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Physiological Determinants > Central Fatigue > Flashcards

Central Fatigue Flashcards

1
Q

Davis and Bailey (1997)

A

Central Fatigue: A subset of fatigue associated with specific alterations in CNS function (can’t be explained by dysfunction in the muscle itself)

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2
Q

James et al (1995)

A

Central Fatigue may come about as a result of conscious/unconscious mechanisms

Subject may decide the sensations are unacceptable and reduce the level of activity

Alternatively, afferent feedback from working muscles, joints or tendons may inhibit motor activity - leading to performance loss, that voluntary effort can’t overcome

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3
Q

Chen et al (2006)

A
  • Incremental ramp test
  • Yelling or control (measuring VO2)
  • 10% increase in VO2 with yelling
  • No difference in HR
    Increase in VE with yelling (VE is reflective of central motor drive from brain)
    Increased TTE, PO, iEMG

iEMG = Integrated electromyographic activity in muscle

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4
Q

Millet et al (2002)

A

Prolonged Exercise and Central Drive

Assessed VA (MVC’s)

27% reduction in VA - emphasises role of central fatigue in endurance running = can voluntarily activate their muscles less

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5
Q

Lepers et al (2002)

A
  • Cycle 55% VO2 max for 5 hours
  • Measured MVC every hour and fall in muscle interpolation (activation)
  • Evidence that peripheral fatigue happened first, followed by central fatigue
  • Suggests contractile changes occur early, followed by impaired central drive
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6
Q

Ross et al (2010)

A

Repeated Prolonged Exercise and Central Drive

  • Tour De France (20 days)
  • Twitch interpolation method
  • Assessing VA of quadriceps

Decreased VA indicates a reduction in the number of motor neurons voluntarily recruited by the subject (central fatigue)

30% reduction in MEP in response to TMS
- Can’t be sure where the issue is but we know it is there

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7
Q

Del Coso et al (2008)

A

Strategies to minimise central fatigue:

  • 7 trained cyclists
  • Measured VA pre/post cycling
  • Caffeine preserves central fatigue
  • CHO + Electrolyte + Caffeine = VA is highest
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8
Q

Vitor-costa et al (2015)

A

Transcranial direct current stimulation (TDCS)

  • Electrocute part of brain to increase performance
  • TDCS before cycling TTE 80% peak power
  • No difference in RPE/HR between conditions
  • But is increased TTE - don’t know why…
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9
Q

Triscott et al (2008)

A

Potential recovery strategies:

  • Comparing non trained, endurance trained and resistance trained
  • MEP
  • Bicep curls to fatigue
  • Recovery measured in non-exercising arm
  • See small degree of central fatigue in non-exercising arm, meaning it can’t be the muscle
  • We get more recovery in endurance trained only - suggests you need a good base of training (e.g. endurance) even though you would expect resistance training to recover best as always doing it… although not the case.
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10
Q

Amann and Dempsey (2008)

A

2 constant load cycling tests on separate days

  • first: cycling to voluntary exhaustion at 83% Wpeak
  • second: identical duration at 67%Wpeak (time matched)
  • Muscle fatigue measured using femoral nerve stimulation
  • Greater reduction in quad twitch force after exhaustive exercise trial than in time matched (more central fatigue)
  • They then asked participants to do a 5km TT on bike (4 min rest)
  • iEMG (excitability of muscle) = after exhaustive trial there was a reduction in iEMG (lower PO in 5km TT)
  • Pre-existing muscle fatigue had a substantial dose-dependent inverse effect on CMD
  • Doesn’t matter which trial, after the 5km TT – always get the same reduction in twitch force (doesn’t matter what did beforehand /level of fatigue before – cannot exceed this level = THRESHOLD)
  • Therefore, there is a critical threshold of fatigue (and associated sensory tolerance)
  • Participants must have ‘chosen’ an associated power output during the TT low enough to prevent further fatigue as they’ve already hit the threshold
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11
Q

Amann et al (2008)

A

Pharmacological interventions to prevent afferent feedback

  • 8 cyclists - two 5km TT
  • Lumbar epidural of lidocane (in spine) to block afferent feedback
  • iEMG 9% higher suggesting a greater CMD (muscle is seeing more electrical feedback than usually would)
  • Brain doesn’t know the conditions in the muscle so continues to stimulate the muscle via efferent output
  • Power output decreased(jelly legs from epidural)
  • VE expresses CMD
  • With epidural theres an increase in CMD, expressed by VE - suggests we have prevented fall in CMD as prevented afferent feedback
  • Afferent blockage increased CMD but PO also decreased
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12
Q

Amaan et al (2009)

A
  • 8 cyclists, 3 5km TT with fentanyl
  • Higher EMG demonstrates lower inhibition of CMD
  • Not aware of conditions within the muscle
  • CMD now less restricted
  • Fentanyl (reduced afferent feedback) allowed the development of muscle fatigue far beyond the levels observed in other trials
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13
Q

Sidhu et al (2014)

A
  • Cycling - looking at fatigue in the non-active limb
  • Fentanyl used to knock out afferent feedback
  • If on fentanyl never reduced MVC
  • Superimposed twitch increased with control trial only
  • Cortical VA went down pre and post in control, no difference on fentanyl
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14
Q

Foster et al (2014)

A
  • Wingate tests x 8
  • With or without 1.5g paracetamol
  • increase in mean power output in sprints 6,7,8 with paracetamol - didn’t see anything before that
    No difference in physiology or perceptual mesures
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15
Q

Amaan et al (2006)

A
  • Manipulating oxygen conditions
  • Normoxia – normal air
  • Hyperoxia – more than 21% oxygen
  • Hypoxia – less oxygen
  • Iso-oxia – measured oxygen in blood, if drops below certain level gives them extra bump – clamping oxygen
  • Observed differences in CMD between conditions
  • Peripheral fatigue was the same throughout all trials
  • Neural drive (outflow from brain) increased with hyperoxia
  • Lower iEMG even within the first 60s in hypoxia (i.e. before any excessive homeostatic stress)
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16
Q

Crewe et al (2008)

A
  • Cycling until exhaustion in different PO in either 15 or 35 degrees
  • RPE increased linearly in all trials (expected)
  • Rate of increase was greater in the hotter and harder trials
  • Rate of increase in RPE can be used to predict trial duration/performance
  • When expressed as a percentage of trial duration - increase in RPE is linear amongst all trials
  • This rate is set very early on (at exercise onset) - can predict how long they’ll go for
  • Given that volitional exercise is terminated at max RPE, the brain integrates this information and subconsciously forecasts the exercise duration that can be maintained
  • RPE is higher in hotter condition when just sat on bike – suggests that the brain generates a conscious sensation of exertion in a forecasted manner (teleoanticipation)
17
Q

Paterson and Marino (2004)

A
  • Make different groups do 3 trials
  • trial 1 = 30km, trial 2=30km, 36km and 24km, trial 3 = 30km.
  • Tell them they’re doing 30km every time
  • There was a significant difference compared to 30km in the 36km and 24km in the third trial and a significant difference between groups
  • No difference in HR
18
Q

Marcora et al (2009)

A

90 mins of demanding cognitive tasks then cycled to exhaustion at 80%W peak

  • TTE significantly lower following demanding cognitive function tasks
  • No difference in physiological parameters (including VE)
  • Mentally fatigued participants achieved their max RPE much earlier than disengaged from the exercise
  • Provides experimental evidence that mental fatigue limits exercise tolerance in humans
19
Q

Williamson et al (2001)

A

Hypnosis, completed 3 identical constant load cycling bouts
- At minute 10 - participants were informed that they would start cycling uphill, downhill or remain

  • Cerebral blood flow significantly changed in uphill and downhill
  • Manipulation of effort senses can alter patterns of brain activation and elicit CDV changes
20
Q

Noakes (2011) - Further reading not on slides

A
  • Previous research suggests no role for the brain in the regulation of exercise performance.
  • The Central Governor Model: States fatigue is purely an emotion, function of which ensuring exercise terminates before there is a catastrophic biological failure.
21
Q

Letter to the editor: Noakes and Tucker (2008) - Further reading not on slides

A
  • Letter to Dr Marcora
  • ‘We argue that the integration of this information generates a conscious perception of effort, measured as RPE, which regulates the extent of skeletal muscle activation during exercise in order to insure that a potentially catastrophic failure of homeostasis does not occur.’
  • ‘Unlike Dr. Marcora’s model in which the RPE is purely
    a consequence of increasing motor drive to the exercising
    muscles and is of no particular relevance, the RPE is a central component of the central governor model. For it provides the conscious perception of the potential
    consequences of all the numerous physiological changes
    that develop during exercise.’
22
Q

Mauger (2010) - Further reading not on slides

A
  • Cycling with Acetaminophen (paracetamol)
  • Cycled with higher mean PO, increased HR and B La
  • No changes in perceived pain or exertion
  • Completion time = significantly faster
  • Supports notion that exercise is regulated by pain perception (increased pain tolerance can improve exercise capacity)

Physiological Determinants (3 decks)

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