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MEDSCI second half > Energetics of muscle fatigue & training > Flashcards

Energetics of muscle fatigue & training Flashcards

1
Q

Muscle Fatigue

A

Defined as a reversible failure to maintain the required, or
expected, power output, leading to reduced muscle performance.
Protective strategy to prevent cellular damage.

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2
Q

Muscle Fatigue Aetiologies not yet clearly established:
• Many potential sites between ?
• Performance enhancing techniques used by athletes frequently
target pathways that are ______to cause muscle fatigue: eg?

A

the brain and the contracting
muscle.
assumed
eg. creatine supplementation, carbohydrate loading,high altitude training.

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3
Q

Where does Fatigue occur?

A

Central fatigue

Peripheral fatigue

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4
Q

Central fatigue

A

• CNS command – reduced excitatory input
• Motor neuron signal – altered input from
sensory fibres
Likely more relevant in untrained individuals

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5
Q

Peripheral fatigue

A
  • Neuro-muscular transmission
  • Muscle fibre action potential
  • Excitation-contraction coupling
  • Depletion of substrates for metabolism
  • Accumulation of waste-product
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6
Q

How is Fatigue Studied?

Many experimental approaches:

A
  1. Trained athlete
  2. Exercising volunteer subject
    (sedentary vs. active)
  3. Experimental animals
  4. Isolated whole muscle
  5. Isolated single fibre (myocyte)
  6. Contractile proteins in a test-tube
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7
Q

Summation & tetanus

A

single, summation, unfuzed, fused

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8
Q

Exhaustion (fatigue) occurs at the intersection of what lines on force vs time graph.

A

max force

required output

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9
Q

Alterations in time taken to fatigue will occur with:

A
  1. Inc or dec in required force
  2. Inc or dec in maximum force muscle can produce
  3. Changes in the intrinsic fatiguability of muscles
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10
Q

How does a Fast-twitch fiber Type II, fatigue

A

(easily fatigued):

↓↓ Ca2+ and ↓↓ force

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11
Q

How does a Slow-twitch fibre Type I, Soleus fibre fatigue

A

fatigue-resistant):
Ca2+ and force relatively stable, even after
1000 pulses.

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12
Q

What kind of fiber?
predominantly anaerobic metabolism
- short bursts of fast contractions (e.g. sprinters)

A

Fast-twitch fiber (Type II, easily fatigued):

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13
Q

What kind of fiber?
predominantly aerobic metabolism
- rich in capillaries and mitochondria (dark)
- continuous extended contractions over time (e.g. marathon
runners)

A

Slow-twitch fibre (Type I, fatigue-resistant e.g. Soleus)

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14
Q

Fatigue at the Cellular level

A 
• Changes in pH
(due to accumulation
of waste products)
• Accumulation of
phosphate (Pi)
• Decreased Gibbs free
energy of ATP
• Excitation-contraction
coupling impairment
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15
Q

Effects of decreased pHi

A

• At rest pHi ~7.05, following exhaustive exercise pHi ~6.5
• Competition of H+ with Ca2+ for binding sites on
Troponin-C – right-shift of the Force-[Ca2+]i relation
= ↓ Ca2+ sensitivity of the myofilaments
• Inhibition of Na-K-ATPase, myosin ATPase, cross-bridge
interaction

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16
Q

HOWEVER:
Following exhaustive exercise, ____recovers faster than ___
indicating that pH may contribute to fatigue but cannot be the sole cause.

A

force

pH

17
Q

_________________

imaging is used to quantify Pi and PCr

A

Nuclear magnetic resonance (NMR)

18
Q

Pi and PCr levels during fatigue?

A
  • ↓ PCr with exercise
  • ↑ Pi with exercise
  • coincident with ↓ force production
19
Q

Possible Actions of Pi during fatigue

A

• “Direct” inhibition of rotation of the actomyosin cross-bridge
(Pi is bound to myosin head)
• Effects (direct or indirect) on SR Ca2+
release and Ca2+-force dependence
- reduce Ca2+ release (inhibit RyR,
precipitation Ca2+-Pi )
- increase Ca2+ force activation threshold
• “Indirect” energetic effect:
- reduction of Free Energy of ATP hydrolysis (ΔGATP)

20
Q

Role of Gibbs Free Energy (ΔGATP)

A

∆GATP is the energy released by ATP hydrolysis (kJ/mol)
• Depends on the concentrations of reactants and products
• ∆GATP is usually negative, because it is releasing energy

21
Q

Gibbs Free Energy (ΔGATP)

The more negative GATP, the more ?

A

energy is transferred.

22
Q

∆G required by ATPases is positive b/c they gain energy from

A

ATP

23
Q

How can ΔGATP diminish while [ATP] remains constant?

A

as [CrP] falls, [Pi] rises but [ATP] and [ADP] stay constant.

24
Q 
High value of K means
the reactions are
driven far to the right
and [\_\_\_] maintained
at the expense of [\_\_\_].
A

ATP

PCr

25
Q

Exhaustive Exercise
Increased [Pi
] will cause a decrease in

A

ΔGATP

26
Q

Exhaustive Exercise

• If ΔGATP falls sufficiently then work of ATPases will be

A

compromised.

27
Q

Exhaustive Exercise

• Metabolic end-products may inhibit

A

muscle activation

& force development.

28
Q 
Fatigue:
excitation-contraction coupling
1. Na+ and K+ ionic gradients
not fully restored = ?
2. Signal to open Ca2+
channels is ?
3. Inhibition of SERCA pump
= 
4. ↓ Ca transient =
A

impaired membrane excitability
impaired
↓SR Ca stores,
↓ force

29
Q

Effects of aerobic training occur WHERE and WHAT?

A

Heart ↑ cardiac output
Increases O2 delivery to the muscles
Circulation ↑ plasma volume
Increases stroke volume and thus cardiac output.
Increases skin blood flow to optimise thermoregulation
Blood
vessels
↑ capillary proliferation
Increases O2 delivery and diffusion into the muscles
Myocytes ↑ mitochondria
Increases O2 extraction
Myocytes Enzyme adaptation
Optimizes metabolism
Increased reliance on fat thus reduced lactate production

30
Q

Many potential sites of fatigue between the

• Can be either “_____” or “_________”.

A

brain and the contractile protein interactions.
central
peripheral

31
Q

• Peripheral (cellular) fatigue may be a result of:

A
  • Decreased energy supply and GATP
  • Increased end-product accumulation
  • Excitation-contraction coupling impairment
32
Q

• Training induces changes in

A 
muscle structure and
function to optimize O2 delivery and extraction

MEDSCI second half (10 decks)

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