L6.1 Skeletal muscle fatigue Flashcards

1
Q

What is skeletal muscle fatigue and how does it differ from weakness?

A
  • Fatigue definition: Loss of max or potential performance
  • Weakness definition: Inability to develop an initial force
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2
Q

What is central fatigue and what are the 2 school of thoughts associated with it?

A
  • Due to emotional & physiological factors
    • ↓ motivation
    • ↓drive of motor neurons
    • Impaired spinal transmission
    • Neuromuscular transmission failure
    • ↓recruitment of motor units & firing frequency
    • Inhibitory afferent muscle inputs
  • 2 school of thoughts:
    • Sense muscular effort due to pathway reaching conscious centres
      • “Tells” muscles what to do
    • Sense of effort from afferent info from active muscles
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3
Q

What are the arguments FOR and AGAINST central fatigue?

A
  • FOR:
    Auditory/visual stimuli → ↑ force
    Electrical stimulation of fatigued muscles → ↑ force
  • AGAINST:
  • During voluntary muscle fatigue → electrical stimuli was unable to restore tension
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4
Q

What is peripheral fatigue

A
  • Neural, mechanical or biochemical
  • ↓force & slower force developed
  • Relaxation prolonged
    • ↓cross-bridge cycling
    • ↓SR pump functions (↓reuptake)
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5
Q

Peripheral fatigue in - NMJ?

A
  • Depletion of neurotransmitters (x Ach) - unlikely
    • Perhaps only during prolonged isometric contraction
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6
Q

Peripheral fatigue in - T-tubules?

A
  • K+ accumulation in t-tubules
  • K+/Na+ exchange failure
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7
Q

What are the 2 types of peripheral muscle fatigue?

A
  • High frequency fatigue:
    • Fast onset, fast recovery
    • Likely to be caused by t-tubules conduction failure
  • Metabolic fatigue:
    • Slow onset, slow recovery
    • Characterised by metabolic stress
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8
Q

ATP

A
  • FOR
    • Mismatch btw supply & demand
    • ATP also required for cellular homeostasis
    • Fatigue → protective mechanism → ↓rate of ATP hydrolysis
  • AGAINST
    • Intramuscular ATP falls only to 60% at fatigue
    • At ↓[ATP], resting fatigue muscles would be rigor
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9
Q

ATP & ADP balance

A
  • ADP competes with ATP for sites on RyR → ↓ RyR opening and thus Ca2+ release
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10
Q

Lactic acid & lactate

A
  • ↑ lactate → ↑ H+ → ↓ pH
    • Especially during high intensity → fast twitch = fewer mito → less mito take up H+ → acidosis
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11
Q

pH

A
  • FOR
    • H+ → ↓ force:
    • ↓sensitivity of trroponin for Ca2+
    • Slows glycolysis
    • Interferes with actin-myosin cross bridge cycling
  • AGAINST
    • Mcardle’s disease: ↓ muscle glycogen phosphorylase → no glycogen breakdown, no glycolysis & thus no lactate/H+ accumulation
    • Yet still fatigues more rapidly
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12
Q

Other biochemicals

A
  • Ca2+
    • Caffeine → ↑ Ca2+ release after fatigue → ↑ force
  • Pi
    • ↑ ex → accumulate Pi → ↓ msucle fibre force by 30%
    • ↓ free [Ca2+] in SR
  • Mg2+
    • Harder for DHPR to open RyR
  • ROS
    • ↑ ex → ↑ ROS → damage SR → alters Ca2+ release
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