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HES 319 > Exam 3 (final) > Flashcards

Exam 3 (final) Flashcards

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1
Q

what is happening at the molecular level during muscle fatigue

A

lower amount of cross-bridges able to form means we ultimately decrease force production

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2
Q

how does the EMG signal usually change with force from muscles that are NOT fatigued?

A

As the force goes up so does the EMG and vice versa. If you are holding a constant force, the EMG is constant as well.

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3
Q

when a muscle is fatigued - what happens to the central drive from the brain to the motor neurons ?

A

we increase the central drive to the muscle to increase motor unit recruitment OR increase firing rate of current active motor units. This is all done to compensate for the failure occurring in the muscle (failure in the muscle fibers)

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4
Q

what is muscle fatigue?

A

activity-related impairment of the physiologic processes that are involved in the production of muscle force.

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5
Q

during what type of contractions can be study muscle fatigue? (four total)

A
  1. sustained max
  2. repetitive max
  3. sustained sub-max
  4. repetitive sub-max
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6
Q

what are the sites in the neuromuscular system which fatigue can occur?

A

a.Central drive to the motor neurons
b.Activation of motor units and muscles
c.Neuromuscular propagation
d.Excitation-contraction coupling
e.Availability of energy substrates
f.The intracellular environment
g.Contractile apparatus
h.Blood flow to the muscle

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7
Q

what is the EMG signal actually showing us?

A

gross command from the brain to the muscle

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8
Q

what happens to MU as fatigue occurs?

A

discharge of MU decreases as fatigue increases. Think about the force-frequency relationship (higher frequency is greater force) so with decreased frequency of discharge we ultimately have decreased force production

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9
Q

In a non-fatigued state if you stimulate the nerve or muscle how much force is produced (same or different amount)

A

you will produce the same amount of force between the nerve and muscle stimulated separately.

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10
Q

What did we find out from the experiment that stimulated the nerve directly during a fatigued state (every 15 seconds stimulated muscle directly)

A
  • over time the force produced from nerve only stimulation was a fraction of the force produced during non-fatigued state
  • yet every 15 seconds when they stimulated the muscle they still produced a higher amount of force still
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11
Q

in fatigued state, when we stimulate the muscle directly and still get a higher force production what does this mean for the site of fatigue occuring?

A

shows the motor neuron can fail to convey activation signal to muscle
- connection between spinal cord and muscle can fail
- AP not able to excite the sarcolemma

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12
Q

what is happening at the NMJ during fatigue that prevents a motor neuron from exciting muscle fibers enough during muscle fatigue

A

AP are traveling down the motor neuron too quickly and do not allow enough time for acetylcholine reuptake process.
- so with less acetylcholine available we cannot excite the motor end plate and result in a AP on the sarcolemma
- with less AP traveling down t-tubules we have less Ca2+ released and thus less cross-bridges able to form.

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13
Q

What does TMS do?

A

transcranial magnetic stimulation

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14
Q

what is the learning point from the experiment using TMS over the elbow flexor portion of the motor cortex

A
  • when TMS is applied to this area of the brain after a fatigue test we see and even greater force production after stimualtion.
  • this illustrates that failure at the motor cortex level can occur too (brain itself can contribute to fatigue)
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15
Q

what happens to discharge of individual motor units during fatiguing contractions ?

A
  • firing rate of MU decrease as fatigue increases
  • this occurs because we have increased intramuscular pressure that clamps down on vessels and decreases our ability to bring in nutrients and get waste products out
  • as the chemical environment changes this is sensed by chemoreceptors which travel to spinal cord and up to brain. in the spinal cord this excites an inner IPSP that travels back and decreases force output
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16
Q

what metabolites increase in concentration during a fatigue muscle contraction that contribute to decreases M.U discharge

A

ADP
H+ ions

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17
Q

why does the chemical environment changes from muscle fatigue lead to decreased force output?

A
  1. we see less excitation of neurons due to chemical environment exciting IPSP that inhibits motor neurons
  2. inhibitory at both spine (IPSP inner neurons) and brain
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18
Q

why do we see decreased MU firing as fatigue increases (why does the body do this)

A

it is a protective factor that protects the muscle environment changing too much that would be destructive

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19
Q

with less MU firing, what happens to whole muscle force

A

less tetanic force (remember force-frequency relationship)

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20
Q

what are peripheral mechanisms that contribute to fatigue?

A

activation failure due to lower amount of ATP
1. na/k pump
2. K+ channels in sarcolemma
3. Ca2+ pump dysfunction
4. pH change in environment

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21
Q

explain the “battle of the dendrites”

A

motor neurons are receiving both IPSP (from inner neurons) and EPSP (from brain due to you telling your brain to increase force) but over time the IPSP will always win because it increases over time as the environment of the muscle changes

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22
Q

what are the major determinants of strength of a muscle

A
  1. physiological cross sectional area
  2. activation of M.U and discharge rate
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23
Q

how do the two major determinants of muscle strength alter number of cross-bridges able to form

A
  1. the amount of actin and myosin available is directly correlated to number of muscle fibers (more physiological cross sectional area = more actin and myosin available)
  2. neural activation changes as you increase M.U firing. if you recruit the max amount of M.U and firing at highest frequency = maximal force produced
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24
Q

what are the two major adaptations due to strength training

A
  1. neural
  2. hypertrophic muscle adaptations
    Both increase number of cross-bridges engaged
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25
what is the list of ways neural adaptations influence strength gains after training?
1. strength increases more than muscle size 2. specificity of training impact strength and force production 3. increase in magnitude of EMG 4. effects of imaginary strength training 5. cross-education 6. recruitment/activation of M.U
26
what is the percent increase of strength and muscle size after 60 day robust strength training program
8% increase in muscle size and 20% increase in strength
27
how would an exercise scientist express the relative changes of muscle size and strength
specific tension: amount of force specific to the size of the muscle - (newtons of force / cross-sectional area)
28
what can be determined if the specific tension of a muscle is increasing?
means the numerator (newtons of force) is increasing more than the denominator (size of muscle). this illustrates the idea that strength increases more than the size of the muscle
29
how does the principle of specificity relate to neural adaptations
changes in strength are greatest when the training matches the test completed - training fast muscle contraction results in strength changes greatest when completing fast contractions ie: football lineman
30
how do we know specificity changes are due to neural changes and not muscle ?
if it were muscle the bars on the graph would all be the same height
31
if you train dynamic contractions (lift and lower) are you better at 1RM or MVC
1 RM
32
what does a larger EMG signal after strength training suggest
highlights brain is better able to drive M.U in muscles
33
what is the EMG signal represent
gross reflection of the activation from the brain (summed sarcolemma AP)
34
what does the results of the imaginary strength training experiment show us?
even just imaging completing a muscle contraction can lead to increase strength (22%) compared to group who actually trained (28%) - only thing changing is neural - no actual contractions are occurring so cannot be due to hypertrophy
35
what is cross-education?
training only one limb and seeing and increase in strength in the other limb that was not trained - only reason is neural adaptations
36
how does the activation and behavior of M.U changes after training?
1. firing rate of single M.U increases and total force produced increases after ballistic training (doubled rate)
37
what are the different potential sites of neural adaptations due to strength training
Enhanced brain output (imaginary contraction) Greater activation of synergist muscles Enhanced coupling among spinal interneurons that produce cross-education Greater muscle activation (EMG signal increasing) Heightened excitability and altered connections onto motor neurons
38
What is the general timing of the onset of neural adaptations vs. muscle adaptations in response to regular strength training?
Neural adaptations dominate the beginning of strength increases during a training program. At about week 4 a switch over occurs and we see increases in hypertrophy (muscle adaptations) start to increase more and neural factors decrease
39
Appreciate the specifics of the adaptations of muscle and muscle fibers to strength training.
1. Increased protein synthesis from stimulation of nucleus (transcription and translation) - Due to mechanical stress to muscle cell -Results in more cross bridges 2. Morphological changes -Fiber hypertrophy -Increase in cross-sectional area (30-70%) after training -Shift in fiber types (more type 2) -Fiber hyperplasia (more fibers possibly due to splitting) -Increase density of contractile proteins -Whole muscle hypertrophy
40
How does the muscle cell nucleus receive the signal that it needs to respond to the strength training stimulus with an appropriate adaptation?
1. biochemical signals activated at focal adhesions when you lift weights due to acidification 2. mechanical stimulation at integrins
41
how does the mechanical stimulation signal cell nucleus to respond to strength training
After heavy load training puts tension on tendons that it is not used to to causes mechanical stress that is transmitted through integrins converted to chemical messaging MAPK -> nucleus -> transcription -> translation of actin, myosin and other contractile proteins needed for cross-bridges
42
how does the chemical environment signal to cell nucelus that you lifted weights?
Other receptors in sarcolemma that are activated by chemical change due to multiple repeated contractions (acidification) that lead to protein transcription and translation as well g-protein linked receptors Tyrosine kinase receptors
43
what are the alterations to muscle fibers after strength training
- use muscle biopsy to find out - area of type 2 and type 1 investigated and found that type 2 area increased more - this occurs because you use type 1 for everyday life and stimulate type 2 more with this type of activity.
44
what is the difference between hyperplasia and hypertrophy ?
hyperplasia: increase in total amount of muscle cells hypertrophy: increase in size of muscle cells
45
what is the significance of hyperplasia to muscle strength increase? more or less important compared to hypertrophy?
- not a lot of scientific evidence for hyperplasia - cannot test in humans only have animal studies to back up
46
what is the gene that is not functionally properly in animals like Belgium cow
- myostatin which decreases muscle hypertrophy and size
47
how can we measure whole muscle size, how does it change after strength training
- use MRI scan - increases in muscle size are the area between the two lines on the graph - illustrate an increase in proteins available for more cross bridge formation - even with same training load people respond differently to training
48
describe magnitude and timeline of decline in muscle strength with age
- greatest decrease in strength after 70-80 yrs old
49
what is the difference between longitudinal and cross-sectional data
Longitudinal studies: follow a group of people overtime Cross-sectional data: looking at people at those distinct age groups
50
Describe the difference between muscle strength and power.
Muscle strength: max force in a few seconds Muscle power: force x distance (work) / time -This is the ability to move a submaximal load in certain time
51
What is the significance of power loss with aging?
Power is more correlated with physical function (gait speed, climbing stairs, getting out of a car, off a chair, etc)
52
Be familiar with the major contributors (the major things that change) to neuromuscular decline in aging.
1. Aging reduces number of alpha motor neurons in ventral horn of human spinal cord, ventral root, and nerves 2. Motor unit remodeling
53
What happens to motor neurons in aging?
apoptosis
54
What are the consequences of neuromuscular remodeling after motor neuron death? Motor unit size? Motor unit number?
Muscle fibers are de-innervated and recruited partly to be re-innervated to other nearby motor neurons to create a larger motor unit size. Also less amount of motor units
55
What major phenomena contribute to the decline in whole muscle size with aging? Muscle fiber loss? Atrophy of muscles fibers?
We see a large decrease in muscle fiber amount as you get older usually after 60 which contributes largely to the decrease in muscle size
56
What is sarcopenia? Why is it not a good thing?
Sarcopenia: is the decline in muscle mass and increase in fat mass related to age. It is not a good thing.
57
Fiber types and aging? Shifts in proportion of different types? Areas? The result on speed of contraction is?
number of muscle fibers decreases with age - proportional (amount) of type 1 and type 2 decline roughly the same BUT the size of type 2 decreases more - with less fast twitch fibers we see slower contraction
58
what behavior reinforces the less forceful and fast contractions
- pain - fear of injury
59
Are there inherent changes in force production in muscle fibers?
We see a decrease in size which smaller fibers are associated with less force generation. But even for fiber of the same size, old people still produce less force. Slower contractions due to M.U twitches and whole muscle twitches are slower M.U twitches may be larger, but whole twitches are reduced
60
What is neuromuscular slowing? What contributes to it? Muscle changes? Changes in neurons?
Nerve conduction velocity is reduced with aging -Demyelination of individual neurons -Decreased distance between nodes of Ranvier on neuron -Preferential disappearance of fast, large diameter neurons (fast twitch)
61
what are the consequences of neuromuscular slowing
- movement speed, reaction time, and protective movements
62
Is force decrease larger from just nerve or muscle stimulation
Larger decrease in force from repetitive nerve stimulation compared to intermittent muscle stimulation
63
what is jiggle?
variability of the shape of motor unit action potentials. Due to how well A.P is transmitted from neuron -> muscle fibers
64
what is jitter?
variability of timing of neuron and muscle fibers AP. Due to integrity of NMJ
65
what does the findings of the jitter and jiggle research present about aging and masters athletes
stability of neuron to muscle transmission better in those with more motor units remaining
66
what aspects of neuromuscular integrity was maintained in master athletes compared to aged matched sedentary individuals
- number of motor units - motor unit size (smaller because they did not have restructuring occur) - excitable muscle mass

HES 319 (3 decks)

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