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FHB I - Cardiac Unit > Striated and Smooth Muscle > Flashcards

Striated and Smooth Muscle Flashcards

1
Q

What is a motor unit?

A

single motor neuron and all of the corresponding muscle fibers it innervates

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2
Q

Describe striated and smooth muscle

A

Striated- cardiac and skeletal (organized in sarcomeres)
cardiac (single unit - myocytes connected through low resistance gap junctions)
skeletal (multi-unit … every single skeletal muscle cell has nerve connected to it..each muscle fiber is innervated by only one nerve ending)

smooth muscle- most predominant in body, around blood vessels, can be single or multi unit

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3
Q 
Describe the following terms:
fascicles (a group of muscle fibers)
fascicles
myofiber
myofibrils
myofilaments

Give a summary of skeletal muscle structure.

A

fascicles- a group of muscle fibers

myofiber = muscle fiber = muscle cell

myofibrils (composed of many repeating sarcomeres)

myofilaments (myosin and actin filaments)

  • muscle is composed of fascicles
  • each fascicle contains bundle of muscle fibers (cells)
  • within each fiber are myofibrils composed of thick and thin filaments
  • arrangement of filaments gives muscle its striped (striated) appearance
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4
Q

Describe the connective tissue sheaths of muscle
endomysium
perimysium
epimysium

A

endomysium- surrounds individual fibers, contains capillaries
perimysium- surrounds each fascicle, contains blood vessels and nerves
epimysium-surrounds entire muscle

epimysium, perimysium and endomysium all come together at ends of muscles to form tendons

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5
Q

What is a myofibril composed of?

A

myofibril is composed of many repeating sarcomeres

sarcomere= basic contractile unit (is about 2 microns)

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6
Q 
Describe and draw the sarcomere: 
A band
I band
M line
Z line
H zone

“sliding filament theory”

A

1 sarcomere = Z line to Z line
A band = dark (thick filaments myosin and some overlapping thin filaments actin)
I band- light thin filaments only (actin only)
M line: contains proteins that anchor the thick filaments together (M line inside H zone)
Z line- where actin filaments attach

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7
Q

Describe the thick filament: myosin

A

thick filament = polymer of approx 200 myosin molecules

Myosin binds actin and has ATPase activity

-one myosin protein has 2 heavy chains and 4 light chains

the chains coil to form a rod (tail) region and 2 globular heads (cross bridges)

globular head 1) binds actin
2) contains ATPase activity

Each pair of heads is oriented 120 degrees from the next pair so myosin thick filament interacts with thin filament in 3D

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8
Q

Describe the thin filament: actin, troponin, tropomyosin (What is thin filament composed of? Describe at rest and when activated.)

A

F-actin is a double stranded helix composed of many G-actin monomers (about 360)

the thin filament is a complex of several interacting proteins
F-actin, tropomyosin, troponin-T, Troponin-I, Troponin-C

1 tropomyosin and troponin complex per 7 actin monomers

Each G-actin has a binding site for myosin
At rest: binding site blocked by the troponin-tropomyosin complex
When activated: t-t complex move into the “actin groove” exposing the myosin binding site

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9
Q

What is sarcolemma?

A

plasma membrane of muscle fibers

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10
Q

What are transverse tubules (T-tubule)?

A

invaginations of sarcolemma into the muscle fiber, conduct muscle AP, they are closely apposed to the SR, Dihydropyridine receptor (DHPR) on the T-tubule functions as the voltage sensor

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11
Q

Describe the Sarcoplasmic Reticulum (SR).

A

a special type of smooth endoplasmic reticulum of muscle and store a high concentration of Ca2+. Ryanodine receptor (RyR) or the SR membrane is the Ca2+ releasing channel

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12
Q

Describe muscle triad.

A

association of one T-tubule with 2 adjacent “lateral sacs” of SR

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13
Q

What is SERCA?

A

sarcoplasmic and endoplasmic reticulum Ca2+ ATPase - a Ca2+ ATPase (calcium pump) in the SR membrane

pumps Ca2+ from cytoplasm into SR lumen to restore Ca2+ gradient.

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14
Q

How does the NS communicate with muscle?

A

through neuromuscular junctions. work like a synapse between neurons

  • the impulse arrives at the end bulb,
  • chemical transmitter is released and diffuses across the neuromuscular cleft,
  • the transmitter molecules fill receptor sites in the membrane of the muscle & increase membrane permeability to sodium,
  • Na+ then diffuses in & the membrane potential becomes less negative,
  • and, if the threshold potential is reached, an action potential occurs and travels along the sarcolemma, and the muscle contracts.
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15
Q

What is the neurotransmitter in NMJ?

What is its receptor on the postjunctional membrane?

Describe what happens when the receptor is activated.

A 
Ach
Acetylcholine receptor (AchR) - it is nicotinic in nature and when activated by Ach, it opens as a cationic channel (mainly Na+) ...receptor has 5 subunits

Released Ach is rapidly hydrolysed to inactive choline and acetate, catalysed by the enzyme acetyl cholinesterase

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16
Q

What is excitation-contraction coupling?

A

A process whereby membrane depolarization (electrical) is transformed into a chemical signal to initiate muscle contraction

Ca2+ (calcium) is the link between excitation and contraction

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17
Q

What are the six steps in muscle contraction?

A
  1. Excitation-Contraction Coupling
    a. Action potential travels into T-tubule
    b. Depolarization activates DHPR
    c. DHPR conformational change activates RyR
    d. Ca2+ release from SR
    e. Ca2+ initiates muscle contraction
    f. SERCA pumps Ca2+ back into SR lumen (muscle relaxes)
  2. Ca2+ binds troponin
  3. Troponin/tropomyosin move to actin groove
  4. myosin binds actin
  5. Crossbridge cycle/Powerstroke
  6. Calcium sequestration = relaxation
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18
Q

Label/Draw graph for events during muscle contraction.

A

See slide 26.

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19
Q

What is the steric hindrance model?

A

Striated muscle contraction is regulated by the thin filament regulatory proteins

At Rest, troponin & tropomyosin inhibit the binding of myosin to actin

(slide 27)

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20
Q

Describe the steps in the steric hindrance model.

A

During activation (by Ca released from SR)

  1. Ca binds troponin C
  2. Conformational change so Troponin I has low actin affinity
  3. Tropomyosin and troponins move into actin groove
  4. Myosin binding site on actin is exposed
  5. Myosin binds actin crossbridge cycle
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21
Q

Describe/draw the cross-bridge cycle.

A

Diagram slide 30.

basic mechanism is the same in all muscles but how activation occurs varies among muscle types

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22
Q

Describe the muscle sarcomere: sliding filament model.

A

Free energy from cleavage of Mg*ATP induces a bend in myosin head from a 90 to 45 degree angle

Actin filaments slide toward the H zone, pulling the Z lines inward

Sarcomere shortens and muscle contracts

This happens in a wave - not synchronous for each sarcomere

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23
Q

How is the strength of muscle contraction regulated?

A
  1. twitch summation
  2. recruitment of additional motor units
  3. muscle fiber thickness
  4. length of fiber at onset of contraction (length-tension relationship)
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24
Q

Describe frequency summation.

What is happening when someone is exerting a muscle as hard as they are able?

A

Frequency summation - For skeletal muscles, the force exerted by the muscle is controlled by varying the frequency at which action potentials are sent to muscle fibers. Action potentials do not arrive at muscles synchronously, and during a contraction some fraction of the fibers in the muscle will be firing at any given time. Typically when a human is exerting a muscle as hard as they are consciously able, roughly one-third of the fibers in that muscle will be firing at once, but various physiological and psychological factors (including Golgi tendon organs and Renshaw cells) can affect that. This ‘low’ level of contraction is a protective mechanism to prevent avulsion of the tendon - the force generated by a 95% contraction of all fibers is sufficient to damage the body.

25
Q

What is twitch summation?

A

The length of a single muscle twitch is much longer than a single action potential

  • Multiple action potentials can fire during a single muscle twitch
  • Each action potential will cause the release of additional Ca2+
  • cumulative increase in Ca2+ = more available thin filaments so more crossbridges interact
26
Q

Describe muscle fiber thickness.

A

more sarcomeres in parallel add force (ex: each sarcomere produces approx. 0.3N of force)

side by side total 0.3 N (more or more sarcomeres would break if force was greater than 0.3)

stacked on top of e/o total is 0.9N

27
Q

Describe the length of fiber at start of contraction. What if it is too short? Too long?

A

If Sarcomere is too short - steric hindrance
If Sarcomere is too long – not enough crossbridges overlap with actin so less force

i.e. Length-Tension Relationship

28
Q

Draw/diagram the force-velocity relationship.

A

Slide 39 and slide 40

at maximum velocity no load, actin myosin ATPase activity

at maximum load, no shortening, number of actin-myosin interactions (cross-bridges)

29
Q

What is an isotonic contraction?

A

In an isotonic contraction, tension remains unchanged and the muscle’s length changes. Lifting an object off a desk, walking, and running involve isotonic contractions. A near isotonic contraction is known as Auxotonic contraction.

30
Q

What are two types of isotonic contractions?

A

There are two types of isotonic contractions: (1) concentric and (2) eccentric. In a concentric contraction, the muscle tension rises to meet the resistance, then remains the same as the muscle shortens. In eccentric, the muscle lengthens due to the resistance being greater than the force the muscle is producing.

31
Q

Describe concentric contractions.

A

muscle actively shortening

32
Q

Describe eccentric contractions.

A

Muscle actively lengthening
physiologically common
muscle injury and soreness associated
exercise with eccentric contractions increase muscle strength

33
Q

Describe isometric contractions.

A

muscle activity held at a fixed length

34
Q

Describe passive stretch.

A

muscle passively lengthening likely resulted from a giant protein called “Titin” within muscle fiber

35
Q

Describe an eccentric contraction induced injury.

How can muscle injury be detected?

A

See slide 42.
Left: Protocol to induce eccentric muscle contractions in human quadriceps femoris muscles.

Right: Electron micrograph demonstrating control muscle vs. the muscle that has undergone eccentric injury. Note the loss of Z-disk alignment.

Loss of cytoskeletal proteins (eg. desmin) following eccentric contraction.

Muscle injury can also be detected by elevated serum CK levels.

36
Q

What are some major ATP consuming processes?

A

In contracting muscle: Actomyosin ATPase (i.e. crossbridge cycle) accounts for 50 – 70% of all ATP consumed

Other ATP-consuming processes:
SERCA (sarcoplasmic reticulum Ca2+ ATPase) – 20-30%
Na/K ATPase -

37
Q

What are the 3 sources of muscle ATP?

A

1) Creatine phosphate:

Creatine-P + ADP  Creatine + ATP

  • reaction catalyzed by creatine kinase (CK)
  • Rapid release of ATP
  • Creatine is the first energy store used & depleted during muscle contraction (only for the first few seconds of intense activity)*
    2) Oxidative phosphorylation:
  • in mitochondria
  • requires O2 (aerobic)
  • efficient but slow synthesis of ATP (30 ATP per glucose)
  • myoglobin (O2 binding protein) gives muscle red color
  • starting material = glucose or fatty acids

3) Glycolysis—anaerboic exercise

  • fast synthesis of ATP, but LESS efficient
  • used when little O2 available
  • glycolytic muscle is whiter (less myoglobin), has fewer mitochondria, fewer vessels
  • GLYCOLYSIS PRODUCES LACTATE*
38
Q

What is the first energy store used and depleted during muscle contraction?

A

Creatine is the first energy store used & depleted during muscle contraction (only for the first few seconds of intense activity)

39
Q

How would muscles with high demand for oxidative phosphorylation appear?

A

muscles with high demand for Oxidative phosphorylation appear red (myoglobin), have LOTS of MITOCHONDRIA, and lots of blood vessels

40
Q

How many ATP per glucose?

A

Consumed -2, produced -6…net is 6 ATP per glucose

Glycolysis—anaerboic exercise

  • fast synthesis of ATP, but LESS efficient
  • used when little O2 available
  • glycolytic muscle is whiter (less myoglobin), has fewer mitochondria, fewer vessels
  • GLYCOLYSIS PRODUCES LACTATE*
41
Q

Describe 3 types of fatigue:
Central fatigue
Muscle fatigue
Neuromuscular fatigue

A

Central fatigue: can be overcome by “psyching up”

Muscle fatigue: -lactate is generated from glycolysis in the absence of sufficient oxygen, leads to fatigue

  • decreased pH—inhibits enzymes
  • also depletion of energy reserves

Neuromuscular fatigue— myasthenia gravis, etc. not common in healthy people

42
Q

What are Type I Fibers?

A

SLOW

  • myosin ATPase is slower, so slower contraction
  • Oxidative phosphorylation is primary energy source (after creatine stores used up)
  • Endurance, do NOT fatigue easily (little lactate produced)
  • postural muscles have more type I fibers
  • lots of mitochondria, blood vessels, myoglobin
43
Q

What are Type II Fibers?

A
  • FAST*
  • myosin ATPase activity is faster
  • May use GLYCOLYSIS (after creatine stores used up)
  • Fatigue more EASILY (make LACTATE)
  • found in muscle used for FAST & FORCEFUL movement
  • less vasculature, less myoglobin, fewer mitochondria
44
Q

If you were training for distance running, which type II fiber is best?

If you want to train for sprinting, which type II fiber is best?

A

?

45
Q

Describe:
Fast Twitch White IIB
Fast Twitch Red IIA
Slow Twitch I

A

Fast twitch white IIB- v high glycolytic activity, low oxidative activity, high MHC-ATPase twitch speed, low fatigue resistance, short term phasic

fast twitch red IIA- moderate glycolytic activity, v high oxidative activity, high MHC-ATPase twitch speed, high fatigue resistance, sustained phasic

slow twitch I- low glycolytic acvitiy, moderate oxidative activity, low MHC-ATPase twitch speed, v high fatigue resistance, sustained tonic

46
Q

Describe the difference between skeletal and cardiac muscle EC coupling.

A

Skel muscle- mechanical coupling
Cardiac muscle- Ca induced Ca release

See slide 51

47
Q

Describe smooth muscle structure

A

Distributed around hollow organs such as digestive tract, airway, vasculature, urogenital tract et al.
Propelling the contents of the organ, or increasing the resistance to flow
Thick filaments regulated.
In response to either electrical or hormonal signals.
Exhibit the ability to remain contracted for extended period at low levels of energy consumption (vascular tone  blood pressure).
Circumferentially or longitudinally

48
Q

Describe smooth muscle: give examples of single unit/multi unit
tonic/phasic

A

Single unit: electrically coupled; stimulate one cell is followed by stimulation of adjacent smooth muscle cells; this results in a wave of contraction, as in peristalsis. The electrical signal may be initiated by a pacemaker cell. (intestine connected by gap junctions just like heart)

Multiunit: not electrically coupled. Eg. Vas deferens of the male genital tract and the iris of the eye.

OR

tonic (continuously active)_ vascular
phasic (rhythmic)- GI tract

49
Q

What does smooth muscle contractile apparatus attach to?

A

dense bodies

50
Q

Describe some key facts about smooth muscle (t-tubules, sarcolemma, gap junction…)

A

No t-tubules
Sarcolemma contains caveolae, which represent invaginations of SL
Gap junction for electrical coupling and chemical communication

not striated bc even though there’s actin and myosin, they’re randomly distributed in the cell

51
Q

Describe the mechanism of smooth muscle contractile protein activation.

A

Slide 56.

52
Q

Describe how the exciation pathway in smooth muscle involves Ca.

A

See slide 57.

53
Q

Describe how the Basal tone varies in smooth muscle types.

Describe sphincters, blood vessles/airways, stomach/intestines, esophagus and urinary bladder

A

See slide 59

54
Q

Describe smooth muscle E-C coupling.

A

turned on by nerves attached to individual cells in multi units or nerves that attach through junctions in single unit
smooth muscle also reacts to circulating hormones that bind to surface receptor.
normally a combo of all

See slide 60.

55
Q

Describe pathways for smooth muscle activation that do not require membrane depolarization.

A

hormone receptor stimulation leads to formation of IP3, cAMP, cGMP or the activation of a ligand operated Ca2+ channel.

IP3: causes release of Ca2+ from SR via IP3 receptor, leading to MLCK-dependent contraction via Ca2+-Calmodulin

cAMP, stimulates PKA to: 1) phosphorylates MLCK decreasing its Ca2+-sensitivity, 2) increases SR Ca2+ pumping: relaxation (β2 AR)

cGMP, stimulates MLC phosphatase, decreasing myofilament activation: relaxation (Nitric oxide [NO]). importantly in vascular smooth muscle (Note: in the vascular system NO is released by endothelial cells, e.g. in response to ACh, which subsequently affects smooth muscle cells; in the absence of endothelial cells (i.e. absence of NO) ACh leads to smooth muscle contraction by the direct effect of ACh on smooth muscle cells).

Similar downstream effects can also be accomplished by agents that reduce the rate of cAMP or cGMP breakdown, thereby increasing their levels in the cell (good examples include caffeine and Viagra)

56
Q

Describe pathways for smooth muscle activation that do require alterations in membrane potential.

A

Depolarization-induced Ca2+ entry into smooth muscle cell

Voltage gated Ca2+ channel: varies Ca2+ and, thus, contractile state

Ligand bound Ca2+ channel  sufficiently activate voltage-gated Ca2+ channel: varies Ca2+ and, thus, contractile state

Moderate depolarizations of resting membrane potential activate small tonic amounts of Ca2+ current that can keep intracellular [Ca2+] tonically high

Ca2+ entry leads to Ca-CaM and MLCK, but can also be amplified by CICR (via RyR)

Spread of the depolarization via gap junctions is important in single-unit smooth muscle activation.

57
Q

Review the modulation of smooth muscle activity by nt, hormones, and local factors.

A

Slide 63.

58
Q 
Review the comparisons among skeletal, smooth and cardiac muscle.
Striations
Actin and myosin
level of control
neuronal input
neuroeffector junction
hormonal control
source of Ca
regulatory protein that binds Ca
gap junctions
pacemaker activity
myosin ATPase activity
recruitment
A

Slide 64.

FHB I - Cardiac Unit (23 decks)

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