Skeletal Muscle Fatigue Flashcards
Skeletal Muscle Fatigue
a) The inability to maintain the required power output which is related to a decline in either force or velocity
b) A condition in which there is a loss in the capacity for developing force or velocity of muscle resulting from muscle activity under a demand/load which is reversible by rest
c) The inability to maintain the required power output which is related to a decline in force, velocity and power which is reversible
Sites of Fatigue
Central and Peripheral
Components of Central
1) Planning of voluntary movement (includes motivation)
2) Motor cortex and the supraspinal outpouts (includes cooardinated afferemt amd efferent signals)
3) Upper motor neurons
4) Lower motor neurons
Components of Peripheral
5) Neuromusclar Junction
6) Sarcolemma and T-Tubule
7) Sarcoplasmic Reticulum
8) Metabolic systems
9) Actin-Myosin Interaction
Central Fatigue
Centeral Governor Model (CGM):
A regulatory mechanism in the brain selects an optimal ‘pace’ that will preserve homeostasis by continuosly adjusting intensity during exercise
Peripheral Fatigue Sites: Impact on Neuromuscular Junction (NMJ)
No biochemical evidence that NMJ blockage is a primary cause of fatigue during exercise
Peripheral Fatigue Sites: Impact on Sarcolemma and T- Tubule System
The quality of the Action Potentials (electrical signals) are changed
Membrane Potential
Resting membrane potential is due to alot of sodium inside and outside
Peripheral Fatigue Sites: Sarcolemma and T- Tubule System #1
- Fatigue at the sarcolemma site is associated with a change in membrane potential:
- Sodium (Na+) and Potassium (K+) imbalancL Na+/K+ ATPase becomes inhibited, membrane may become ‘leaky’ to ions
- Exercise increase blood potassium levels - ) Sodium potassium pump itself starts shutting down
- ) The membrane itself becomes leaky
- ) Increase of blood potassium
Peripheral Fatigue Sites: Sarcolemma and T- Tubule System #2
- Fatigue at T-Tubule site is associated with a drop in the strength or size (amplitude) of the action potential:
- Na+; K+ ion imbalance continues
- Electrical signal not sufficient to activate ion channels in T-Tubules system to release calcium
Peripheral Fatigue Sites: Impact on Sarcoplasmic Reticulum (Ca2+ movements) #3
- A rediuction in the amount of Ca2+ being released from the sarcoplasmic reticulum, due to:
- Depressed Ca2+ release from the SR
- The calcium remaining in SR is more difficult to release- increased Ca2+ staying in SR
- Decrease Ca2+ return to SR- relaxation becomes a concern
- Generally referred to as Calcium Overload
Peripheral Fatigue Site: Actin-Myosin Interaction-Contractile Force Generation
I. Increasing inorganic phosphate (Pi) in cytoplasmic space
IV. Build up of ADP slows down the A-M ATPase activity- crossbridge cycling rate
II. Increasing hydrogen ions levels will decrease the pH
III. With lower pH a decreased sensitivity of troponin (on actin filament) to calcium
Peripheral Fatigue Site: Metabolic Pathways
A. Phosphagen Sources
i) Reduced levels or lower supply of creatine phophate (P) or phosphicreatine (PCr)
B. Anaerobic Glycolysis
i) Lower supply- reduced glycogen concentrations
ii) Build up or accumulation of intracellular components - H+
iii) POSSIBLY lactate itself
C. Aerobic- Oxidative Phosphorylation
i) Depleted glycogen will lower pyruvate supply and reduce ATP production
ii) Possible role of reactive oxygen species, but limited evidence