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SF1.12 Muscle Physiology (ZACHOW) > Part 1: Muscle Physiology > Flashcards

Part 1: Muscle Physiology Flashcards

1
Q

To perform work and generate power, all muscles require:

A

ATP and calcium

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2
Q

Load of skeletal muscle, load of smooth muscle, load of cardiac muscle:

A
  • Skeletal: gravity
  • Smooth: blood pressure, food/digestion
  • Cardiac: blood pressure
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3
Q

Sources of calcium and ATP for skeletal muscle:

A
  • Ca2+: intracellular
  • ATP: stored, phosphagen, glycolytic, oxidative phosphoryation, fatty acids
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4
Q

Sources of calcium and ATP for smooth muscle:

A
  • Ca2+: extra- and intracellular
  • ATP: oxidative phosphorylation
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5
Q

Sources of calcium and ATP for cardiac muscle:

A
  • Ca2+: extra- and intracellular
  • ATP: oxidative phosphorylation, fatty acids
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6
Q

Functions of skeletal muscle:

A
  • Ambulation, posture
  • Displacing mass
  • Glucoregulation
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7
Q

Function of cardiac muscle (myocardium):

A

Moving blood volume

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8
Q

Function of smooth muscle:

A
  • Changing lumenal diameter
  • Digestion
  • Blood pressure
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9
Q

Hierarchy of muscle structure:

A
  1. Whole muscle
  2. Fascicles
  3. Muscle fibers/cells (covered with satellite cells)
  4. Myofibrils
  5. Sarcomeres
  6. Myofilaments
  7. Actin
  8. Myosin
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10
Q

The three types of troponin and their roles:

A
  • Troponin I (anchor to actin)
  • Troponin C (calcium binding)
  • Troponin T (anchors to tropomyosin)
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11
Q

What protein is interwoven into the actin filament and binds myosin?

A

tropomyosin

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12
Q

Structure of muscle myofilaments:

A
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13
Q

Process of voluntary muscle contraction:

A
  1. Brain initiates movement.
  2. Brain signal travels down spinal cord descending tracts.
  3. Signal leaves spinal cord through ventral root.
  4. Signal travels on alpha and gamma motor neurons to muscle fibers.
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14
Q

A motor unit consists of:

A

Motor neuron + fiber(s) it innervates

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15
Q

What motor neurons are involved in voluntary skeletal muscle contraction?

A

alpha and gamma motor neurons

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16
Q

Steps in neuromuscular transmission to muscle contraction:

A
  1. Action potential reaches motor neuron terminus. Voltage-gated calcium channels open, calcium influx, acetylcholine synaptic vesicles released.
  2. Acetylcholine binds to cholinergic-nicotinic (CN) receptors on the post-synaptic membrane of the muscle cell. Small sodium influx generates end plate potential.
  3. Endplate potential opens voltage-gated sodium channels, sodium rushes in and causes action potential firing in the muscle cell.
  4. Action potential travels down T-tubules of muscle cells and activates dihydropyridine receptors (DHPRs).
  5. DHPRs activate ryanodine receptors (RYRs), which are calcium channels. Calcium influx into the sarcoplasm of the T-tubule from the sarcoplasmic reticulum.
  6. Elevated sarcoplasmic reticulum calcium levels. Calcium binds to troponin C, causing conformational change in troponin C. Tropomyosin on actin revealed.
  7. Myosin head binds to tropomyosin on the actin.
  8. Myosin head changes conformation, power stroke occurs, which releases ADP + Pi from the myosin head.
  9. ATP binds to myosin head, myosin dissociates from tropomyosin/actin.
  10. ATP is hydrolyzed to ADP + Pi.
  11. Myosin head binds to tropomyosin. Repeat power strokes continue so long as increased calcium levels in the sarcoplasmic reticulum keep tropomyosin exposed.
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17
Q

Alpha and gamma motor neurons use what neurotransmitter/receptor to generate an end plate potential in muscle cells?

A
  • Neurotransmitter: acetylcholine
  • Receptor: cholinergic-nicotinic (CN)
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18
Q

Cholinergic-nicotinic (CN) receptors are:

A
  • ligand-gated sodium channels activated by acetylcholine.
  • activation generates an end plate potential.
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19
Q

What occurs when acetylcholine from a motor neuron crosses the synaptic cleft and binds to cholinergic-nicotinic (CN) receptors on the membrane of a muscle cell?

A
  • Small sodium influx generates end plate potential.
    • Endplate potential opens voltage-gated sodium channels, sodium rushes in and causes action potential firing in the muscle cell.
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20
Q

Once an action potential is generated in a muscle cell, where does it go and what does it activate?

A
  • Action potential travels down T-tubules of muscle cells and activates dihydropyridine receptors (DHPRs), which activate ryanodine receptors (RYRs), which are calcium channels.
21
Q

Dihydropyridine receptors (DHPRs):

A
  • receptors located in the T-tubules of muscle cells
  • activated by calcium
  • activate ryanodine receptors (RYRs)
22
Q

Ryanodine receptors (RYRs):

A
  • Calcium channels activated by dihydropyridine receptors (DHPRs).
  • Cause a calcium influx into the sarcoplasm of the T-tubule from the sarcoplasmic reticulum.
23
Q

What occurs in muscle cells when there is a sudden elevation in sarcoplasmic calcium levels?

A

cross-bridge cycling

  1. Calcium binds to troponin C, causing conformational change in troponin C.
  2. Tropomyosin on actin revealed.
  3. Myosin head binds to tropomyosin on the actin.
24
Q

Steps in cross-bridge cycling:

A
  1. Increased sarcoplasmic calcium levels from RYRs activation.
  2. Calcium binds to troponin C, causing conformational change.
  3. Tropomyosin on actin revealed.
  4. Myosin head binds to tropomyosin on the actin.
  5. Myosin head changes conformation, power stroke occurs, which releases ADP + Pi from the myosin head.
  6. ATP binds to myosin head, myosin dissociates from tropomyosin/actin.
  7. ATP is hydrolyzed to ADP + Pi.
  8. Myosin head binds to tropomyosin. Repeat.
25
Q

Myosin head power strokes continue in muscle cells so long as:

A
  • increased calcium levels in the sarcoplasm keep troponin C structurally altered to keep tropomyosin exposed.
26
Q

What occurs in the muscle cell when myosin powerstrokes occur?

A
  • Muscle contracts (Z-discs move closer to one another)
27
Q

ATP for cross-brdige cycling in skeletal muscle is produced from:

A
  • Sarcoplasmic stores
  • Phosphocreatine
  • Glycolysis
  • Oxidative phosphorylation
28
Q

Fuel for muscle contraction lasting a few seconds:

A

ATP stored in sarcoplasm

29
Q

Fuel for muscle contraction lasting a few seconds to a minutes:

A
  • ATP generated from phosphocreatinine/creatinine kinase
30
Q

Fuel for muscle contraction lasting a few minutes:

A

ATP generated from anaerobic glycolysis

31
Q

Fuel for muscle contraction lasting minutes to hours:

A
  • ATP generated from oxidative phosphorylation/fatty acid metabolism
32
Q

Diagram of muscle contraction fuel over time:

33
Q

When the shift occurs into anaerobic glycolysis and oxidative phosphorylation occurs, what by-products become significant?

A
  • lactate + protons
  • heat
  • carbon dioxide (vasodilator)
34
Q

What two sources of ATP for muscle contraction produce the most ATP?

A
  • oxidative phosphorylaiton
  • fatty acid metabolism
    • occur during sustained muscle contraction (minutes-hours)
35
Q

Steps in muscle relaxation:

A
  1. Motor neuron stops firing action potential, ACh not released.
  2. Muscle cell stops firing action potentials.
  3. DHPRs and RYRs (calcium channel) become inactivated.
  4. Sodium-calcium exchangers (NCXs) and SERCAs pump calcium out of the sarcoplasm back into the sarcoplasmic reticulum surrounding muscle cells.
  5. Troponin C does not have any calcium to bind to, tropomyosin hidden, myosin head cannot bind to tropomyosin and muscle relaxes.
36
Q

In skeletal muscle cells, what pumps out more calcium of the sarcoplasm during muscle relaxation, SERCAs or NCXs?

A
  • SERCAs
  • NCXs pump out relatively few calcium ions
37
Q

In skeletal muscle cells, what pumps out calcium from the sarcoplasm during muscle relaxation?

A
  • SERCA: sarco/endoplasmic reticulum Ca2+ ATPase (MAJOR)
  • NCX: Na+-Ca2+ exchanger (MINOR)
38
Q

What is the stimulus for all muscle contraction?

39
Q

What is the major type of calcium channel present in myocardium?

A

Type L calcium channels

40
Q

Inotropic state occurs when:

A
  • Changes in [Ca2+] are directly proportional to changes in muscle contractility.
  • Occurs in the myocardium of the heart.
41
Q

What is the major mechanism to pump calcium out of myocardium to allow the myocardium to relax?

A

NCX: Na+-Ca2+ exchanger

42
Q

NCX (Na+-Ca2+ exchanger) is what type of transporter?

A
  • secondary transporter:
    • a sodium-potassium ATPase pump drives sodium out of the myocyte, creates a favorable gradient for NCX to pump sodium into the cell while driving calcium out.
43
Q

What organ/hormone controls blood calcium levels?

A

parathyroid gland/parathyroid hormone

44
Q

What does parathyroid hormone promote?

A
  • An increase/maintainence of plasma [Ca2+] via:
    1. calcium resorption from bone
    2. kidney reabsorbtion of calcium from urine
45
Q

Patients with profound hyper- or hypocalcemia will have altered function of:

A

Skeletal and cardiac muscle function

46
Q

Hypercalcemia in patients can be due to:

A

Hyperparathyroidism

CALCIUM IS KEY TO MUSCLE CONTRACTION

47
Q

Hypocalcemia in patients may be due to:

A
  • Hypoparathyroidism
  • kidney failure
  • Vitamin D deficiency

CALCIUM IS KEY TO MUSCLE CONTRACTION

48
Q

Hypocalcemia leads to:

A
  • Motor neuron and skeletal muscle HYPERexcitability via a modulation of Na+ channel stability.
    • Increased INa+.
49
Q

Hypercalcemia leads to:

A
  • Motor neuron and skeletal muscle HYPOexcitability.
  • Raises threshold for voltage-gated Na+ channels.
  • Harder to fire action potentials.

SF1.12 Muscle Physiology (ZACHOW) (5 decks)

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