KINE 2P97 Lecture Notes - Lecture 17: Serca, Motor Drive, Glycolysis
8 May 2018
School
Department
Course
Professor
KINE 2P97
Muscle Physiology & Exercise Metabolism
Regulation and Modulation of Muscle Performance
Muscle Fatigue
- Temporary decline in muscular performance from repeated activation (use)
- Inability to produce or maintain force
- Slowing of shortening velocity and relaxation
- Central
o Brain to a-motor neuron
o Motor drive, capacity for max. voluntary contraction (MVC)
o Psychological – tolerance/pain
- Peripheral
o NMJ to cross-bridge
o Dysfunction to …
Motor unit type & fatigue
- Type I: fatigue resistant
- Type IIa: moderately fatigable
- Type IIb/x: very fatigable
Force-Frequency
- Low frequency causes less fatigue
Exercise Parameters
- Intensity is the primary factor in determining rate of fatigue
- Duty-cycle – fraction of time that a motor unit is active
Fatigue results from
1. Mismatch between energy provision and demand
2. Dysfunction at the level of the myofilaments that leads to
a. Impaired CA2 release
b. Decreased force response to activation signal
ATP/ADP
- Min. ATP required for contraction is 20 um
- ATP is not usually limited at fatigue
- Dec. ATP/ADP RYR dysfunction
- Dec. Ca2+ release dec. force production
- ATP required for active transport of Ca2
o Slowed relaxation time due to high ADP causes leakage from SR and higher
SERCA load
- OVERALL decreased force production through Ca2, dec. SR pumping and RYR function
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Document Summary
Temporary decline in muscular performance from repeated activation (use) Central: brain to a-motor neuron, motor drive, capacity for max. voluntary contraction (mvc, psychological tolerance/pain. Peripheral: nmj to cross-bridge, dysfunction to . Intensity is the primary factor in determining rate of fatigue. Duty-cycle fraction of time that a motor unit is active. Fatigue results from: mismatch between energy provision and demand, dysfunction at the level of the myofilaments that leads to, impaired ca2 release, decreased force response to activation signal. Atp is not usually limited at fatigue. Dec. ca2+ release dec. force production. Atp required for active transport of ca2: slowed relaxation time due to high adp causes leakage from sr and higher. Overall decreased force production through ca2, dec. sr pumping and ryr function. Fatigued muscle fibres have depleted muscle glycogen. Leads to fatigue via dec. provision of substrate: dec. acetyl-coa enters tca cycle, dec. atp production rate. Takes time, only in prolonged higher intensity exercise (75-80 vo2 max 1+hrs)
