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KNPE 227 > Unit Test 2 > Flashcards

Unit Test 2 Flashcards

1
Q

Motor unit activation

A

First step in initiating action potential

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2
Q

Trigger zone

A

Site of action potential; AP initiated when cell body is depolarized past AP threshold

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3
Q

Action potential threshold

A

Critical level to which a membrane potential must be depolarized to initiate AP

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4
Q

Excitatory neurons

A

Cause depolarization of motor nerve; membrane potential becomes more positive

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5
Q

Inhibitory neurons

A

Cause hyperpolarization of motor nerve; membrane potential becomes more negative

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6
Q

Spatial summation

A

When three excitatory neurons fire with their graded potentials being separate and below the threshold, the graded potentials arrive at trigger zone together and sum to create a supra threshold signal, generating AP

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7
Q

What happens if there is an inhibitory neuron present in spatial summation?

A

The sum of one inhibitory and two excitatory will not be enough to generate an AP

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8
Q

Temporal summation

A

When multiple excitatory neurons cause a depolarization that reaches the trigger zone at the same time, and sum to cause a depolarization that triggers AP

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9
Q

Spatial vs temporal summation

A

Spatial: several weak signals from different locations converted to a single one
Temporal: converts a rapid series of weak pulses from a single source of into one large signal

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10
Q

Depolarization

A

Opening of voltage gates Na+ channels

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11
Q

Repolarization

A

Closure of Na+ and opening of K+ voltage-gated channels

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12
Q

Hyperpolarization

A

Voltage gated K+ channels remain open after potential reaches resting level (refractory period)
- necessary for system to rest Na+ and K+ concentrations for next AP

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13
Q

Acetylcholine release

A
  1. AP depolarizes axon terminal
  2. Opening of voltage gates Ca+ channels and
    Ca+ enters the cell
  3. Triggers exocytosis of acetylcholine in the
    synaptic cleft and binds with receptors on
    the postsynaptic cell
  4. ACh diffuses across the synaptic cleft and
    binds with receptors on the postsynaptic cell
  5. Response initiated in the postsynaptic cell
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14
Q

ACh breakdown

A
  1. ACh made from choline and acetyl CoA
  2. ACh broken down by AChesterase in synaptic
    cleft
  3. Choline transported back into axon terminal
    and is used to make more ACh
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15
Q

Excitation of muscle membrane

A

Initiated by ACh in NMJ and triggers contraction by releasing Ca2+ from SR into muscle’s cytosol

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16
Q

ACh breakdown

A
  1. ACh made from choline and acetyl CoA
  2. ACh broken down by AChesterase in synaptic
    cleft
  3. Choline transported back into axon terminal
    and is used to make more ACh
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17
Q

Ca2+ release

A
  1. Somatic motor neuron releases ACh into NMJ
  2. Entry of Na+ through ACh receptor channel
    initiates AP
  3. AP activates DHPR
  4. DHPR activates RYR which triggers the release
    of Ca2+ from SR into cytosol
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18
Q

Contraction

A

Release of Ca2+ into cytosol

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19
Q

Relaxation

A

A muscle will continue to contract until Ca2+ is pumped out of cytosol back into SR by SERCA pumps

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20
Q

Contraction cycle

A
  1. Calcium binds to troponin exposing myosin
    binding sites on actin
  2. Myosin head forms cross-bridge w actin
  3. Pi released from myosin head
  4. Power stroke
  5. ATP replaces ADP on myosin head
  6. Myosin releases actin and moves into cocked
    position
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21
Q

Sliding filament theory of muscle contraction

A
  1. Ap arrives at the axon terminal of a somatic
    motor neuron; axon terminal of the motor
    neuron connects to muscle fibre via
    neuromuscular junction
  2. Stimulates opening of voltage-gated ca2+
    channels and ca2+ enters the axon terminal
    3 Increased ca2+ stimulates exocytosis of
    synaptic vesicles which release Ach into
    synaptic cleft
  3. Ach binds to Ach receptors on postsynaptic
    cell (motor end plate of sarcolemmal)
  4. Ligand-gated Na+/K+ channels open; Na+
    moves into cell, K+ moves out
  5. Depolarization of Sarcolemma causes voltage
    gated Na+ channels to open causing an Ap
    across sarcolemma and T-tubules
  6. DHP channel causes RyR to open and allows
    Ca2+ to leave sarcoplasmic reticulum +
    diffuse into the sarcoplasm
  7. Calcium ions bind to troponin, moving t
    tropomyosin off of the active actin sites
  8. Myosin can bind to actin, forming a cross-
    bridges … then the contraction cycle
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22
Q

Resting membrane potential

A

Negative inside, positive outside

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23
Q

Central fatigue

A

A decrease in the ability of motor neurons to be excited and conduct APs; results in decreased ACh release into NMJ, less excitation and contraction of muscle, decreased force production

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24
Q

Mechanisms of central fatigue

A
  1. Decreased motor outflow
  2. Increased inhibitory nerve activity
  3. Decreased excitability of motor neurons
25
Q

Decreased motor outflow

A
  • Decreased excitatory nerves stimulating motor
    stimulating motor neurons
  • Fewer AP
  • Less ACh release into NMJ
26
Q

Increased inhibitory nerve activity

A
  • Increased effort required to stimulate motor
    neurons
  • A variety of stimuli in exercise muscles can activate group III/IV afferent fibres
  • Fibres inhibit the excitation of motor nerves by
    causing hyperpolarization of motor nerve cell
    bodies
27
Q

Decreased excitability of motor neurons

A
  • Axon membranes become depolarized
    following repeated action potentials
  • Voltage-gated ion channels on motor nerve
    axons can become dysfunctional
  • Decreased excitability
28
Q

Peripheral fatigue

A
  • Decrease in the ability of muscles to respond to increases in Ach
  • The effect of peripheral is less excitation and or contraction of skeletal muscle, and decreased force production
29
Q

Mechanisms of peripheral fatigue

A
  1. Neuromuscular junction failure
  2. Membrane depolarization
  3. Voltage-gated channel dysfunction
  4. DHPR voltage insensitivity
30
Q

Neuromuscular junction and E-C coupling failure

A
  • Membrane depolarization
  • Voltage-gated channel dysfunctional
  • DHPR voltage insensitivity
31
Q

Membrane depolarization

A
  • If the membrane becomes depolarized, action
    potentials are no longer possible
  • Membrane depolarization decreases the
    ability of muscle to respond to increased ACh
  • Resulting in fewer/less powerful contractions
32
Q

Voltage gated channel dysfunction

A

-

33
Q

DHPR voltage insensitivity

A
  • DHPRs can also become dysfunctional during
    intense or prolonged exercise
  • Dysfunctional DHPRs become insensitive to
    changes in voltage across muscle membrane
34
Q

Accumulation of fatigue inducing metabolites

A

↓ ATP
↓ PCr
↑ Pi
↑ H+

35
Q

Decreases in ATP (and PCr)

A
  • Less ATP = Less Ca2+ release
  • Less ATP = less/slower Ca2+ uptake by SERCA
    pump and slower relaxation
36
Q

Pi

A
  • Increased Pi contributes to the development of muscle fatigue in 4 ways
    1. Slowed release of Pi from myosin head and
    decreased rate of cross-bridge cycling
    2. Decreased sensitivity of Troponin C for Ca2+
    3. Inhibition of DHPR and RYR complex
    4. Binding of free Ca2+ in the cytosol
37
Q

H+

A

Increased H+ contributes to the development of muscle fatigue in 2 ways
1. Decreased sensitivity of Troponin C for Ca2+
2. Competes with Ca2+ at the binding site on SERCA

38
Q

Creatine kinase reaction

A
  • Providing an energy reserve in a muscle
  • Highest rate of ATP resynthesis
39
Q

Anaerobic Glycolysis

A
  • The transformation of glucose to lactate when
    limited amounts of oxygen (O2) are available
  • High rate of ATP resynthesis
40
Q

Oxidative phosphorylation (aerobic metabolism)

A
  • Moderate, sustainable rate of ATP resynthesis
41
Q

Key determinant of lactate production

A
  • Pyruvate
  • More substrate = more lactate production
  • The balance of inflow and outflow to acetyl
    CoA and the accumulation of Pyruvate
    determines the rate of production of lactate
42
Q

Hyperoxia

A

A state of excess supply of O2 in tissues and organs

43
Q

Hypoxia

A

Low levels of oxygen in your body tissues

44
Q

Determinants of strength, power and speed

A
  • Fibre distribution
  • Muscle size
  • Metabolic capacity
45
Q

Fibre distribution

A
  • Type IIx superior at producing power
  • Type IIa powerful and resist fatigue
46
Q

Fatigue resistance of muscle fibres

A
  • I > IIa > IIx
  • Type I are more fatigue resistant than IIa
  • Type IIa are more fatigue resistant than IIx
47
Q

Muscle size

A
  • Larger muscles (by CSA) produce greater force
  • Type II fibres are larger than type I
48
Q

Metabolic capacity

A
  • Phosphagen system (PCr) power and capacity
    are important for very brief, very high intensity
    contraction
  • Anaerobic glycolytic power and capacity are important for longer duration sprints
49
Q

Determinants of speed and endurance

A
  • VO2 max
  • Lactate threshold
  • Critical power
  • Efficiency
  • Metabolic capacity
50
Q

VO2 max

A

Sets the upper limit for speed/endurance performance

51
Q

Lactate threshold

A

Highest sustainable intensity without significant lactate accumulation

52
Q

Critical power (MLSS)

A

Highest sustainable intensity

53
Q

Which muscle fibres have the highest efficiency?

A
  • Type I are more efficient than type II
54
Q

Efficiency

A

The amount of work that can be performed for a given energy expenditure

55
Q

What impacts efficiency?

A
  1. Work rate
  2. Speed of movement
  3. Fibre type composition
56
Q

Factors that determine metabolic capacity?

A
  1. Fibre type distribution
  2. Glycogen stores
  3. Fatty acid oxidative capacity
57
Q

Performance

A
  • Endurance performance is greater when muscle glycogen stores are high
  • Increased ability to metabolize fatty acids improves endurance performance because reliance on glycogen is decreased
58
Q

Force of muscle fibres

A
  • IIx >IIa > I
  • Type IIx produce more force than IIa
  • Type IIa produce more force than I

KNPE 227 (2 decks)

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