fatigue Flashcards

1
Q

fatigue

A

less than anticipated response for a given stimulus
- no one cause of fatigue

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2
Q

catastrophe theory

A

failure of one enzyme, system, cell, tissue, organ, or system places an undue burden on related systems such that several may begin to fail simultaneously

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3
Q

what is the reasoning behind the catastrophe theory

A
  • since multiple organs and organ systems are integrated hard to tell when and which one fails
  • body and functions have genetic components from past lifestyles
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4
Q

central fatigue

A
  • fatigue within the nervous system, nervous discharge, not enough glucose (physiological signals –> psychological inhibition)
  • painful afferent inputs from muscles + joints might affect continuing exercise
  • increase in [H+] –> change in pH –> feel pain –> central fatigue
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5
Q

what kind of movements contribute to central fatigue

A

compound movements

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6
Q

possible theories behind the central fatigue theory

A
  • hypoglycemia
  • dehydration
  • NE, dopamine, serotonin levels in the brain
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7
Q

hypoglycemia theory to central fatigue

A

prolonged moderate to high intensity endurance exercise causes liver glycogen depletion

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8
Q

dehydration theory to central fatigue

A

compromises mental functions like processing cognition, memory

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9
Q

NE, dopamine, and seratonin levels in the brain

A

these hormones help to control mood and sleep
- catecholamines like NE and dopamine are synthesized from tyrosine and seratoning from tryptophan
- prolonged exercise increases tyrosine and tryptophan in the brain
- increases synthesis of NE, dopamine, seratonin + excessive cortisol = sense of drowsiness

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10
Q

tyrosine

A
  • the main amino acid that makes you sleepy
  • takes a while to clear
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11
Q

tryptophan

A

amino acid that also affects sleepyness

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12
Q

peripheral fatigue

A

muscles begin to fail

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13
Q

what contribues to peripheral fatigue

A
  • general skeletal muscle relaxation
  • membrane properties
  • metabolite depletion
  • metabolite accumulation
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14
Q

how does muscle relaxation affect peripheral fatigue

A
  • fatigue and muscle relaxation
  • force frequency relationship
  • force-pCa2+ relationshipwhat
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15
Q

what is the fatigue and msucle relaxation correlation in regards to peripheral fatigue

A
  • relaxation is slowed with fatigue (increases the half relaxation time)
  • can lead to greater summation at a given frequency of activation
  • also reduced force generating capacity
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16
Q

what is true peripheral fatigue

A

reduced performance
- can also be a result of leaky SR

17
Q

force frequency relationship in regard to peripheral fatigue

A
  • low frequency fatigue = depressed force @ lower frequencies of activation (maximal force isn’t affected)
  • high frequency fatigue = depresses forced at higher frequencies and normal at low
18
Q

which is mor common low frequency fatigue or high frequency fatigue and why

A

low frequency fatigue bc its more physioligcally possible

19
Q

force pCa2+ relationship in regards to peripheral fatigue

A
  • fatigue muscle has decreased Ca2+ sensitivity due to damaged troponin + tropomyosin
  • Ca2+ elicits lesser force than in fresh muscle
20
Q

membrane properties in relation to peripheral fatigue

A
  • hard working muscles have large extracellular [K+] = lots of AP generated by muscle fiber unable to rapidly restore [K+] gradient across sarcolemma
  • changes RMP = harder excitability
21
Q

what metabolites are depleted in relation to peripheral fatigue

A

depletion in phosphagens, glycogen, and blood glucosew

22
Q

how does depletion of phosphagens affect peripheral fatigue

A
  • ATP is high energy intermediate that supports muscle contraction + other things
  • the immediate source of ATP dephosphorylation is CP
  • during fatiguing exercise muscle CP levels decline (first rapid then slow)
  • tension development and point of fatigue in isometric exercises coincide in CP depletion while ATP remain relatively maintained
23
Q

why is CP related to fatigue

A
  • ATP is compartmentalized: decrease in one area doesn’t mean decrease in all areas
  • ATP is extremely important so to protect itself muscle cells down regulate functions
24
Q

glycogen and metabolism depletion

A
  • depletion seen to be correlated during prolonged submaximal exercise
  • uniform glycogen depletion during moderate load cycling at moderate pedal rate in different muscle fibers
  • low load cycling @ rapid rate = depletion in slow twitch fibers
  • high load cycling @ lower pedal rate = glycogen depletion from fast twitch muscles
25
blood glucose depletion and peripheral fatigue
- if glyvogen foes down during exercise blood glucose rises above pre exercise levels (stimulated by ANS) - limited by the ability of the liver to maintain high rates of glucose release limited by glycogen stores, heptaic glygenolytic and glucogenic enzymes
26
metabolic accumulation and peripharl fatigue
- lactic acid - calcium ions - mitochondrial couploing efficiency - ryanodine receptor fatigue
27
lactic acid accumlation and peripheral fatigue
- lactic acid accumulation seem during short term high intensity exercise - buildup occurs bc production is greater than removal - lactic acid dissociates a proton @ physiological pH = decrease in pH = increase in intramuscular bicarb stores to address increase in H+
28
how does lower pH affect function within the muscle
- inhibits PFK and slows glycolysis - can stimulate pain receptors - affect the frequency + duration of Ca2+ channels being open - H+ can displace Ca2+ from troponin interfering with contraction - can inhibit myosin ATPase = decrease in power output
29
calcium ion accumulation and peripheral fatigue
- Ca2+ loss from SR during excitation-contraction coupling taken up by mitochondria = interfering with mitochondria function - SR ability to release Ca2+ is slowed = reduced intracellular signal for contraction - causes a decrease in sensitity to Ca2+ for actin + myosin = decrease force production - reuptake is also slowed due to depressed SERCA
30
is Ca2+ in the mitochondria bad
- in large amounts yes, but in small amounts may be good - helps to stimulate dehydrogenase in TCA cycle - but Ca2+ excretion uses ATP so O2 is consumed which affects mitochondrial energy potential fo phosphorylation ADP
31
how is the ryanodine receptor affected during Ca2+ accumulation
- decreases force generation related to ryanodine receptors release of Ca2+ - lactate ion interferes = decrease in Ca2+ release