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2C03 > Exam Review > Flashcards

Exam Review Flashcards

1
Q

For fine motor movements (fiber type and #/MU)

A

type I fibers
Few fibers per motor unit

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2
Q

Motoneuron soma size (largest to smallest)

A

IIX-IIA-I

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3
Q

Fiber size-CSA (diameter) (Largest to smallest-males)

A

IIA-IIX-I

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4
Q

Type I muscle fibers characteristics

A

-slow ATP breakdown
-Smaller (diameter)
-More mitochondria
-Better blood supply
-Fatigue resistant
-AKA Slow Oxidative

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5
Q

Type IIA Muscle fiber characteristics

A

-Fast ATP breakdown (fast myosin ATPase)
-Larger than type I
-less mitochondria
-less blood supply
-less aerobic capacity
-AKA fast oxidative-glycolytic

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6
Q

Type IIX muscle fiber characteristics

A

-larger than type I (but smaller than type IIA)
-fewest mitochondria
-least blood supply
-lowest aerobic capacity
-fatigable
-AKA Fast glycolytic (FG)

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7
Q

Determinants of fatigue resistance

A

-mitochondrial size and number
-myoglobin concentration
-muscle fiber diameter (diffusion distance)
-capillarization

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8
Q

Main differences between onion skin and after hyperpolarization models

A

onionskin: lower threshold MU recruited first (size principle) and firing rate increases significantly to increase force- higher threshold MU are recruited but the firing rate is not increase significantly- this is reserved for extreme circumstances- more indicative of voluntary contraction humans
AHP: lower threshold recruited and FR increases slightly, then higher threshold MU recruited- it is these fibers increased FR that result in a great increase in force production

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9
Q

During an Eccentric contraction of the same absolute force as Concentric there are

A

more force/ CB
less CBs needed
less muscle fibers needed
less motor units needed
less motor units activated (Seen on EMG)

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10
Q

For the same relative force, eccentric and concentric contraction have:

A

same number of CBs active
Same number of muscle fibers active
same number of motor units active
same motor unit activation
*** this relation tappers off at very high relative force

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11
Q

Why is there a lower max EMG activation during high velocity Eccentric contraction

A

fear of max eccentric actions
unfamiliar with max eccentric contractions
reflex inhibition- Golgi tendon organs?
- throw voluntary limitation may be present throw baseball as had as can vs pulling arm stretched as much as possible

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12
Q

Firing rate impact on rate of force development

A

higher firing rate
more frequent MAPs
faster rate of Ca2+ release from SR
More rapid onset of CB cycling
Greater rate of force development

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13
Q

Factors impacting EMG magnitude

A

-Number of fiber active (MUs recruited)
-motor action potentials per fiber (firing rate)
-size of fiber
-Amplitude= action potentials on top of each other
-muscle specific differences exist- different distribution of MU in muscles (eye vs quads)

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14
Q

MU recordings overlap force production with MU potentials- take home

A

integrated signals give us better insight, combining both

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15
Q

What happens to Motor unit number estimates with ageing 2 take homes

A

-MUNE (motor unit number estimation?) decreases with ageing in human skeletal muscle
-this is likely due to alpha motor neuron loss in the spinal cord- Motoneuron number decreases
** can somewhat avoid with use it or lose it principle

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16
Q

What happens to relative recruitment threshold after training- take homes (3)

A

-can decreases relative recruitment threshold (gets easier to recruit) after training
-while relationship between recruitment and training (lower threshold) is driven by fibers recruited at higher MVC there is still an overall effect (all fibers easier to recruit with training)
-recruitment threshold gets lower, and also our discharge rate gets faster (recruit and fire faster)

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17
Q

Fatigue: Isometric contractions

A

reduced force
reduced rate of force development (RFD)
reduced rate of force relaxation (RFR)

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18
Q

Fatigue: concentric contractions

A

reduced force
reduced velocity
overall reduced power

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19
Q

Fatigue: eccentric contractions

A

-reduced force- reduced force at given velocity
-reduced velocity? - may or may not- control velocity determined by external load
-mor likely to cause damage

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20
Q

How is exercise intensity expressed
Isometric
weightlifting
isokinetic
aerobic exercise

A

% MVC
% 1RM
Maximal contractions
% V02Max (can go over 100%)

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21
Q

Bottom line on fatigue

A

fatiguing exercise–> various causes/sites of fatigue–> decreases CB function

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22
Q

Effect of fatigue on force-velocity and power-velocity relationships

A

Reduced Isomax (lower force)- reduced number of CBs
Reduced Vmax (lower max velocity)- Reduced rate of CB cycling
lower force at a given velocity (each)
see overall decreased relation and leftward shift
*** major impact on Power- why power athletes need more rest
-Larger impact on CON contraction- can’t rely on positive braking

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23
Q

Sites of fatigue: brain

A

failure of volitional “drive” to motor cortex
decreased excitation of motoneurons
MU dropout and decreased MU firing rates

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24
Q

Sites of fatigue: Spinal cord

A

decreases excitability of motoneurons
reflex inhibition
MU drop out and decreased MU firing rate

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25
Q

Sites of fatigue: NMJ

A

NMJ failure
Muscle fiber drop out

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26
Q

Sites of fatigue: excitation contraction coupling

A

decreased excitability of endplate- decreased MAP size
impaired T-tubule-SR function - No Ca2+ release
excitation contraction coupling failure

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27
Q

Sites of fatigue: muscle fibre

A

direct effect on CB function- eg Lactic acid, H ion, metabolic in nature

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28
Q

Central fatigue

A

decreased MU activation

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29
Q

Peripheral fatigue

A

Neurotransmitter depletion
Reduced membrane excitability- ion exchange (Na, K)
Fuel depletion- ATP, PCr, Glycogen
Metabolic by-products- Pi, H+, heat

30
Q

Fatigue: MU activation

A

Mu dropout
less active fibers
less active CBs
less force/ power generating capacity
also
decreased FR
less summation/fiber
less active CB/fiber
less force/power generating capacity

31
Q

Sustained submax contraction activation fatigue

A

fatigue (decreased # active CB and decreased force/CB)
increase Mu recruitment and increase MU FR (increase # active CB)
Compensates of fatigue- fatigue progresses and process continues until no more MU can be recruited and firing rate can’t increase further- failure (can no longer maintain force)

32
Q

Possible causes for fatigue- 400m race

A

lack of will, neurotransmitter depletion, increased metabolites, decreased membrane excitability, reflex inhibition (caused by increased metabolites)

33
Q

Possible causes for fatigue- 42km race

A

lack of will, neurotransmitter depletion, hypoglycemia, decreased membrane excitability

34
Q

NMJ failure

A

Ach depletion - firing too quickly for too long
reduced endplate excitability- firing too quickly- can’t reestablish resting potential
result: no MAP- fiber dropout

35
Q

Fuel depletion: ATP

A

decreased ATP:
-decreased sensitivity of Ca2+ channels
-Decreased CA2+ release through SR release channels
-Decrease # active CBs

36
Q

Fuel depletion: glycogen

A

Decreased glycogen:
-decreased sensitivity of Ca2+ channels
-decreased Ca2+ release
-Decreased # of active CBs

37
Q

Accumulation of metabolites: Pi

A

Increased Pi:
-decreased Ca2+ release
-decrease sensitivity of Ca2+ channels
(Main metabolite contributing to fatigue)

38
Q

Accumulation of metabolites: H+

A

Increased H+:
-interference of Ca2+ binding to troponin
-Decreased rate of CB activation
-decreased # active CBs
-decreased PH can also inhibit Ca2+ release channels
-Not sure if H+ of lactic acid caused issues

39
Q

Direct effector of CB function: decreased number of active CBs

A

-from decreased ATP- with greater contractile intensity ATP need is increased

40
Q

Direct effector of CB function: Force/ CB

A

-force comes from actin myosin pulling
-increased Pi= decreased bond strength, increased likelihood of detachment
-increased Pi= decreased Ca2+/troponin interaction therefore Ca2+ requirement increased (more for the same force)

41
Q

Direct effector of CB function: H+

A

role is still debated- slows ADP release during the CB cycle- decreases cycling speed- contraction probability decreases, force decreases and number of active CB decreases

42
Q

Major sources of depletion

A

Fuel:
glucose, glycogen, Pcr, ATP

43
Q

Major accumulations

A

metabolites: lactate (and H+), Pi, occurs in both central and peripheral (muscle and brain)

44
Q

Fuel depletion- flow chart

A

decreased Pcr and/ or decreased glycogen
decreased rate of ATP resynthesis
decreased ATP (small initial store)
decrease # active CBs

45
Q

Metabolite accumulation- flow chart

A

Pi:
- decreased force/CB
-impaired E-C coupling–> decreased # active CBs

H+:
-decreased rate of glycolysis–> decreased rate of ATP resynthesis–> decreased ATP stores–> decreased # active CB
-muscle afferents-pain, inhibition
-impaired E-C coupling???–> decreased # active CBs
-Decreased force/CB???

46
Q

High intensity isometric (30s)

A

-limited O2
-decreased ATP
-decreased PCr
-increased Pi
-increased H+

47
Q

High intensity (4-5 mins)

A

-limited O2
-decreased ATP
-decreased Pcr
-increased Pi
-increased H+
-likely some decrease glycogen

48
Q

Low intensity (2hrs)

A

-O2 ok
-significant glycogen depletion
-hypoglycemia (C and P)
-dehydration
-hypothermia (C and P)

49
Q

Muscle vs blood lactic acid exercise intensity and duration

A

muscle lactic acid (H+)- increased with sprint time and distance)
blood lactic acid at finish- decreased with running distance in KM

50
Q

Fatigue: rate of force development- flow chart

A

type IIx MU drop out, decreased MU firing rate
-decreased force and rate of force development–> both caused decreased speed/ velocity performance
also
decrease rate of Ca2+ release/ Ca2+ sensitivity, decreased rate of CB cycling–> decreased rate of force development and decreased Vmax –> both decrease speed/velocity performance

51
Q

Fatigue rate of force relaxation

A

Ca2+ reuptake is active process0- requires ATP – slower Ca2+ reuptake from SR
- decreased Ca2+ ATPase activity; SERCA pump- may be caused by interference from metabolite accumulation

52
Q

Fuel and metabolite clearing/resynthesis

A

-ATP very fast
-PCr fast
-Pi fast
-H+ takes much longer
-glycogen resyntheses take long time

53
Q

Type II- greater metabolic power- fuel/metabolites chart

A

greater decrease in ATP, PCr, glycogen (but also greater storage of ATP and PCR- but slower recover than type II since less mitochondria)
Greater increase in: Pi and H+
compared to type I and average

54
Q

Female muscles: why have greater relative endurance

A

smaller fiber diameter
smaller II/I area ratio
grater capillary density
more elastic tissue (???)
higher % type I fiber
more Fat metabolism (glycogen sparing)
enzymes for oxidative metabolism also more efficient

55
Q

Effects of training on fatigue

A

-greater cardiac output- increased VO2 max- greater absolute and relative endurance
-increased muscle oxidative capacity: increased: mitochondrial density, myoglobin, capillarization–> increased VO2 max, increased relative endurance
Also see overall increased ability to sustain a given % VO2 max

56
Q

Absolute strength directly related to

A

CSA- highly correlated to mass, but CSA is inversely related to Strength/mass
Strength/CSA is unrelated to muscle CSA

57
Q

Mass and area- square cube law

A

Mass is directly related to volume
Area is related to force

58
Q

Type II fiber have a greater

A

specific force and Vmax

59
Q

Ageing: up to age 20

A

increase muscle size (increase fiber size)

60
Q

Ageing: 25-60

A

decrease: CSA, fiber CSA, fiber # (greater loss of type II)

61
Q

Ageing: 60+

A

Decrease: muscle CSA, fiber CSA, fiber #, # motoneurons, # of fibers (greater loss of type II)

62
Q

Neuromuscular compensation results in

A

greater number of fibers per motoneuron

63
Q

Females Vs Males

A

-lower absolute strength- lower CSA
-Greater body fat %- less strength/BM
-Less muscle mass per lean body mass (remove fat)- less strength/LBM
-Lower upper body: lower body muscle mass ratio: bigger difference versus males in upper body strength
-Small difference in strength/CSA- due to males having slightly more type II fibers than females

64
Q

Strength training hypertrophy

A

No addtion of fibers (hyperplasia)
increased number of myofibrils (splitting)
increased number of myofilaments (no change in size)

65
Q

Parallel loss/ growth

A

adding muscle size (add on top or bottom)

66
Q

Series loss/growth

A

-greater optimal zone (stretched-add more)
add left and right

67
Q

Fibers with the same CSA, longer fibers will (more sarcomeres in series)

A

-greater range of motion
increased absolute range of length-tension curve
-greater force at given velocity

68
Q

2 fibers same length, greater CSA (more sarcomeres in parallel)

A

shifts length tension curve higher- retains shape

69
Q

Unipennate, bipennate, fusiform/multipennate

A

unipennate: all force in same direction- greatest force
bipennate: force in 2 directions- slightly less force, but over a greater length
fusiform/multipennate: force in many directions, least force but over the greatest length

70
Q

PCSA

A

muscle volume/ fiber length- better indication of force than ACSA

71
Q

Training neural adaptation

A

what you see first when start training (before hypertrophy), allows increased FR- allows greater FRD, also less co contraction

72
Q

Faster development during training means it is

A

faster to be lost… but maintainemce is easier than development (1x/ week)

2C03 (1 decks)

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