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
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
- Sense muscular effort due to pathway reaching conscious centres
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
4
Q
What is peripheral fatigue
A
- Neural, mechanical or biochemical
- ↓force & slower force developed
- Relaxation prolonged
- ↓cross-bridge cycling
- ↓SR pump functions (↓reuptake)
5
Q
Peripheral fatigue in - NMJ?
A
- Depletion of neurotransmitters (x Ach) - unlikely
- Perhaps only during prolonged isometric contraction
6
Q
Peripheral fatigue in - T-tubules?
A
- K+ accumulation in t-tubules
- K+/Na+ exchange failure
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
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
9
Q
ATP & ADP balance
A
- ADP competes with ATP for sites on RyR → ↓ RyR opening and thus Ca2+ release
10
Q
Lactic acid & lactate
A
- ↑ lactate → ↑ H+ → ↓ pH
- Especially during high intensity → fast twitch = fewer mito → less mito take up H+ → acidosis
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
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