Fatigue Flashcards

1
Q

How is fatige defineid in exercise science?

A

A process involving an exercise-induced reduction in the ability to exert muscle force or power

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2
Q

What are the two main categories or fatigue?

A

Central
Peripheral

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3
Q

What is peripheral fatigue?

A

Fatigue from changes at or distal to the neuromuscular junction

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4
Q

What is central fatigue?

A

A reduction in neural drive to the muscles, not due to muscle contractility changes

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5
Q

What are key metabolic causes of peripheral fatigue?

A

Substrate depletion and accumulation of deleterious metabolites

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6
Q

What activation falure can cause peripheral fatigue?

A

Impaired actin potential propagation

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7
Q

What are four key outcomes of peripheral fatigue?

A

Changes in [Ca2+]
Myofibrillar function
Shortening velocity
Relaxation time

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8
Q

What phosphagens are linked to short, high-intensity fatigue?

A

ATP
Phosphocreatine (PCr)

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9
Q

What happens when PCr is depleted?

A

ATP regeneration is limited, leading to fatigue

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10
Q

What reaction helps buffer H+ during ATP resynthesis?

A

ADP + PCr + H+ <–> ATP + Cr

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11
Q

How long can glycogen support moderate exercise?

A

1.5-2 hours

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12
Q

What happens when glycogen is depleted?

A

Reliance on protein breakdown and reduced performance

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13
Q

How can glycogen depletion be offset?

A

Lactate suttle
Liver glucose release
Carbohydrate loading

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14
Q

What role does lactate plat in fatigue?

A

It allows glycolysis to continue but H+ accumulation can cause issues

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15
Q

What does H+ do in muscle?

A

Inhibits PFK
Displaces Ca2+ on troponin
Stimulation pain receptors

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16
Q

What effect does inorganic phosphate (Pi) have?

A

Inhibits cross-bridge formation and reduces calcium sensitivity

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17
Q

What type of fatigue dominates a 100m sprint?

A

PCr depletion

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18
Q

What type of fatigue dominates repeated sprints?

A

Metabolite accumulation

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19
Q

What causes fatigue in a matathon?

A

Glycogen depletion

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20
Q

What causes central fatigue?

A

Changes in neurotransmitters and afferent feedback reducing motor drive

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21
Q

Why might central fatigue be beneficial?

A

It’s a protective mechanism - part of a negative feedback loop

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22
Q

How can you test if fatigue is central or peripheral?

A

Induce muscle contraction via external action potentials without voluntary effort

23
Q

What is the sewuence from brian to force output?

A

Brain - Spinal cord - Peripheral nerve - Muscle sarcolemma - T-tubules - Ca2+ - Actin-Myosin - Cross-bridge - Force output

24
Q

What are common causes of muscle fatigue?

A

Substrate depletion
Muscle fibre damage
Build-up of metabolic by-products

25
Q

What is DOMS and when does it occur?

A

Delayed Onset Muscle Soreness
12-72 hours post-exercise

26
Q

What determines the ratio of fast glycolytic and slow oxidative muslce fibres?

27
Q

What muscle fibre type is suited for sprinting and weight lifting?

A

Fast glycolytic (FG)

28
Q

What type of muscle fibre is ideal for endurance?

A

Slow oxidative (SO)

29
Q

How does aerobic training affect muscle fibres?

A

Converts some FG to fast oxidative glycolytic - increases mitochondrial volume and oxidative enzyme levels

30
Q

What are key mitochondrial adaptation to endurance training?

A

Larger mitochondria - increased number

31
Q

What happens to glycolytic enzymes?

A

Increases in enzymes like glycogen phosphorylase, phosphofructokinase, and LDH

32
Q

Which oxidative enzymes increase with training?

A

Citrate synthase
Cytochrome c oxidase

33
Q

Do these enzymes becone more efficient?

A

No - they increase in number, not efficiency

34
Q

How does endurance trianing affect fat metabolsim?

A

Increases fat oxidation at rest and during submaximal exercise

35
Q

How does it affect carbohydrate metabolsim?

A

Increases CHO oxidation during max exercise - enchances glycogen storage

36
Q

What other physiological changes occur with endurance training?

A

Improved ionic balance
Better lactate/H+ regulation
Neural and cardiovascular adaptations

37
Q

What vascular change improves nutrient delivery?

A

Increased capillaristion

38
Q

How does postnatal muscle growth occur?

A

Via hypertrophy - enlargment of existing fibres

39
Q

What causes muscle atrophy?

A

Disease or denervation (nerve damage)

40
Q

What happens in long-term denervation?

A

Muscle shrinks to 25% of size and becomes connective tissue (6-24 month)

41
Q

What is a benefit of muscle hypertrophy?

A

Greater strength from more corss-bridges

42
Q

What is a downisde of muscle hypertrophy?

A

Increased diffusion distance for nutrients and waste

43
Q

What causes tetnus?

A

Infection by Clostridium tetani producing the neurotoxin tetanospasmin

44
Q

How does tetanospasmin affect the body?

A

Blocks inhibitory neurotransmitter release in the spinal cord –> uncontrolled excitation –> spasms

45
Q

What is msucle is usually affected first in tetanus?

46
Q

What is Duchenne Muscular Dystrophy (DMD)?

A

A fatal, X-linked disorder
Affects 1 in 3,500 males
Caused by mutation in dystrophin

47
Q

What does dystrophin do?

A

Links actin to the extracellular matrix, stabilises muscle cell membranse during contration

48
Q

What happens without dystrophin?

A

Muscle cells break down under contraction stress and are replaced by connective tissue

49
Q

What is Distal Arthrogryposis?

A

A congenital condition causing contractures in hands and feet

50
Q

What causes Distal Arthrogryposis?

A

Mutation in myosin, tropomyosin, troponin, or myosin-binding protein C

51
Q

What is contracture?

A

Immobility from stiffness/constriciton in connective tissue

52
Q

What structural changes occur from resistance training?

A

Increases in myofibril, mitochondrial, sarcoplasmic reticulum, and organelles

53
Q

What causes strength increases with resistance training?

A

Hypertrophy (more contractile proteins) and neural adaptations