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Flashcards in Fatigue Deck (32)
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1
Q

Fatigue (2)

A
  • inability to maintain a power output or force during repeated muscle contractions
  • protection mechanism
2
Q

Fatigue can be attributed to

A

disturbed homeostasis attributable to work and work environment

3
Q

Force decreases rapidly during

A

short term, high intensity exercise - 30s Wingate

4
Q

fatigue occurs from

A

disruption in the chain of events between CNS and muscle fibre

5
Q

two types of fatigue

A

central - brain, spinal cord
peripheral - neuromuscular junction
- muscle fibre

6
Q

peripheral fatigue

A

force or power deficit that occurs despite optimal activation of the muscle fibers by motoneurons - too frequent of AP

7
Q

where does peripheral fatigue begin

A

transition between peripheral nerve and alpha motor neuron

8
Q

central fatigue

A

Brain stops sending AP /stimulus

9
Q

causes of fatigue (6)

A

complex and interrelated

  • depletion of phosphogen
  • glycogen depletion
  • hypoxia
  • central and neurtal factors
  • reactive oxygen species (free radicals produced by mitochondria)
  • Ionic imbalance (Na&K, Ca&Pi, H&lactate
10
Q

fatigue depends on

A

type of exercise (intensity, duration)

11
Q

Depletion of phosphates are a result of and affects

A

results of depleted intracellar ATP and PC

sprinting, and strength exercise

12
Q

ATP concentration drops to

A

40% of resting levels

13
Q

PC concentrations drops to

A

15% of resting levels

14
Q

glycogen depletion limits

decreases production of

reduces

A

anaerobic glycolysis
pyruvate and oxaloacetate - limiting amt of FA that can be oxidized through beta oxidation
blood glucose limiting availability of glucose to the brain which could potentally impact coordination of neuromuscular pathways

15
Q

glycogen stores

A

muscle - 1-2% ~ 425g - more but less concentrated

liver - 8-10% `80g - more but higher concentration

16
Q

glycogen in other muscles

A

does not move around

17
Q

ionic imbalance of hydrogen accumulation and fatigue (3)

A

decreased activity of many enzymes - PFK, phosphorylate, APTase that are important for ATP production and muscle contraction

  • impaired Ca2+ troponin binding
  • activate pain receptors in muscles - to cause central fatigue (inhibitory mechanism)
18
Q

acidosis due to hydrogen accumulation and fatigue

A

not a significant factor

  • low, non-physiological temps it induces significant fatigue
  • physiological temmps fatigue was less pronounced
19
Q

why do buffering agents benefit performance

A

rid of acid to decrease central fatigue because of te pain receptors

20
Q

Ionic imbalance of Na/K

A

increased intracellular Na and increased extracellular K

21
Q

2 aftermath of Na/K imbalance

A

disrupt AP movement (depolarization/repolarization) alog sarcolemma and into T tubule
reduced excitability of muscle cells

21
Q

How doe imbalance of Na and k happen?

What one reduces more muscle force?

How can it be reversed?

A

Activation of muscle creates quick depolarization which induces ion movements

Elevating extracellular k

By adding lactate

22
Q

Ionic imbalance of accumulation of inorganic phosphate

A

Interferes with ca binding to troponin
it blocks the Ryanodine receptor which controls the release of ca from the sarcoplasmic reticulum
Moves into SR and forms a precipitate with Ca - sequesters ca so it’s not available for cross bridge cycling

23
Q

Hypoxia

A

Reduced oxygenation of hemoglobin units limit aerobic metabolism during high intensity aerobic exercise
More demand on anaerobic metabolism which leads to increased lactate and hydrogen

24
Q

Three factors that contribute to hypoxia

A

Arterial hypoxemia
Pollution
Altitude

25
Q

Mt Everest vo2max

A

25%of sea level

26
Q

What can happen with diminished oxygen

A

Exercise induced asthma

27
Q

Reactive oxygen species

What is it?

What does it do -3

A

Superoxide with an unpaired electron/free radicals
Damage cellular proteins, DNA
inhibit ca binding to troponin
Reuptake of ca into SR inhibited

28
Q

Central/neural fatigue definition

A

Exercise induced reduction in maximal voluntary contraction that is not companied by the same reduction in maximal evocable force

29
Q

MVC

A

Force generated with fdbk and encouragement when the subject believes it is maximal effort

30
Q

Maximum evocable force

A

Force generated by muscle or group of muscle when additional electrical stimulation does not augment force

31
Q

Central fatigue characterized by 2

A

Loss of drive/motivation - due to alterations in brain neurotransmitters (ratio of serotonin to dopamine) - serotonin associated with lethargy increase in serotonin and decrease in dopamine
Pain intolerance - pain receptors from afferent signals from hydrogen, brain refusing to send stimulus