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Physiology and Pharmacology > Muscle > Flashcards

Muscle Flashcards

1
Q

what is skeletal muscle responsible for?

A
  • voluntary movement of bones that allows locomotion
  • control of inspiration by contraction of diaphragm
  • skeletal-muscle pump allows venous return to the heart
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2
Q

what is the structure of striated muscle?

A
  • myofibres joined into fascicle bundles
  • myofibres contain myofibrils which are broken down into sarcomeres
  • sarcomeres contain actin and myosin myofilaments
  • sarcomeres align with each other to form striated appearance
  • each myosin is surrounded by 6 actin filaments
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3
Q

what are the different bands and lines of a sarcomere?

A
  1. Z-line
  2. M-line
  3. I-band
  4. A-band
  5. H-band
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4
Q

what is the Z-line?

A
  • at end of each sarcomere for anchor point of actin

- coordinates myofilament above, below and adjacently

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5
Q

what is the M-line?

A
  • anchoring point of myosin
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6
Q

what is the I-band?

A
  • the sarcomere between 2 Z-lines

- appears light colour in electron microscopy due to presence of actin only

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7
Q

what is the A-band?

A
  • where actin and myosin overlap for muscle contraction

- appears dark on electron microscope due to presence of both actin and myosin

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8
Q

what is the H-band?

A
  • contains only myosin so appears lightly lighter than A-band
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9
Q

what happens to the I-band and A- band during muscle contraction?

A
  • I-band shortens as actin is pulled across myosin

- A-band stays the same length as myosin fibres have a fixed length

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10
Q

how is contraction of skeletal muscle initiated?

A
  1. ACh is released from NMJ and binds to nAChRs on plasma membrane of muscle fibre, causing influx of Na+, depolarisation, and AP triggering
  2. depolarisation passes along sarcolemma and through T-tubules
  3. T-tubules form a triad with the sarcoplasmic reticulum (SR), causing depolarisation in the SR
  4. this depolarisation causes SR to release stored Ca2+, causing an increase in intracellular Ca2+
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11
Q

what is the process of cross-bridge formation and skeletal muscle contraction?

A
  1. actin and myosin are in attached state
  2. ATP binds to myosin head, causing it to dissociate from actin
  3. ATP is hydrolysed to ADP + Pi, causing conformational change of myosin
  4. myosin head relaxes then extends to a resting conformation, and can interact if actin further down
  5. myosin head binds to new actin-myosin binding site to form new cross-bridge and Pi is released to strengthen the interaction
  6. myosin head undergoes conformational change to pull actin over the myosin (contraction)
  7. ADP is released, returned to attached state until ATP binds again
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12
Q

how is skeletal muscle summated in its contraction?

A
  • contraction depends on frequency of stimulation
  • contraction is slower than AP, so sarcolemma is prepared for contraction before the muscle is relaxed
  • increased stimulation before muscle is relaxed causes twitching, then unfused tetanus state, then fused tetanus state
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13
Q

what is the unfused tetanus state?

A
  • if frequency of stimulation is increased to the muscle, muscle is continuously tense and cannot relax
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14
Q

what is the fused tetanus state?

A
  • if frequency of stimulation is extremely high for the muscle, there is continuous contraction due to constant Ca2+ influx
  • muscle stays contracted
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15
Q

what are slow oxidative muscle fibres?

A

Type I:

  • resistant to fatigue
  • use oxidative phosphorylation to generate ATP in aerobic respiration
  • high in mitochondria levels
  • red in colour due to high levels of myoglobin so high O2 storage
  • low glycogen store
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16
Q

what are fast oxidative muscle fibres?

A

Type IIa:

  • resistant to fatigue
  • use oxidative phosphorylation for ATP in aerobic respiration
  • highest in mitochondria levels
  • red in colour due to high levels of myoglobin so high O2 storage
  • abundant glycogen stores
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17
Q

what are fast glycolytic muscle fibres?

A

Type IIx/IIb:

  • fatiguable but generate power quickly
  • white in colour due to low myoglobin levels so low O2 store
  • undergo anaerobic respiration
  • highest glycogen stores for glucose to generate ATP in glycolysis
  • fewer mitochondria
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18
Q

what is an example of a type I muscle?

A

Soleus

  • resistant to fatigue
  • controls posture when standing
  • if contracting for an hour, it will still generate the same levels of force
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19
Q

what is an example of a type IIa muscle?

A

Gastrocnemius:

  • generates more power when walking and jogging
  • can fatigue within 6 minutes
  • by an hour, it can no longer contract
  • more rapid contraction and generation of higher tension
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20
Q

what is an example of a type IIb/IIx muscle?

A

biceps branchii:

  • generates power strokes via anaerobic respiration
  • rapid contraction and generation of force
  • rapid fatigue within 2 minutes and muscle can no longer contract
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21
Q

what are slow muscle fibres?

A
  • half the diameter of fast fibres

- take longer to contract after nerve stimulation

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22
Q

what are fast muscle fibres?

A

take 10 milliseconds or less to contract

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23
Q

how does the NMJ work>

A
  1. AP enters presynaptic terminal
  2. depolarisation causes Ca2+-voltage gated channels to open
  3. influx of Ca2+ causes fusion of vesicles with presynaptic membrane to release ACh into cleft
  4. ACh binds to nAChRs and opens Na+ channels
  5. Na+ influxes into muscle membrane, depolarising it and generating an AP
  6. Na+ channels close and K+ channels open to repolarise the synapse
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24
Q

what is the mechanism of botulinum toxin on the NM?

A
  • endoproteinase that cleave SNARE proteins which are required for docking of vesicles during exocytosis of ACh
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25
Q

what symptoms does botulinum toxin cause for muscles?

A
  • food poisoning, muscle weakness, paralysis, leading to death

1st symptoms = dry mouth and double vision

2nd symptoms = GI issues such as diarrhoea and vomiting

3rd symptoms = paralysis of limbs and repsiratory muscles

26
Q

what are the clinical uses of botulinum toxin?

A
  • treatment of strabismus (crosseyed) by injection into periocular muscles
  • blepharospasm (uncontrolled eyelid movements)
  • cosmetic treatments: BoTox (toxin A)
27
Q

what is aerobic endurance training?

A
  • sustained, low level exercise over long distances/periods
  • training above threshold
  • threshold increases as fitness increases
  • stimulation of slow fibres
  • conversion of IIx and IIa into more fatigue-resistant fibres, but generate less power
  • no change in muscle strength
  • angiogenesis
28
Q

what is angiogenesis?

A

formation of new blood capillaries through muscle for efficient O2 delivery
- reduces diffusion distance from blood to muscle

29
Q

what is anaerobic training?

A
  • brief, high intensity excerise
  • stimulation of fast fibres
  • no change in no. muscle fibres or distribution
  • enlargement of myofibril size by addition of new myofilaments to muscle
  • causes hypertrophy
30
Q

what is hypertrophy?

A

increased diameter of muscle fibre

31
Q

what energy stores does the body rely on in the first 2 mins of excerise?

A
  • stored energy

- anaerobic glycolysis

32
Q

what are the 3 sources of energy production?

A
  1. immediate energy supply from ATP and PCr stores in muscle
    - depletes within 30 seconds
  2. glycolysis under anaerobic conditions to supply ATP
    - covers next minute of exercise and becomes less efficient
  3. oxidative phosphorylation under aerobic conditions takes over
33
Q

what occurs in the immediate stage of energy release?

A
  • muscle cells have reserves of ATP and phosphocreatine (PCr)
  • ADP accumulates in the cell to drive oxidative phosphorylation and Krebs cycle
  • build up of ADP, AMP and Pi stimulate metabolic pathways (oxidative phosphorylation)
  • creatine is recycled into PCr in mitochondria when at rest as there is an increased O2 demand
34
Q

what occurs in the anaerobic (nonoxidative) phase of energy release?

A
  • anaerobic metabolism via glycolysis

- muscle fibres store 300-400g glycogen

35
Q

at what 2 points in anaerobic glycolysis do substrates enter?

A
  1. glycogenolysis of glycogen produces glucose-1-phosphate
    - glucose-1-phosphate is converted to glucose-6-phosphate
    - enters glycolysis at reaction 2
  2. uptake of glucose from blood by GLUT4
    - glucose enters glycolysis to produce pyruvate
    - pyruvate is converted to lactate
36
Q

why is the anaerobic state of energy release inefficient?

A
  • 2ATP molecules per glucose

- H+ from lactate lowers cell pH and leads to muscle fatigue

37
Q

what is the aerobic (oxidative) phase of energy release?

A
  • O2 delivery to tissue is increased, stimulating oxidative phosphorylation
  • process is slower but more efficient
  • 30ATP per glucose
  • glucose is sourced from blood following breakdown of glycogen stores in liver
  • lactate is released from type IIx is converted back to pyruvate to feed oxidative phosphorylation
38
Q

how are waste products used to aid extended periods of exercise?

A
  • lactate and alanine are used by liver to generate new glucose
  • lactate is released from non-exercising muscles
  • body redistributes glycogen stores
  • increased circulation of fatty acids which muscles can uptake
  • breakdown of triacylglycerols stored in the muscle
39
Q

how efficient is the muscle metabolism in aerobic conditions?

A
  • 38ATP produced in ideal conditions via liver and kidney

- usually 30ATP during muscle contraction (lower yield)

40
Q

what is central muscle fatigue?

A
  • minor factor in trained exercise

- mind over matter

41
Q

what is peripheral muscle fatigue?

A
  • at level of muscle fibre

- production of lactate and H+ ions lowering pH of muscle cells

42
Q

what is fatigue?

A
  • inability to maintain a desired output

- decline in force and velocity of muscle shortening

43
Q

what is high-frequency fatigue?

A
  • alteration in Na+/K+ balance across membrane in type II fibres
  • resting potential is changed so it is harder to trigger APs
44
Q

what is low frequency fatigue?

A
  • reduced Ca2+ release from SR

- more apparent in at low frequency stimulation in type I fibres

45
Q

what is ATP depletion in fatigue?

A
  • intense stimulation can cause large drops in ATP near sites of cross-bridge formation and ATPases
46
Q

what causes lactic acid build up?

A
  • high rates of lactate production leads to cellular acidification
47
Q

what is glycogen depletion in fatigue?

A
  • loss of an easy glucose source
48
Q

what is cardiac muscle?

A
  • specific to the heart
  • cardiomyocytes are striated
  • myocytes are shorter, more branched and joined by intercalated discs
  • electrical coupling between adjacent myocytes by gap junctions
  • AP initiated in SAN pacemaker and propagates between myocytes via gap junctions to cause contraction
49
Q

what is smooth muscle?

A
  • involved in control of organ systems: digestive, urinary and reproductive
  • control blood vessel and airway diameter
  • circulating hormones, ANS or inflammatory mediators control smooth muscle
  • non-striated
  • actin fibres join at dense bodies and thick filaments intersperse around thin ones
  • large variation in AP depending on muscle type
  • some cannot generate APs but respond to graded changes in Vm
50
Q

what are the 2 classes of smooth muscle?

A
  1. multiunit
    - nerve fibres come to each individual muscle cell
    - lots of innervation
  2. unitary
    - AP stimulates one muscle cell
    - gap junctions enable AP to be dispersed to other muscle cells
    - enables coordinated contraction
    - less innervation
51
Q

what is excitation-contraction coupling in skeletal muscle?

A
  • mechanism to increase intracellular Ca2+

- depolarisation activates L-type Ca2+ channels in T-tubule membrane

52
Q

what 2 effects does excitation-contraction coupling have on skeletal muscle?

A
  1. leads to opening of L-type Ca2+ channels and influx of Ca2+ into sarcoplasm
  2. causes mechanical tethering between L-type Ca2+ channels in T-tubule and ryanodine receptors in the SR membrane
    - ryanodine channels open and Ca2+ moves into sarcoplasm

ryanodine receptors are Ca2+ release channels

53
Q

what is excitation-contraction coupling in cardiac muscle?

A
  • cardiac T-tubules are close to one branch of SR so is called dyad
  • there is no mechanical tethering between L-type Ca2+ channels in T-tubules and the ryanodine receptors in the SR
  • influx of Ca2+ through L-type channels activates ryanodine receptors to open
  • Ca2+ enters sarcoplasm

known as calcium induced calcium release (CICR)

54
Q

what does removal of calcium from the sarcoplasm cause?

A
  • termination of muscle contraction
55
Q

what are the 3 ways in which Ca2+ is removed from the sarcoplasm?

A
  1. Plasma Membrane Calcium ATPase (PCMA)
    - PCMA is an active transport pump and requires hydrolysis of ATP to pump Ca2+ out of cell
  2. sodium/calcium exchanger (NCX)
    - relies on Na+ conc gradient
    - 3Na+ are transported into sarcoplasm while 1 Ca+ is transported out into extracellular space
  3. back into SR stores via SR Ca2+ ATPase
    - uses ATP hydrolysis to pump Ca2+ back into SR
    - buffering proteins combine with 50Ca2+ to increase storage capacity
56
Q

what is excitation-contraction coupling in smooth muscle?

A
  • smooth muscles lack triads/dyad T-tubule and SR structures
  • they use caveolae which contain voltage-gated Ca2+ channels
  • peripheral SR encircles caveolae as a nearby Ca2+ store
  • central SR runs through enter sarcoplasm as a general Ca2+ store
57
Q

how are L-type Ca2+ channels activated in smooth muscle?

A
  • change in membrane potential, or an ATP, leads to CICR via activation of ryanodine receptors in the SR
58
Q

what is the role of Gq-coupled receptors in smooth muscle?

A
  • they are activated and cause IP3 production and IP3 receptor stimulation in SR membrane
59
Q

how is sarcomere contraction similar in skeletal and cardiac muscle?

A
  • both contain tropomyosin which interweaves around actin
  • both contains a troponin complex with can block the actin-myosin binding site
  • in the absence of calcium, troponin complex prevents myosin head forming a cross-bridge with actin
60
Q

what is the role of calcium and troponin in skeletal and cardiac muscle cross bridge formation?

A
  1. troponin T binds to tropomyosin, troponin C binds to calcium, troponin I lays over binding site
  2. increase in Ca2+ levels causes calcium to bind to TnC
  3. this causes conformational change in TnT, causing it to pull tropomyosin and TnI out of the binding site
  4. cross-bridge formation can now occur
  5. as Ca2+ levels decrease, original conformation returns and the binding site is blocked again
61
Q

what is the mechanism of contraction in smooth muscle?

A
  • there is no troponin in smooth muscle
  • calponin and caldesmon tonically inhibit actin-myosin interaction
  • stimulation of contraction involves stimulation of calmodulin by Ca2+ binding
62
Q

what are the downstream effects of calmodulin during contraction of smooth muscle?

A
  1. activation of Myosin Light Chain Kinase (MLCK)
    - phosphorylates MLC to cause change in myosin head angle
  2. removes inhibitory effects of calponin and caldesmon to allow cross-bridge formation
  3. stop contraction by dephosphorylating MLC via MLC phosphatase (MLCP)

Physiology and Pharmacology (13 decks)

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