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Human Physiology (BIOL 2410/2420) > Skeletal + Cardiac muscle > Flashcards

Skeletal + Cardiac muscle Flashcards

1
Q

What are the three types of muscle and where are they found?

A

Skeletal muscle: make up musclar system

Cardiac muscle: found only in heart

Smooth muscle: appears throughout body as components of organs and tubes

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2
Q

What are the structures of the three types of muscle?

A

skeletal: multinucleated due to fusion, striated, long and stacked in parallel

cardiac: uninucleated and unfused, striated, stacked from end to end and connected via intercalated disk

smooth muscle: uninucleated, not striated, stacked in sheets or tubes

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3
Q

What part of the nervous system controls skeletal muscle?

A

Neurons in CNS control muscle via upper motor neurons and lower motor neurons.

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4
Q

What is the difference between upper and lower motor neurons?

A

upper: cell body in primary motor cortex synapses on lower motor neurons on spinal cord

lower: cell body in spinal cord sends axons to synapse on motor units

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5
Q

What is the pathway of muscle control from the primary motor cortex?

A
  1. Neurons in primary motor cortex send axons through white matter in brain
  2. Axons descend through midbrain and medulla, switching sides at medulla pyramids
  3. Motor neurons send out axons through VENTRAL roots and make neuromuscular junctions
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6
Q

What is a motor unit?

A

One motor neuron and all of the muscle cells it innervates.

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7
Q

What is the neuromuscular junction?

A

Synapse between lower motor neurons and muscle cell consisting of many nicotinic Acetylcholine receptors and voltage gated Na+ channels

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8
Q

How does the nueromuscular junction cause an action potential in the muscle?

A
  1. Action potential travels down to axon terminal, and depolarization allows VG Ca2+ channels to bind
  2. VG Ca2+ channels open, allowing Ca2+ inside, which triggers exocytosis of ACh vesicle
  3. ACh is released into cleft and binds to many nicotinic ACh receptors, allowing them to open.
  4. Open nACh receptors allow influx of Na+, triggering opening of other VG Na+ channels
  5. Mass influx of Na+ causes a massive EPSP, guaranteeing the trigger of an action potential in the muscle.
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9
Q

What is the structure of a large muscle?

A

Muscle is made of multiple fascicles, which are bundles of fibers held together via connective tissue.

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10
Q

What are the organelles of a muscle cell?

A

Sarcoplasmic reticulum: endoplasmic reticulum and mass Ca++ storage

Sarcolemma: cell membrane of muscle cell

T-tubules: tubes made of invaginated sarcolemma running perpendicular to myofibril at ends of A bands

Myofibril: long chains of sarcomeres, the contractile elements of a muscle fibre

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11
Q

What are the parts of a sarcomere?

A

A band: section of overlapping thick and thin filaments

H zone: section of thick filaments between ends of thin filaments

I band: section of thin filaments between ends of two thick filaments

M line: Column where rows of thick filaments connect

Z disk: column where rows of thin filaments connect

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12
Q

What is the difference between thick and thin filaments?

A

Thick: made of myosin tails connected at the M line and branching out into two heads

Thin: made of chain of actin surrounded by Titin, tropomyosin, troponin and nebulin

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13
Q

What is a myosin crossbridge?

A

Bridge between myosin tail and actin filament consiting of twisted hinge region and globular heads. Each head has an actin binding site and myosin ATPase.

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14
Q

What is actin’s role in the muscle?

A

Primary structural component of thin filaments made of spherical G-actin monomers in a long chain. Each actin molecule has a binding site for attachment with myosin head to form the cross bridge.

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15
Q

What is tropomyosin?

A

Threadlike molecule interacting with actin along spiral groove. Covers myosin binding sites to prevent crossbridge formation

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16
Q

What is troponin’s structure?

A

Regulatory protein with subunits to bind to tropomyosin, actin, and Ca++

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17
Q

What is the effect of Ca++ on troponin?

A
  1. When not bound to Ca++, troponin stabilizes tropomyosin in blocking position over actin cross bridge
  2. When Ca2+ binds to troponin, tropomyosin moves away from blocking position, exposing binding site and creates crossbridges.
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18
Q

What is titin?

A

Giant elastic protein that joins M-lines to Z-lines at opposite ends of a sarcomere. This stabilizes position of thick filaments in relation to thin filaments, and improves muscle’s elasticity.

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19
Q

What is nebulin and myomesin?

A

Nebulin: aligns actin filaments

Myomesin: creates the M-line that joins thick filaments together

20
Q

What is the sliding filament hypothesis?

A
  1. at relaxed state myosin + ADP + Pi is weakly bound to actin and tropomyosin partially blocks binding site on actin
  2. Ca++ levels increase and bind to troponin, which pulls tropomyosin away from actins binding site allowing cross-bridge formation and power stroke
  3. Myosin releases Pi causing head to swivel and pull actin towards M-line
  4. At end of power stroke, ADP is released and myosin binds rightly to actin.
  5. Cycle continues until tropomyosin covers the actin again
21
Q

What are the parts of the sarcoplasmic reticulum?

A

Ca++ ATPase transporter: pumps Ca++ from cytoplasm into SR

Calsequestrin: soaks up Ca++ ions and ensures high Ca++ concentration inside the sarcoplasmic reticulum

22
Q

How do the DHP and Ryanodine receptor work together?

A

dihydropyridine receptor is a voltage gated Ca++ channel on the T-tubule that is connected to the ryanodine receptor.

Opening of DHP via action potential mechanically opens ryanodine receptor on sarcoplasmic reticulum, releasing massive amounts of Ca++ into the cytoplasm

23
Q

What is the full pathway of muscle contrcation?

A
  1. AP from lower motor neuron releases ACh into neuromuscular junction
  2. ACh binds to the many receptors, allows entry of Na+, triggers VG Na+ channels, allows entry of even more Na+, causing large EPSP
  3. AP invades T-tubule system and triggers voltage gated DHP receptor
  4. DHP receptor opens, which mechanically opens RyR channel on sarcoplasmic reticulum
  5. Sarcoplasmic reticulum releases large amounts of Ca++, increasing Ca++ concentration
  6. Ca++ binds to troponin which causes a confiirmational change, pulling tropomyosin away from myosin binding site on actin of thin filament
  7. Exposed myosin binding site allows globular head to bind and induces power stroke.
  8. Power strokes slide actin filaments towards centre of sarcomere
  9. When action potentials stop arriving at NMJ, ACh dissociates from ACh receptors, free Ca++ is pumped back into SR via Ca++/ATPase transporter, tropomyosin moves back into position, and actin + myosin slip past each other via titin
24
Q

How does rigor mortis occur?

A
  1. Intracellular Ca++ leaks out of SR
  2. Ca++ increase allows troponin-tropomyosin to expose myosin binding site
  3. Myosin creates cross bridges and holds tightly, but cannot separate and make a power stroke without ATP
25
Q

What are the processes in contraction relaxation that require ATP?

A
  1. Splitting of ATP by myosin ATPase for power stroke
  2. Ca++/ATPase transporter to bring Ca++ back to sarcoplasmic reticulum
  3. Na+/K+ ATPase to maintain resting membrane potential
26
Q

Where does the muscle get ATP for contraction?

A
  1. Minimal stored ATP
  2. Creatine phosphate: first energy source tapped at onset of contractile activtiy after stored ATP is used
  3. Oxidative phosphorylation: takes place in mitochondria if sufficient O2 is present
  4. Glycolysis: supports anaerobic or high-intensity exercise
27
Q

When and how is Creatine phosphate used?

A

When: first few minutes of exercise when ATP is low, provide 4-5x energy of stored ATP for a few minutes

How: In times of low ATP, Creatine kinase dephosphorylates creatine-phosphate and transfers it to an ADP molecule, creating useable ATP

28
Q

What is oxidative phosphorylation and when is it used?

A

What: Process that uses stores of glyocgen in muscleto creates a good yield of ATP with an adequate supply of oxygen.

When: used during first 30 mins of exercise)

29
Q

How does the body maintain adequate oxygen for oxidative phosphorylation?

A
  • Increased ventilation (oxygen inhaltion)
  • increase heart rate and force of contraction (increased rate of sending oxygen to muscle)
  • dilate skeletal blood vessels (allow more oxygen in at a time)
30
Q

What is anaerobic glycolysis and when is it used?

A

When: primary source of ATP when oxygen supply is limited (intense exercise)

What: process that produces 2 ATP per glucose molecule with a few enzymes involved, but occurs rapidly. Lactic acid is produced as a result of lack of oxgen which acidifies the muscles and causes fatigue.

31
Q

What causes muscle fatigue?

A

Central: psychological

Peipheral: decrease in release of Ach, receptor desensitization, changes of muscle RMP, impaired Ca++ release by SR, intracellular pH of muscle, muscle damage

32
Q

How does muscle tension develop during on muscle twitch?

A
  1. Latent period (5-10ms)
  2. Contraction phase followed by relaxation phase (10-100ms)
33
Q

How is maximum tension reached?

A

Summation of tension via summed twitches. Fatigue causes muscles to lose tension despite continuing stimuli due to Ca++ saturation on myosin binding sites.

34
Q

What are the three types of motor units?

A
  1. Slow twitch oxidative (red muiscle)
  2. Fast twitch oxidative (red muscle)
  3. Fast twitch glycolytic (white muscle)
35
Q

What are slow twitch oxidative muscle fibers? Why?

A

SLOW FATIGUE RESISTANT: Small fibres that generate small amounts of tension for long periods of time without running down energy stores. This is due to large numbers of mitochondria + well vascularized and contains myoglobin to facilitate oxygen transfer from blood.

36
Q

What are fast oxidative glycolytic muscle fibres?

A

FAST FATIGUE RESISTANT: larger fibres than slow twich and generate a lot of tension moderately fast. They’re somewhat resistant to fatigue due to moderate # of mitochondria.

37
Q

What is fast twitch glycolytic muscle fibres?

A

Largest fibres made of white muscle (little myoglobin) and generate the most tension. They fatigue rapidly due to their few mitochondria and tendency for anaerobic catabolism.

38
Q

How are motor units recruited in a muscle?

A

1st: small motor neurons to slow twitch fatigue resistant, each motor unit has only a few fibres

2nd: larger motor neurons to motor unit in fast fatigue resistant fibres

3rd: Largest motor neurons to motor unit that contains the most fibres, including fast fatiguable fibres.

39
Q

Why are motor units recruited in smallest to largest?

A

It is easier to bring a small neuron to threshold than a large neuron

40
Q

How do cardiac muscles maintain functional syncytia?

A

Cardiac muscle cells are interconnected by intercalated discs formed by desmosomes and gap junctions.

41
Q

what are the three types of cardiac muscle cells?

A
  1. Myocardial Autorhythmic Cells: Initiate + maintain electrical activity in the heart, do not contract.
  2. Conducting cells: conduct electrical signals throughout the heart. Do not contract.
  3. Myocardial contractile cells: 99% of cardiac muscle, do mechanical work of pumping and electrically joined by gap junctions.
42
Q

How is electricity conducted in the heart?

A
  1. Cardiac impulse originates at sinoatrial node
  2. Action potential spreads throughout right and left atria via internodal pathway
  3. From internodal pathway, signal is passed through atrioventricular node
  4. Atrioventricular node is briefly delayed to ensure atrial contraction before ventricle.
  5. Impulse travels down septum through L and R branches of the bundle of His
  6. Rest of ventricular cells activated by cell-to-cell spread of impulse due to gap junctions
43
Q

What is pacemaker potential?

A

Constant change of potential in autorythmic cells, preventing a resting membrane potential.

44
Q

What are the steps in the action potential of contractile cells?

A
  1. Na channels open causing rapid depolarization
  2. Na+ channels inactivate
  3. Ca+ channels open letting in Ca++ and K+ begins to open, causing early repolarization
  4. K+ channels open and K+ leaks out causing rapid final repolarization
45
Q

Why does the plateau (repolarization) of contractile cells take so long?

A

Plateau occurs primarily due to prolonged activation of L-type Ca++ channels which are slow. This ensures adequate ejection of blood.

46
Q

What is the difference between the refractory period of a skeletal muscle vs a cardiac muscle?

A

skeletal: Refractory period is short compared to the time required for development of tension. This allows summation and constant muscle contraction

cardiac muscle: refractory period is as long as the development of tension. This prevents summation and constant muscle contraction.

47
Q

How is the excitement-contraction coupling in cardiac contractile cells different from skeletal muscle?

A

Instead of depolarization across T-tuble causing VG DHP to open and with it open the RyR, depolarization across T-tuble causes influx of Ca++ which opens the RyR.

Human Physiology (BIOL 2410/2420) (15 decks)

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