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Pathophysiology > Muscle Physiology > Flashcards

Muscle Physiology Flashcards

1
Q

Excitability

A

Capacity to respond to AP

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2
Q

Contractility

A

Ability to shorten and create a pulling force

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3
Q

Extensibility

A

How much the muscle can stretch

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4
Q

Elasticity

A

Ability to recoil to original length after stretch.

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5
Q

Epimysium

A

Dense connective tissue that surrounds the entire muscle tissue.

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6
Q

Perimysium

A

continuous layer of collagen connective tissue that separates the skeletal muscle tissue into muscle fascicles.

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7
Q

Endomysium

A

Delicate network of connective tissue which surrounds individual muscle fibers. Contains vessels and nerves that supply the muscle fibers as well as proteoglycan for ion exchange and metabolic exchange.

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8
Q

Skeletal muscle attributes

A

Striated; voluntary; innervated by somatic motor neurons; multiple nuclei; rapid contractions.

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9
Q

Sarcolemma

A

Surrounds sarcoplasm (membrane of each muscle cell) where change in membrane potential and muscle contraction begin.

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10
Q

T-tubules

A

Extensions of cell membrane that wrap around the entire cell and transmit APs so the entire muscle contracts simultaneously.

Encircle sarcomere near zones of overlap.

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11
Q

Myofibril

A

Lengthwise subdivisions of muscle fiber. Responsible for contraction.
Made of thick (myosin) and thin (actin) filaments.

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12
Q

Sarcoplasmic reticulum

A

Surrounds muscle cells; Helps transmit APs to T-tubules.

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13
Q

Cisternae

A

made up of T-tubules and run alongside t-tubes. Transmits AP for simultaneous contractions.

Concentrates Ca2+ and releases to sarcomeres to begin contraction.

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14
Q

Components of the Triad

A

1 T-Tubule
and
2-terminal cisternae

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15
Q

A-band

A

Overlap area

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16
Q

I band

A

Has thin filaments but no body of thick filaments.

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17
Q

M line

A

Midline of sarcomere

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18
Q

Z lines

A

Defines the edges and differentiates sarcomere units.

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19
Q

H band

A

Only at rest, contains only myosin.

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20
Q

Chitin

A

Stabilize thick filaments and attach to Z line.

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21
Q

4 proteins of thin filament

A

1.F-actin (2 twisted ropes of G-actin)
2. G-actin
3. Nebulin (holds strands together)
4. Tropomyosin

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22
Q

Tropomyosin function

A

Regulates access of actin binding proteins to filaments

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23
Q

thick filament attributes

A
  1. Have myosin heads & tails that move as one.
  2. Each thick filament is surrounded by 6 thin filaments
  3. Thick filament is stationary
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24
Q

Thin filment attributes

A
  1. Has 2 a helical actin chains connected by nebulin.
  2. Tropomyosin has to move out of the way to allow mysoin to bind.
  3. Each actin molecule has a binding site for myosin head.
  4. Thin filaments come closer together, no shortening occurs
  5. H and I bands shorten, A band stays the same.
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25
Q

Troponin function

A

Binds with Ca2+ to move tropomyosin away from actin

26
Q

Cross-Bridge-Theory

A

When sufficient Ca 2+ is present the myosin heads hinge drawing thin filaments towards each other and the sarcomere shortens.

27
Q

How Myosin gains energy

A

Have ATP binding sites for actin and ATP.

ATP hydrolyzes in to ADP a Pi, which in turn energizes the myosin cross-bridge.

(In cadavers there is no ATP to bind and detach the myosin and actin which is how rigor mortis sets)

28
Q

Contraction aspects

A
  1. When all sarcomeres shorten, then contraction occurs. Bends at 45 degree angle.
  2. ADP and Pi stay bound to myosin head until ATP comes to release it.
29
Q

T-tubule, Calcium, cisternae, troponin, and tropomyosin integration

A
  1. APs propagated into T-tubule and enters via gap junction.
  2. AP is 1-2 milliseconds, then Calcium is released from cisternae ( millisecond after AP).
  3. Membrane is repolarized by the the time calcium is at its peak.
  4. Calcium unbinds from troponin and tropomyosin moves back into position.
30
Q

Motor Unit funciton

A

composed of all of the muscle fibers innervated by a single alpha motor neuron.

31
Q

Integration of membrane and Ach release

A
  1. The release of acetylcholine occurs when an action potential is relayed and reaches the axon terminus in which depolarization causes voltage-gated calcium channels to open and conduct an influx of calcium, which will allow the vesicles containing acetylcholine for release into the synaptic cleft.
  2. Ach is reversibly bound will not stay attached to receptors free Ach is hydrolyzed to choline acetate to be reused later.
32
Q

Frequency differences in muscle contraction

A
  1. Low frequency - twitches
  2. Intermediate frequency - unfused tetanic contractions
  3. High frequency- fused tetanus ( no breaks)
33
Q

Isometric contraction

A

Muscle contraction without shortening or movement.

34
Q

Isotonic contraction

A

Muscle contraction with shortening and movement drawing muscle fibers closer togerther.

35
Q

Load vs. Velocity

A

As load decreases, the rate of muscle shortening increases.
The point of maximal muscle shortening occurs at zero load.

36
Q

ATPases action

A
  1. Cleave ATP - ADP + Pi
37
Q

Calcium ATPase Action

A

Pumps calcium back into SR

38
Q

Determinants of Muscle Force

A
  1. Frequency
  2. Recruitment
  3. Recruitment of motor units progresses from small alpha motor neurons to larger alpha motor neurons
39
Q

Types of Skeletal muscle types

A

Type 1 - Slow oxidatitive - slow to fatigue, use oxygen and glucose to produce ATP.
Type 2A - Fast Oxidative - fast contractions under primary aerobic respiration, can switch to anaerobic respiration (glycolysis), can fatigue more quickly.
Type 2B - Fast glycolytic - fast contractions and primarily use anaerobic glycolysis. These fatigue the most quickly.

40
Q

smooth muscle locations

A
  1. walls of hollow organs
  2. blood vessels
  3. eyes
  4. glands
  5. uterus
  6. skin
41
Q

Morphology and structure of smooth muscle

A
  1. smaller than skeletal
  2. fibers are spindle shaped
  3. dense bodies inside the cell - connected via desmin
42
Q

Single Unit smooth muscle aspects

A
  1. Visceral muscle
    (blood vessel, intestine, ureter, uterus)
  2. use gap junctions and contract as a unit
  3. spontaneous action potentials
43
Q

Multi unit smooth muscle aspects

A
  1. locations - airways, iris, ciliary body, piloerector muscles
  2. no gap junctions
  3. no spontaneous activity
  4. fibers structurally independent
  5. many nerve endings
  6. Autonomic neural stimulation
44
Q

Smooth muscle aspects of contraction

A
  1. calcium binds calmodulin (messenger protein)
  2. calcium-calmodulin complex joins with myosin kinase and activates this phosphorylating enzyme.
  3. Activated myosin kinase transfers a phosphate head to the head of myosin LC
  4. Phosphorylated myosin head binds to actin
  5. contraction
45
Q

Smooth muscle relaxation

A
  1. Removal of calcium
  2. hydrolysis of myosin phosphate via myosin phosphatase

**Calcium for contraction primarily comes from the extracellular sources.

46
Q

Smooth muscle calcium mediators

A
  1. Neural Signals
  2. Hormonal stimulation
  3. Stretch of smooth muscle fiber
  4. change in the chemical environment
47
Q

local factors affecting smooth muscle tone

A

PO2
PCO2
[H+] or pH
Adenosine
Lactate
↑Temperature
[K+]
Change in calcium permeability
Activated second messengers
cAMP
cGMP

48
Q

smooth aspects compared to skeletal

A

smooth
No striated banding pattern
No distinct sarcomeres
No transverse tubules
Very few SR
Actin and myosin filaments

Ca++-dependent excitation-contraction coupling
Site of Ca++ regulation: Myosin
Source of Ca++: SR & extracellular
Connections between individual smooth muscle (SM) cells
Unitary SM: Gap junctions
Multiunit SM: Electrically separate

skeletal
Striated muscle
Distinct sarcomeres
Transverse tubules
SR major site of Ca++ storage
Myofibrils contain actin and myosin filaments
Ca++-dependent excitation-contraction coupling
Site of Ca++ regulation: Troponin
Source of Ca++: SR
Individual muscle fibers are electrically separate

49
Q

Cardiac muscle elements

A

The muscle cells are arranged in a branching pattern
Each cell contain only 1-2 nuclei
Cardiac muscle is striated

50
Q

How calcium works with heart muscle

A
  1. requires CA++ to allow actin to bind to myosin
  2. Some of the CA++ required must enter from the outside of the cell
  3. The CA++ will enter through voltage dependent calcium channels (also known as “L” channels). - “L” channels are sometimes referred to as Slow Calcium Channels
  4. This influx of calcium from the outside of the cell occurs during the cardiac muscle action potential. Even though the calcium enters as part of the action potential mechanism–it is also important for the contraction action.
51
Q

How calcium effects cardiac and skeletal

A

Since cardiac muscle has functional “L” calcium channels – and skeletal muscle cells do not – a calcium channel blocker drug will affect cardiac muscle and not skeletal muscle (example Verapamil)

52
Q

Why cardiac muscle has a prolonged absolute refractory period?

A

To ensure that the heart can refill with blood in diastole.

If the heart chamber cannot fill it has no blood to empty into the next chamber or into the next blood vessels

If a heart muscle goes into Tetany called Cardiac Flutter or Fibrillation

53
Q

Length of cardiac absolute refractory period

A

over 200 msec ( almost the entire length of one cardiac contraction).

54
Q

Pacemaker cells

A
  1. Have automatic rhythm
  2. can spontaneously fire an AP
55
Q

Pacemaker structures in order of “fail safe”

A
  1. SA node - 60-80 APs / min
  2. AV node - 40-60 APs / min
  3. Bundle of HIS 20-40 APs / min
  4. Bundle Branches 10-20 APs /min
56
Q

Connective Tissue of Muscle

A
  1. Epimysium
    Dense regular c.t. surrounding entire muscle. Separates muscle from surrounding tissues and organs
    Connected to the deep fascia.
  2. Perimysium
    Collagen and elastic fibers surrounding a group of muscle fibers called a fascicle. Contains blood vessels and nerves

Endomysium
Loose connective tissue that surrounds individual muscle fibers
Also contains blood vessels, nerves, and satellite cells (embryonic stem cells function in repair of muscle tissue.

**Collagen fibers of all 3 layers come together at each end of muscle to form a tendon or aponeurosis.

57
Q

Cross-bridge nuance

A
  1. Through the attachment-detachment-attachment cycle, the myosin heads or cross bridges “walk” along an actin filament to pull it inward relative to the stationary thick filament.
  2. Because of the way the myosin molecules are oriented within a thick filament, all the cross-bridges stroke towards the center of the sarcomere.
    At any time during contraction, part of the cross bridges are attached to the thin filaments and are stroking, while others are returning to their original conformation in preparation for binding with another actin molecule.

3.Thus, some cross-bridges “hold on” while others “let go”. Otherwise, the thin filaments would slip back to their resting position b/w strokes.
The detachment of the myosin head from the actin cannot take place until and unless a new ATP does not attach to the myosin head. This is important when death occurs, no more ATP is available and thus, rigor mortis occurs.

58
Q

Mechanism of skeletal contraction

A
  1. Width of sarcomere decreases from 2.2 to 2 or less. Length of thick and thin filament remain the same.
  2. Power stroke pull the Z discs towards the center of the sarcomere
    Results in app. Of the Z discs
    Cyclic attachment-detachment-attachment of myosin head to actin, till there is complete overlap of thick & thin filaments
  3. Decrease in I-band and H-band, A-band stays the same
59
Q

Cardiac contraction

A
  1. The CA++ will enter through voltage dependent calcium channels (also known as “L” channels).
  2. These “L” channels are sometimes referred to as Slow Calcium Channels
  3. This extracellular CA++
    is taken up by Troponin-C to assist directly with contraction. -it also assists with opening of the CA++ -release channels in the cardiac muscle cell SR.
60
Q

Calcium importance in Cardiac contraction

A

Since the amount of calcium available to troponin C is important to the strength of contraction in both skeletal muscle and cardiac muscle and some of the calcium for cardiac muscle contraction must come from the extracellular fluid – the blood (extracellular fluid) calcium level is more important to cardiac muscle than skeletal muscle.

61
Q

Problems encountered if the cardiac resting potential is less negative than -90mv

A
  1. If the membrane potential is less neg (-60 instead of -90) some of these Na+ channels will be in an inactivated state thus INSENSITIVE to opening.
  2. This insensitivity to opening will lead to a decrease response to excitation of the cardiac cell membrane (Not all Na+ channels are open)

3.This will cause a delay in the conduction through the heart which will increase the risk of for a cardiac arrhythmia.

Slow the heart rate=BRADYCARDIA

62
Q

How the plateau phase of cardiac cycle is maintained.

A

All of this sustained by a balance between the inward movement of Ca++ through “L” Ca++ channels and the outward movement of K+ through SLOW K+ channels

Pathophysiology (11 decks)

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