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KNPE327 > Review > Flashcards

Review 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 threshold
The graded potentials arrive at trigger zone together and sum to create a supra threshold signal and an AP is generated

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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 reach trigger zone at 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 diff locations converted to a single one
Temporal: converts a rapid series of weak pulses from a single source 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 reset 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 cell
  3. Triggers exocytosis of acetylcholine in synaptic vesicle
  4. Ach diffuses across synaptic cleft and binds w receptors on postsynaptic cell
  5. Response initiated in 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 intro 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 intro 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 axon terminal of a somatic motor neuron; axon terminal of motor neuron connects to muscle fibre via neuromuscular junction
② stimulates opening of voltage gated ca2+ channels and ca2+ enters axon terminal
3 Increased ca2+ stimulates exocytosis of synaptic vesicles which releases Ach into synaptic cleft
④ Ach binds to Ach receptors on postsynaptic cell (motor end plate of sarcolemmal)
③ Ligand gated Na+/K+ channels open; Na+ moves into cell, K+ moves out
⑥ Depolarization of Sarcolemma causes voltage gated Na+ channels to open causing an Ap across sarcolemma and T-tubules
⑦ DHP channel causes RyR to open and allows Ca2+ to leave sarcoplasmic reticulum + diffuse into sarcoplasm
⑧ calcium ions bind to troponin, moving tropomyosin off of the active actin sites
⑨ Myosin can bind to actin, forming cross bridges … then 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

Decrease in the ability of motor neurons to be excited and conduct APs; everything upstream Ach being released at NMJ

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24
Q

Effect of central fatigue

A

Decreased Ach release into NMJ, less excitation and contraction of skeletal muscle and decreased force production

25
Q

Mechanisms of central fatigue

A
  1. Decreased motor outflow
  2. Increased inhibitory nerve activity
  3. Decreased excitability of motor neurons
26
Q

Decreased motor outflow

A
  • Decreased excitatory nerves stimulating motor neurons
  • Fewer AP
  • less ACh release into NMJ
27
Q

Increased inhibitory nerve activity

A
  • increased effort required to stimulate motor neurons
  • results from activation of group III/IV afferent nerves bc they cause hyperpolarization rather than depolarization
  • hyperpolarization requires more effort to excite
28
Q

Decreased excitability of motor neurons

A
  • voltage gated ion channels dysfunctional
  • axon membrane depolarized following repeated AP
  • axons can’t conduct AP= decreased ACh release into NMJ
29
Q

Peripheral fatigue

A

Decrease in the ability of a muscle to respond to increases in ACh

30
Q

Mechanisms of peripheral fatigue

A
  1. NMJ failure
  2. Accumulation of fatigue inducing metabolites
31
Q

Neuromuscular junction failure

A

Decreased function of muscle membrane and DHPR/RYR)

32
Q

Accumulation of fatigue inducing metabolites

A
  1. Decreases in ATP and PCr
  2. Pi
  3. H+
33
Q

Decreases in ATP (and PCr)

A

ATP stimulates RYR mediated Ca2+ release which stimulates contraction
Required for rapid uptake of Ca2+
Phosphocreatine system is first defence against decrease in ATP which increases breakdown of PCr

34
Q

Pi

A
  • slowed release of Pi from myosin head and decreased rate of cross bridge cycling
  • decreased sensitivity of troponin C fore Ca2+ (decreases number of crossbridges formed)
  • inhibition of DHPR and RYR complex
  • Binding of free Ca2+ in cytosol (less Ca2+ in cytosol =less force)
35
Q

H+

A

Decreased sensitivity of troponin C for Ca2+
Competes w Ca2+ binding site on SERCA
Decreased ATP stmulates glycolysis which increases lactate and H+ accumulation

36
Q

Creatine kinase reaction

A

PCr + ADP = ATP + Cr
- generates greatest sustainable max power, fatigues fast
- sprinting and powerlifting

37
Q

Anaerobic Glycolysis

A

Negative relationship with ATP
Positive relationship with ADP
- high power, more fatigue resistant

38
Q

Oxidative phosphorylation (aerobic metabolism)

A
  • lowest power output, high maximal capacity
39
Q

Key determinant of lactate production

A

The balance in activation btwn the conductances for inflow and outflow of pyruvate
- Inflow to pyruvate: ADP and AMP
- Outflow to pyruvate: PFK- PDH activity
*More pyruvate = more lactate

40
Q

Hyperoxia

A
  • excess O2
  • increases aerobic ATP production bc system is better able to match ATP inflow to outflow
  • Don’t require the activation of PCr or glycolysis and therefore reduce fatigue inducing metabolites
  • less of an increase in ADP and Pi
41
Q

Hypoxia

A
  • low O2
  • decreases production of ATP
  • drives breakdown of PCr
  • activates glycolysis = accumulation of H+
  • increased ADP and Pi
42
Q

How does higher intensity exercise use more ATP?

A

Increases activity of ATPases which increases outflow from the ATP pool

43
Q

Determinants of strength, power and speed

A
  1. Fibre distribution
  2. Muscle size
  3. Metabolic capacity
44
Q

Fibre distribution

A
  1. Slow twitch: oxidative type I
    - most fatigue resistant
    - lowest force output
    - endurance athletes
  2. Fast twitch
    a) Type IIa oxidative glycolysis (longer sprints, lifting weights with higher reps)
    x) Type IIx fast glycolytic (100m sprints, heavy weight 1-3 reps) *PCr
45
Q

Force of muscle fibres

A

Type IIx>Type IIa>Type I

46
Q

Fatigue resistance of muscle fibres

A

Type I>Type IIa>Type IIx

47
Q

Muscle size

A

Bigger muscles= more force production
Cross sectional area: Type IIx>Type IIa>Type I

48
Q

Inflows to ATP pool

A

Three 3 metabolic pathways

49
Q

Outflow from ATP pool

A

ATP hydrolysis

50
Q

Metabolic capacity

A

PCr power and capacity imp for brief, high intensity contraction
Anaerobic glycolytic power and capacity imp for longer duration sprints

51
Q

Determinants of speed and endurance

A
  1. VO2 max
  2. Lactate threshold/ critical power
  3. Efficiency
  4. Metabolic capacity
52
Q

VO2 max

A

Sets upper limit for speed/endurance performance
Higher relative max = greater absolute performance

53
Q

Lactate threshold

A

Highest sustainable intensity without significant lactate accumulation
Higher the threshold, the higher sustainable work rate

54
Q

Critical power (MLSS)

A

Highest sustainable intensity
Once you go over critical power threshold, you go from performing a sustainable work rate to fatiguing very quickly
Past the critical threshold, PCr and anareboic glycolysis kick in whereas before you would have been using aerobic metabolism

55
Q

Which muscle fibres have the highest efficiency?

A

Type I

56
Q

Efficiency

A

Amount of work you do that can be performed for a given energy expenditure
Work/energy expenditure
- highest power output for the same VO2

57
Q

What impacts efficiency?

A
  1. Work rate: efficiency decreases at higher intensities
  2. Speed: everyone has a most optimal and most efficient speed; if you work above or below this speed it decreases efficiency
  3. Fibre composition: type I more efficient than type II
58
Q

Factors that determine metabolic capacity?

A
  1. Fibre type distribution: type I for endurance
  2. Glycogen stores: when stores are high, endurance performance high (Type I preserves longer than Type II)
  3. Fatty acid oxidative capacity: increased ability to metabolize fatty acids improved endurance performance bc reliance on glycogen is decreased
59
Q

Performance

A

Impacted by body weight

KNPE327 (8 decks)

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