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Muscle & Exercise Physiology > Lecture 16 - Mechanisms of skeletal muscle fatigue > Flashcards

Lecture 16 - Mechanisms of skeletal muscle fatigue Flashcards

1
Q

What is muscle fatigue?

A

Force loss during a sustained maximum voluntary contraction

loss of maximum or potential performance

need to be careful which aspect of performance is being considered

'’A failure to maintain the required or expected force’’

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2
Q

What is the distinction we need to be clear about when talking about ‘fatigue’

A

need to be clear about which aspect is under consideration - i.e sensations and perceptions of exhaustion or changes in muscle function

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3
Q

True or False

The extend of fatigue may vary according to the method of testing

A

true

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4
Q

changes in function may appear greater for _____ contractions than for _____stimulation

A

changes in function may appear greater for voluntary contractions than for tetanic stimulation

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5
Q

True or False

The fatigue levels may differ if muscle is tested at one frequency of stimulation than another

A

true

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6
Q

What things does the rate of fatigue depend on?

A

muscles employed

the relative intensity of the exercise

whether contractions are intermittent or continous

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7
Q

What is the definition of weakness?

A

an inability to develop an initial force appropriate for the circumstances

e.g elederly person with atrophied muscle unable to get up from a chair

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8
Q

What are the two potential sites of Muscle Fatigue?

A

Central - Brain and spinal cord; involves motivation and central motor pathways

peripheral - peripheral nerves and muscles involves sites within motor units (i.e motor neurons, peripheral nerves, motor endplates, muscle fibres)

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9
Q

What are the factors of central fatigue?

A

emotional and psychological factors which infleunce our motivation to perform a task

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10
Q

How does the CNS contribute to muscle fatigue?

A

reduced supraspinal ‘‘drive’’ of MNs

Impaired SC transmission

neuromuscular transmission failure

recruitment of MUs

reduced motor unit firing frequency

inhibitory input from muscle afferents

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11
Q

What are the two schools of thought regarding the origins of the sense of muscular effort?

A

A) A sense of muscular effort due to a collateral pathway reaching a conscious centre - ‘‘telling’’ the muscle what to do

B) sense of effort due to afferent information from active (contracting) muscle - comes from what the muscle is doing

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12
Q

How do some experiments argue AGAINST a central mechanism for fatigue?

A

there is no difference in force output of voluntary contraction vs. force output with electrical stimulation

during voluntary muscle fatigue - imposing electrical stimulation was unable to restore tension (in some studies)

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13
Q

How do some experiments argue FOR a central mechanism for fatigue?

A

Shout during exertion = increase force

electrical stimulation of fatigued muscle = increase force

contractions of fatigue with eyes closed, simply opening the increases force

alterations in CNS arousal can facilitate MU recruitment

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14
Q

The majority of evidence indicates that central factors play a ___ role in mediating fatigue

A

lesser

there’s still alot of debate on this

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15
Q

Given central factors may not be the major cause of fatigue, what are the factors that can contribute to peripheral fatigue?

A

neural

mechanical

biochemical

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16
Q

what are the changes from fresh to fatigued muscle fibres?

A

Force is decreased

Force is developed more slowly

relaxation is prolonged - thought to be due to a decreased rate of cross-bridge detachment. Also impairment of SR pump functiom such that the reuptake process fails or takes longer

This tells us there are some biochemical changes - intracellular metabolic disturbances

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17
Q

What is Excitation-contraction?

A

E-c coupling is defined as the events that include depolarisation of the t-system that activates specialised voltage sensors (DHPR), which in turn open ryanodine receptors (RYR, also called Ca release channels) in the adjacent SR membrane, allowing Ca to enter cytoplasm and intiate crossbridge cycling

18
Q

What are the considerations when looking at the NM junction as a source of peripheral fatigue?

A

supplies of NT are exhausted?

insufficient ACh to transmit presynaptic AP

below threshold for AP

^ Evidence is mostly against this.

perhaps could occur during prolonged isometric contraction, but NOT during intermittent activation

19
Q

At change in frequency stimulation to a lower level will result in a rapid increase in force - what does this indicate?

A

failure of AP

loss of membrane excitability - K+ accumulation in the t-tubules

impairment of the Na/K exchanger mechanisms

Simply by switching the to lower frequency, the exchanger is back in action and we get a restoration of acitivity and hence, force

20
Q

High frequency fatigue will involve

A

fast onset
fast recovery - will be able to to produce the same level of force quicky

occurs during exercise that requires intense, near maxial muscle contraction

21
Q

metabolic fatigue will involve

A

slower onset

slower recovery

induced by less intense, submaximal contraction

characterised by metabolic stress, including acidosis and phosphocreatine depletion

recovery can be hours-days

22
Q

What is the most likely cause of high frequency fatigue?

A

T-tubule conduction failure - we know the force recovers quickly, hints at what mechanism it is

23
Q

What are the potential biochemical factors to fatigue?

A

loss of glycogen, ATP (fatigue could be a protective mechanism against total ATP depletion - it is required from cellular homeostasis)

accumulation of lactate and H+

accumulation of Pi

accumulation of ADP

fall in PCr

24
Q

Intramuscular ATP falls to only __% of pre-exercise levels at fatigue, due CP buffering

A

60%

25
Q

If low ATP caused fatigue, resting fatigued muscles would develop…

A

tension from rigor cross-bridges

26
Q

The rateof ATP _____, however, is reduced at fatigue

A

ATP hydrolysis

27
Q

Why does High-intensity resistance training result in acidosis (the burn)?

A

The body’s more explosive fast twitch MUs are recruited to overcome the resistance loads

The fuel for is energy demand comes primarily from the anaerobic metabolism

Fast-twitch muscle fibres have fewer mitochondria than slow twitch

Thus, during high-intensity resistance training there is a greater accumulation of protons causing acidosis

28
Q

How does H+ reduce force?

A

reducing the sensitivity of the troponin for Ca

slowing glycolysis

interfereing with actin-myosin cross-bridge cycling

29
Q

while a fall in pH may play some role int he development of fatigue…

A

it cannot be the only cause

Fatigue is multi-factorial

30
Q

how does lactate affect fatigue?

A

lactate is likely not the cause of fatigue Acidity associated with increase lactate accumulation may actually help delay the onset of muscle fatigue

31
Q

What is the evidence against pH and lactate as influencing fatigue?

A

McArdle’s disease

deficiency in muscle glycogen phosphorylase

results in muscles that are unable to break down glycogen

no glycolysis, therefore lactate or H+ accumulation, et fatigue is more rapid in McArdle’s patients

32
Q

Ca2+ is a critical factor in ____

A

fatigue

33
Q

Higher Ca2+ concentration results in…

A

more force

34
Q

During intense activity and high energy demand, Pi accumulates from..

A

the splitting of ATP and breakdown of PCr

35
Q

True or False

accumualtion of Pi reduces muscle fibre force by up to 30%

A

true

just these kind of metabolites accumualting in a bath drops the levels of force

tells us the myofilaments are highly sensitive to the circulating environemnt

36
Q

Mg2+ can compete where in the contraction mechanism?

A

at the binding site of troponin. Mg2+ competes with Ca2+

Can therefore inhibit SR Ca2+ release

37
Q

Summarise how the metabolic changes during exercise affect the fatigue levels

A

Increase lactate has little or no effect

Pi and Mg2+ decrease myofibrillar function

Pi reduces the free [Ca2_] in the SR

H+ may have little effect on overall E-C coupling

ADP competes with ATP for sites on RyR, thsu reducing RyR opening and Ca2+ release

increase in Mg2+ makes it harder for DHPR to open RyR

A decrease in ATP decreases RyR opening

38
Q

How are ROS said to effect fatigue?

A

THought to cause damage to the SR leading to alterations in Ca2+ release

39
Q

Could antioxidant supplementation prevent or reduce radical-induced damage to skeletal muscle?

A

recent studies say it has no beenfit

40
Q

What is the most likely to cause fatigue, peripheral or central factors?

A

peripheral

Pi

decreased SR Ca2+ release

not lactate or H+ accumulation

ROS

Muscle & Exercise Physiology (34 decks)

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