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BIOSCI107 > Module 7 (ET muscle) > Flashcards

Module 7 (ET muscle) Flashcards

1
Q

Types of muscles

A

Skeletal, cardiac and smooth

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2
Q

Striated muscle

A

Skeletal and cardiac; highly ordered contractile system leading to a banded appearance with bands occurring with a periodicity of about 2um

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3
Q

Non-striated muscle

A

Smooth muscle

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4
Q

Voluntary muscles

A

Skeletal; responsible for the movement of limbs; attached to bones which act as levers to provide a greater range of movement

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5
Q

Involuntary muscles

A

Cardiac for pumping blood; smooth for lining blood vessels and hollow organs, responsible for altering their dimensions; may have intrinsic contractile activity whose amplitude and/or frequency is modulated by nervous system input (myogenic); others may be quiescent and their contraction initiated by autonomic nervous system input

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6
Q

Motor unit

A

A group of muscle cells which are innervated by a single motor neuron

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7
Q

Structure of skeletal muscle

A

Most highly ordered of muscles; attached to bones via tendons; the cells (muscle fibres) are up to 35cm long and 0.1cm wide; cells composed of fibrils which run the length of the cell and contain highly organised contractile filaments; SR surrounds the fibril and stores calcium, releases it to activate contraction

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8
Q

Fibrils in skeletal muscle

A

Run the length of the cell; made up of alternating bands of myosin and actin filaments which interdigitate

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9
Q

Sarcomere

A

Basic contractile element; consists of an array of thick and thin filaments, attached to Z-discs at each end; t-tubules invaginate the surface membrane of the cell (sarcolemma) and are surrounded by the SR

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10
Q

Thin actin filaments

A

Globular proteins that form thin filaments within the cell; may have accessory proteins attached to them which regulate their activity (such as troponin and tropomyosin)

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11
Q

Thick myosin filaments

A

High molecular weight protein that is formed from two high molecular weight sub-units which each have a tail that wind around each other in a double helix and a globular head able to hydrolysed ATP; accessory proteins regulate this ability

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12
Q

A-band

A

Thick filaments run the entire length; some thin filament

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13
Q

I-band

A

Thin filaments run length

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14
Q

Z-disc

A

Coin-shaped sheet of proteins that anchors the thin filaments and connects myofibrils to one another

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15
Q

H-zone

A

Lighter mid-region where filaments do not overlap

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16
Q

M-line

A

Line of protein myomesin that holds adjacent thick filaments together

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17
Q

T-tubules

A

Deep invaginations continuous with the sarolemma (cell membrane) and circle each sarcomere at each of the junctions of the A and I bands; allows APs to be carried deep within the cell

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18
Q

SR

A

Sarcoplasmic reticulum; calcium storage site; terminal cistenae lie close to the T-tubules

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19
Q

Sliding filament theory

A

Sarcomere shortens as the thin filaments are pulled over the thick filaments; Z-line pulled toward M-line; I band and H zone become narrower

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20
Q

Cross-bridge cycle

A

Cross-bridge formation; power stroke; detachment; energisation of myosin head

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21
Q

Cross-bridge formation

A

Myosin binds to the actin binding site to form a cross-bridge; can only occur in the presence of calcium when the myosin biding site on actin is exposed; the myosin head has already hydrolysed ATP so ATP needs to be available

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22
Q

The power stroke

A

ADP is released; myosin head rotates to its low-energy state (about 45degrees to the actin) pulling with it the thin filament; result is shortening of the sarcomere

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23
Q

Detatchment

A

A new ATP molecule bind to the myosin; the actin-myosin bond is weakened and the myosin detaches; if there is no ATP, rigor mortis (stiffness) will occur because there is no energy available and the myosin stays attached to the actin

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24
Q

Energisation of the myosin head

A

Myosin head hydrolyses the ATP to ADP and Pi; the myosin head moves back to its high energy (cocked) conformation about 90degrees to the actin

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25
Q

Importance of calcium

A

Calcium ions provide the on switch for the cross-bridge cycle to begin; when it binds with troponin, the tropomyosin moves to expose the myosin binding sites on actin; the cross-bridge cycle will continue as long as calcium remains above the threshold

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26
Q

Calcium regulation

A

In skeletal muscle, the opening of calcium channels in the SR allows the movement of calcium ions into the cytosol; active transport pumps (Ca2+ ATPase) are constantly moving Ca2+ from the cytoplasm back into the SR

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27
Q

Isotonic

A

Contraction where the tension developed in the muscle remains almost constant while the muscle changes length;shortening; tension constant; velocity variable

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28
Q

Isometric

A

Contraction where the tension developed does not exceed the resistance of the object and there is no change in muscle length; no shortening; length constant; tension variable

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29
Q

Length-tension relationship

A

During an isometric contraction; at the level of the sarcomere, the maximum active force (tension developed) is dependent on the degree of actin and myosin overlap

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30
Q

Optimal resting length

A

The greatest tension produced due to maximum number of cross-bridges formed; 2.0-2.2.um

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31
Q

Sarcomere length decreases

A

Decrease in length reduces tension due to extensive overlap; no tension can form when thick filaments meet Z-lines and sarcomeres cannot shorten; <2.0um filaments collide and interfere

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32
Q

Sarcomere length increases

A

Reduced size of zone of overlap means fewer cross-bridges are formed and reduced tension; zero zone of overlap results in zero tension due to no interactions between thick and thin filaments; >2.2um active forces decline as the extent of overlap between filaments reduces

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33
Q

Total tension

A

Active + passive forces; as muscle is stretched the connective tissue around the muscle cells resists the stretch (passive force); total tension is the sum of the active tension dependent on the sarcomere length and passive tension

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34
Q

Neuromuscular junction

A

Synaptic cleft; chemical synapse between the motor neuron and muscle fibre

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35
Q

ACh released into neuromuscular junction

A

An AP travels down the motor neuron; at the axon terminal Ca2+ channels open and the ions enter the axon terminal; triggers the vesicles containing ACh to fuse with the terminal membrane which releases ACh into the neuromuscular junction (synaptic cleft)

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36
Q

Activation of ACh receptors

A

The binding of ACh to the receptors on the muscle end plate causes opening of the ligand-gated ion channels; opening of these channels allows movement of predominantly Na+ into the muscle cell and depolarises it; short lasting as ACh is broken down by an enzyme

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37
Q

A muscle AP is triggered

A

If sufficient ligand-gated channels are opened, the end plate potential reaches threshold; voltage-gated Na+ channels open and an AP is triggered; the AP is then propagated along the sarcolemma and int the T-tubule system

38
Q

AP in skeletal muscle

A

Small increase in sodium ion permeability causes volatge-gated Na+ channels to open and the ions rush in - depolarisation; channels close and the voltage-gated K+ channels open - begins repolarisation; channels close and the RMP stabilises, concentrations of both ions is restored

39
Q

Excitation contraction coupling

A

Transient depolarisation during AP in skeletal muscle is conducted into the interior of the cell by the t-tubules where is causes the calcium channels in the SR to open; this allows calcium to bind to the troponin, which changes shape and exposes tropomyosin; contraction can occur

40
Q

Calcium released from the SR

A

AP is conducted down the t-tubules coming in close contact with the SR; results in voltage-gated Ca2+ channels in the SR to open, ions are released into the cytosol

41
Q

Ca2+ binds with troponin

A

When Ca2+ concentrations reach a critical threshold, the myosin binding sites on the actin filaments are exposed, allowing the cross-bridge cycle to occur

42
Q

Contraction ends

A

Calcium is actively pumped back into the SR via Ca2+ ATPase pumps; troponin moves back and covers the myosin binding site

43
Q

Muscle metabolism: creatine phosphate

A

For brief periods (<15s), creatine phosphate can act as an ATP store; creatine phosphokinase transfers Pi from Creatine-Pi to ADP to give ATP; anaerobic

44
Q

Anaerobic glycolysis

A

Good for short intense exercise (fast but inefficient); dominant system from about 10-30s of maximal effort; build up of lactate and H+ limits duration to max 120s

45
Q

Aerobic metabolism

A

Efficient, but comparitively slow; requires oxygen, therefore good blood supply; max 300W; important for postural muscles and endurance exercise

46
Q

Control of muscle tension

A

Increasing the frequency of stimulation (number of APs in one motor neuron); recruiting additional motor units

47
Q

Type 1 muscle fibre

A

Slow fibres which have a low maximum ATPase rate and lower maximum force production; mainly oxidative in metabolism and have large amounts of myoglobin and mitochondria (red colour); have extensive high energy phosphate stores which are replenished by slow aerobic metabolism; slow twitch

48
Q

Type 2A muscle fibre

A

Fast fibres that have a high ATPase rate; can have a high oxidative capacity and glycolytic capacity in metabolism; have very large amounts of myoglobin and mitochondira (red colour); high oxygen demand is offset by them having small diameter to facilitate diffusion of oxygen across the cell; fast twitch

49
Q

Type 2B muscle fibre

A

Not common in humans; fast fibres that have a high ATPase rate but low oxidative capacity; primarily glycolytic in metabolism with low amounts of myoglobin and mitochondria (white colour); large diameter makes them fatigue rapidly but generate large forces

50
Q

Type 1 muscle fibre e.g.

A

Maintaining posture, walking; low intensity exercise; units with neurons innervating the slow efficient aerobic cells

51
Q

Type 2 muscle fibre e.g.

A

Jumping, weight lifting; high power output exercise; units with the neurons innervating the large fibres that fatigue rapidly but develop large forces

52
Q

Rate of stimulation

A

A single stimulus is delivered and the muscle contracts and relaxes; if another stimulus is applied before the muscle relaxes completely, the more tension results; temporal/wave summation, results in unfused/incomplete tetanus; at higher stimulus frequencies, there is no relaxation at all between stimuli and this is fused/complete tetanus

53
Q

Temporal summation

A

Occurs when there is an increased frequency of APs; a twitch lasts longer than an AP

54
Q

Recruitment

A

As more motor units are recruited to innervate a number of muscle fibres, the amount of force developed increases; generally, small oxidative motor units are recruited first and fewer large glycolytic motor units are recruited last; contractile function can be graded by recruitment of different motor units

55
Q

Cardiac muscle

A

100um long; branched; myogenic (involuntary); atrial cells joined to each other by gap junctions that allow electricity to spread from one cell to the next, no t-tubules and contract relatively weakly; ventrical cells are branched and have numeroid gap junctions that join them to form sheets that divide and wrap around the ventricles, well developed t-tubule system occurs at level of z-discs

56
Q

Heart

A

Cardiac muscle cells are found mostly in the left ventricle; heart has numerous mitochondria and myoglobin; primarily oxidative and deep red; each cell has 1-3 nuclei and growth occurs mainly through hypertrophy with little cell division

57
Q

ventricular muscle cells

A

100um x 30um; 1-3 nuclei; lots of mitchondria; needs lots of oxygen for oxidative metabolism; SR not as extensive as skeletal muscle

58
Q

Intercalated discs

A

Desmosomes prevent cells from seperating during contraction; contain gap junctions that allow the APs to be carried from one cell to the next; allows for co-ordinated contraction of all the myocytes (unlike skeletal where fibres are recruited by motor neurons)

59
Q

Sino-atrial node

A

Group of specialised cells in the right atria of the heart where APs are initiated

60
Q

Ventricular myocyte AP

A

AP initiated in sino-atrial node, spreads throughout the atria and then via specialised conducting cells to the ventricles; AP is long lasting (>100ms) due to presence of additional ionic currents that hold the cell depolarised for a period comparable to that of a twitch (heart beat); has plateau phase due to presence of large sustained Ca2+ current

61
Q

Re-excitation of cardiac muscle

A

Membrane is highly polarised during most of the twitch and so it is unlikely that re-excitation will occur - the cells are refractory; troponin only has one calcium binding site so the calcium transient is of much lower amplitude than skeletal - leads to troponin not being fully staurated

62
Q

AP vs contraction in skeletal vs cardiac

A

Skeletal: brief AP done before contraction, which is longer
Cardiac: long AP done at the same time as contraction

63
Q

Stages of AP in cardiac muscle cell

A

Rapid depolarisation due to fast opening of voltage-gated Na+ channels
Plateau please due to slow opening of voltage-gated Ca2+ channel
Repolarisation due to closing of Ca2+ channels and opening of K+ (outward) channels

64
Q

Structural basis for EC-coupling in ventricular cardiomyocytes

A

LTCC: L-type volatge-gated calcium channel
RyR: ryanodine receptor (calcium channel in SR)
NCX: sodium/calcium exchanger
NKA: sodium/potassium ATPase

65
Q

Cardiac muscle EC-coupling 1

A

Depolarisation opens voltage-gated fast Na+ channels in the sarcolemma; reversal of membrane potential; depolarisation wave opens slow (L-type) Ca2+ channels in the sarcolemma (DHPR); Ca2+ influx balanced by a Na+/Ca2+ exchanger

66
Q

Cardiac muscle EC-coupling 2

A

Ca2+ influx triggers opening of Ca2+ sensitive channels in the SR, ions flow into cytosol; raised intracellular Ca2+ concentration allows Ca2+ to bind to troponin and this switches on the contractile machinery

67
Q

Relaxation in cardiac muscle

A

Ca2+ transport out of the cytosol with SR Ca2+-ATPase and sarcolemmal Na+/Ca2+ exchange

68
Q

Regulation of cardiac output

A

CO (how much blood comes out of the heart) = SV (stroke volume) x HR (heart rate)

69
Q

Heart rate

A

Set by the pacemaker cells in teh sin-atrial node; rate can then be modified, especially via the autonomic nerves releasing NTs

70
Q

Stroke volume

A

Reflects the tension developed by the cardiac muscle fibres in one contraction

71
Q

Pacemaker cells

A

In SA and AV node; slow depolarisation due to If current; depolarisation where Ca2+ channels open at threshold, produces rising phase of AP sustained opening of slow Ca2+ channels; repolarisation due to Ca2+ channels inactivating and K+ channels opening

72
Q

Autonomic innervation of the heart

A

Vagus nerve: parasympathetic which decreases heart rate and releases ACh
Sympathetic cardiac nerves: increase heart rate and force of contraction (release noradrenaline)

73
Q

Regulation of contractile force in cardiac

A

Increase rate of firing (automaticity); increase the dimensions of the ventricle (stretch); use NTs to alter rate and calcium handling (direct and rate effects)

74
Q

Modulation of force with automaticity

A

Change in amplitude of the calcium transient whcih modulates the availability of actin binding sites for myosin and the number of attached cross-bridges; Ca2+ from previous AP that hasn’t left the cytosol yet can be used for the next AP

75
Q

Modulation of force with muscle length

A

When length is suddenly increased, there is an immediate increase in force development due to the increased interaction between actin and myosin followed by a slow increase in the amplitude of the calcium transient over several beats

76
Q

Modulation of force by NTs

A

Sympathetic cardiac nerves: increase heart rate and force of contraction (release noradrenaline)
Parasympathetic cardiac nerves: release ACh which slows the discharge of SA cells and reduce heart rate which decreases the force of contraction

77
Q

Length-tension relationship skeletal vs cardiac

A

Active tension are the same; passive tension is different (more resting tension in heart) so the total tension is greatest in cardiac

78
Q

Neural control of stroke volume

A

Noradrenaline released by sympathetic nerves leads to increased cytosol calcium due to increased heart rate shortenening time for extrusion; more Ca2+ comes into cell during AP and more released from SR; increased sympathetic stimulation results in increased output at any filling pressure due to increase in inotropy and heart rate

79
Q

Smooth muscle found

A

Airways; bladder and reproductive organs; blood vessels; iris and ciliary muscles in eye

80
Q

Structure of smooth muscle

A

Very long and thin with a singal central nucleus and tapered at the ends (spindle shape); may be connected to each other by dense bodies or by gap junctions and groups of cells may be electrically connected; considerable shortening can occur because contractile machinery is poorly organised; SR is poorly developed and spread throughout the cell; no troponin and t-tubules

81
Q

Single unit smooth muscle

A

Sheets of cells that are electrically coupled and act in unison (as one unit); often spontaneously active; found in most blood vessels and hollow organs

82
Q

Multi unit smooth muscle

A

Tissue made of discrete bundles of independent cells which are densely innervated and contract only in response to its innervation; vas deferens, iris, piloerectors

83
Q

Initiation of contraction smooth muscle

A

Ca2+ ions enter cytosol from EC fluid via voltage-dependent or voltage-independent Ca2+ channels or SR; ions bind to and activate calmodulin which then activates myosin light chain kinase (MLCK; enzyme); MLCK activates the myosin by phosphorylation it which activates the myosin ATPases; activated myosin forms cross bridges with actin of the thin filaments and shortening begins

84
Q

Relaxation in smooth muscle

A

Contraction ends when a myosin light chain phosphatase dephosphorylates the myosin light chain; Ca-ATPase in cytoplasm membrane reduces intracellular Ca2+

85
Q

Arrangement of smooth muscle in hollow organs

A

Outer longitudinal layer and an inner circular layer; are at right angles to each other

86
Q

Basic cellular structure of smooth muscle

A

No t-tubules (cavolae instead to increase the SA and helps get more APs into the centre); dense bodies (act like z-lines to anchor actin to sarcolemma); gap junctions electrically connect the cells together; intermediate filament is cytoskeleton element; poorly developed SR

87
Q

Regulation of calcium in smooth muscle

A

Via voltage, hormones, neurotransmitters and specific ions; calcium source is from EC membrane and SR

88
Q

Activation of myosin by MLCK smooth

A

Myosin does not hydrolyse ATP unless it is first phosphorylated; MLCK phosphorylates the light chain in the presence of the activated calmodulin

89
Q

MLCK and MLCP smooth

A

Increased MLCK activity (Ca2+ regulated) will facour contraction; increased MLCP activity will favour relaxation; when intracellular Ca2+ drops, MLCP activity will dominate

90
Q

Modulation of smooth muscle contraction

A

Stretch; neurotransmitters; hormones; environment; histamine; adenosine; prostacyclin; nitric oxide

91
Q

Innervationof smooth muscle

A

Autonomic nerve fibres branch and form diffuse junctions with underlying smooth muscle fibres; varicosities in the terminal axons contain NT; NT is secreted into matric coating and diffuses to the muscle cells

92
Q

Smooth muscle response to stretch

A

It will initially contract, effectively resisting the stretch, stretch-activated calcium channels; over time will slowly relax and adapt to the change in length via calcium-dependent K+ channels, hyperpolarising the membrane potential

BIOSCI107 (7 decks)

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