: brings bones together
• Extensor: moves bones away

24
Q

What is the level of organization for skeletal muscle?

A

Skeletal muscle > muscle fascicle > muscle fiber > myofibril > sarcomere > thick filament > thin filament

25
Q

What is F-actin?

A

F-Actin: back bone of thin filaments, double stranded alpha helical polymer of G-actin molecules. Contains binding site for thick filaments (myosin).

26
Q

What is tropomyosin?

A

Tropomyosin: two identical alpha helicies that coil around each other and sit in the two grooves formed by actin strands, regulates the binding of myosin to actin.

27
Q

What is the Troponin complex? What does it consist of?

A

Troponin complex: heterotrimer consisting of
[1] troponin T (TnT):binds to a single molecule of tropomyosin
[2] troponin C (Tnc):Ca2+ binding site
[3] troponin I (TnI):under resting conditions is bound to actin inhibiting contraction
Situated ~ every 7 actin molecules

28
Q

What are thick filaments? What is the structure of thick filaments?

A
  • Consist of a bundle of Myosin molecules
    -Two intertwined heavy chains
    -Each heavy chain contains two light chains: essential light chain (MLC-1), regulatory light chain (MLC-2)
  • Myosin head contains a region for binding actin as well as a site for binding and hydrolyzing ATP (ATPase).

-Regulatory light chain regulates ATPase activity of myosin
-Essential light chain stabilizes myosin head

29
Q

What are additional proteins titian and nebulin? What do they do?

A

Titin- a very large protein extending from M line to Z line, appears to be involved in stabilization of thick filaments and the elastic recoil behavior of muscle.

Nebulin- a large protein that interacts with the thin filaments, believed to regulate the length of thin filaments and contribute to the structural integrity of myofibrils.

30
Q

What are the different components of the sarcomere? (Z disk, I bands, A band,H zone, M line)

A

Z disk-zigzag protein structure that is the attachment site for the thin filaments

I bands-Lightest band of sarcomere, region occupied only by thin filaments

A band-Darkest band of sarcomere, encompasses entire length of the thick filament, including very dark area where thin and thick filaments overlap

H zone-Central region of A band, consists only of thick filaments.

M line-proteins form the attachment site for the thick filaments, equivalent to z disk for thin filaments

31
Q

What events lead up to skeletal muscle contraction?

A

Events in CNS > Events at neuromuscular junction > excitation contraction coupling > Ca2+ signal > contraction relaxation cycle&raquo_space;Muscle twitch , sliding filament theory

Excitation-contraction coupling: an action potential initiated in the skeletal muscle fibre results in an increase in intracellular (sarcoplasmic) Ca2+

32
Q

What brain regions are involved in voluntary movement?

A

Primary motor cortex
-basal ganglia
-premotor cortex (motor association) -thalamus
-midbrain
-cerebellum

  • Corticospinal Tract: descending tract (ventral and interior lateral white matter)
  • Upper motor neuron: brain to spinal cord
  • Alpha (lower) motor neuron: spinal cord to muscle
33
Q

What is a motor unit? What is an alpha motor neuron?

A

Alpha (lower) motor neuron: from spinal cord to muscle
-A single motor neuron and all the muscle fibres it innervates is known as a motor unit.
-The area where the motor neuron makes synaptic contact
with the muscle fibre is known as the neuromuscular junction .

34
Q

What is ALS?

A

Amyotrophic lateral sclerosis (ALS)
- Neurodegenerative motor neuron disease
- Upper and/or lower motor neurons degenerate leading to muscle atrophy and weakness from disuse .

10% are genetically inherited as dominant traits (familial)
25% of these are due to a mutation in gene(s) producing superoxide dismutase
- enzymes that catalyze the dismutation of superoxide (O2−) into oxygen and hydrogen peroxide.
- Important antioxidant defense
- Eventual respiratory failure

35
Q

What are the three components of the neuromuscular junction?

A

Three components of neuromuscular junction:
1. Presynaptic motor neuron filled with synaptic vesicles
2. The synaptic cleft
3. The postsynaptic membrane of the skeletal muscle fibre.

36
Q

In the neuromuscular junction… What is the motor end plate, Junctional folds, acetylcholine?

A
  • Region of sarcolemma at the neuromuscular junction is referred to as the motor end plate
  • Junctional folds on sarcolemma increase surface area
  • Motor neuron vesicles contain acetylcholine
37
Q

What happens when an action potential arrives at the muscle axon terminal?

A
  • An action potential arrives causing voltage gated Ca channels to open. Ca entry causes synaptic vesicles to fuse with the presynaptic membrane and release ACh into the synaptic cleft.
  • Post synaptic cleft is modified into a motor end plate.
38
Q

What does the nicotinic acetylcholine receptor do?

A
  • Nicotinic cholinergic receptor binds two ACh molecules, opening a nonspecific mono alert cation channel. The open channel allows Na and K to pass. Net Na influx depolarize the muscle fiber.

Nicotinic acetylcholine receptor:
- Sarcolemma of muscle fibre contains nicotinic acetylcholine receptors.
- Member of cys-loop receptor family of ligand gated ion channels; classified as a monovalent cation channel (permeable to Na+ and K+.)

39
Q

What are the events at the neuromuscular junction?

A
  1. Motor neuron action potential moves down neuron
  2. Ca enters voltage gated channels
  3. Acetylcholine release
  4. Acetylcholine binding opens ion channels
  5. Na enters muscle generating excitatory end plate potential.
  6. Local current between depolarized end plate and adjacent muscle plasma membrane
  7. Muscle fiber action potential initiation
  8. Propagated action potential in muscle plasma membrane
  9. Acetylcholine degration.
40
Q

What ceases neural transmission?

A

Once AP’s stop firing in the alpha motor neuron acetylcholine in the synaptic cleft must be removed and will diffuse away or be broken down to acetate and choline by the enzyme acetylcholinesterase.

Choline is transported back into the motor neuron and combined with Acetyl CoA produced from mitochondria by the enzyme choline acetyltransferase to make acetylcholine.

41
Q

What is myasthenia gravis?

A

• Means severe weakness of muscle
• Disorder of neuromuscular transmission
• Can be restricted to extraocular muscles or generalized
• Autoimmune: body produces antibodies that bind to ACh receptors
• Impedes activation of AChR and eventually decreases number.
• Degeneration of postjunctional folds

42
Q

What is the Sarcoplasmic reticulum?

A

Specialized Ca2+ storage organelles known as sarcoplasmic reticulum are strategically organized with the T-tublules

43
Q

What is excitation-contraction coupling?

A

• The process by which electrical excitation of the surface membrane triggers an increase of [Ca2+]i in muscle is known as excitation-contraction coupling

44
Q

Where do T tubules attach to the myofibrils?

A

T-tubules penetrate the muscle fibre and surround the myofibrils at two points in each sarcomere, at the A and I band junctions

45
Q

Action potentials propogate from the … to the … along the …

A

Action potentials propagate from the sarcolemma to the interior of muscle fibres along the transverse tubule network

46
Q

What is a DHP receptor?

A

DHP receptor: L-type Ca2+ channel -voltage sensitive

47
Q

What is s RyR?

A

RyR-ryanodine receptor
-Ca2+ release channel on SR

48
Q

What are the steps of the initiation of a muscle action potential?

A
  1. Somatic motor neuron releases ACh at the neuromuscular junction
  2. Net entry of Na through ACh receptor-channel initiates a muscle action potential
49
Q

What are the excitation contraction coupling steps of a muscle action potential?

A
  1. Action potential in t tubule alters conformation of DHP receptor
  2. DHP receptor opens RyR ca release channels in Sarcoplasmic reticulum and Ca enters cytoplasm

-Ca2+ can also enter the sarcoplasm through L-type Ca2+ channels
-Besides mechanically, ryanodine receptors can also be activated by Ca2+ (Ca2+ induced Ca2+ release)
-But Ca2+ - induced Ca2+ release and Ca2+ entry from ECF is NOT vital in skeletal muscle

50
Q

What does an increase in [Ca2+]i trigger?

A
  • An increase in [Ca2+]i triggers contraction by removing the inhibition of cross bridge cycling
    -Ca2+ binds low affinity sites on troponin C which induces a conformational change in the troponin complex:
    -causes the troponin complex as well as tropomyosin to move revealing the myosin binding site on the actin.
51
Q

What are the steps of a muscle cell action potential?

A
  1. Muscle cell action potential propogated into T tubules
  2. Ca released from lateral sac
  3. ca binding to Troponin removes blocking action of tropomyosin
  4. Cross bridge cycling bind and generate force
  5. Ca taken up
  6. Ca removal from Troponin restores tropomyosin blocking action.
52
Q

What are the steps of the power stroke?

A

When intracellular Ca is elevated tropomyosin shifts allowing myosin to bind actin

  1. ATP binding: ATP binds to the head of myosin heavy chain reducing affinity of myosin for actin.
  2. ATP hydrolysis: ATP is broken down to ADP and inorganic phosphate (Pi) resulting in the myosin head pivoting around hinge into cocked state. The cocked head is now aligned with and binds to a new actin molecule on thin filament.
  3. The powerstroke: Dissociation of Pi from myosin head strengthens bond between actin and myosin AND triggers power stroke, a conformational change in which the myosin head returns to its un-cocked state and while doing so pulls the actin filament generating force and motion.
  4. ADP release: Dissociation of ADP from myosin causes myosin to remain bound to actin until ATP initiates the cycle again.
53
Q

How does contraction terminate?

A
  • Termination of contraction requires removal of Ca2+
  • Once the AP has subsided Ca2+ must be removed so that the myosin binding site on actin can be covered by tropomyosin
  • Ca2+ can be removed to the extracellular space by the Na-Ca exchanger or by the Ca2+ pump which uses ATP.
    -would eventually deplete the cell of any Ca2+, leaving the SR empty and because of this plays a minor role.

BMSC 207 (5 decks)

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