Fatigue Flashcards
(32 cards)
Fatigue (2)
- inability to maintain a power output or force during repeated muscle contractions
- protection mechanism
Fatigue can be attributed to
disturbed homeostasis attributable to work and work environment
Force decreases rapidly during
short term, high intensity exercise - 30s Wingate
fatigue occurs from
disruption in the chain of events between CNS and muscle fibre
two types of fatigue
central - brain, spinal cord
peripheral - neuromuscular junction
- muscle fibre
peripheral fatigue
force or power deficit that occurs despite optimal activation of the muscle fibers by motoneurons - too frequent of AP
where does peripheral fatigue begin
transition between peripheral nerve and alpha motor neuron
central fatigue
Brain stops sending AP /stimulus
causes of fatigue (6)
complex and interrelated
- depletion of phosphogen
- glycogen depletion
- hypoxia
- central and neurtal factors
- reactive oxygen species (free radicals produced by mitochondria)
- Ionic imbalance (Na&K, Ca&Pi, H&lactate
fatigue depends on
type of exercise (intensity, duration)
Depletion of phosphates are a result of and affects
results of depleted intracellar ATP and PC
sprinting, and strength exercise
ATP concentration drops to
40% of resting levels
PC concentrations drops to
15% of resting levels
glycogen depletion limits
decreases production of
reduces
anaerobic glycolysis
pyruvate and oxaloacetate - limiting amt of FA that can be oxidized through beta oxidation
blood glucose limiting availability of glucose to the brain which could potentally impact coordination of neuromuscular pathways
glycogen stores
muscle - 1-2% ~ 425g - more but less concentrated
liver - 8-10% `80g - more but higher concentration
glycogen in other muscles
does not move around
ionic imbalance of hydrogen accumulation and fatigue (3)
decreased activity of many enzymes - PFK, phosphorylate, APTase that are important for ATP production and muscle contraction
- impaired Ca2+ troponin binding
- activate pain receptors in muscles - to cause central fatigue (inhibitory mechanism)
acidosis due to hydrogen accumulation and fatigue
not a significant factor
- low, non-physiological temps it induces significant fatigue
- physiological temmps fatigue was less pronounced
why do buffering agents benefit performance
rid of acid to decrease central fatigue because of te pain receptors
Ionic imbalance of Na/K
increased intracellular Na and increased extracellular K
2 aftermath of Na/K imbalance
disrupt AP movement (depolarization/repolarization) alog sarcolemma and into T tubule
reduced excitability of muscle cells
How doe imbalance of Na and k happen?
What one reduces more muscle force?
How can it be reversed?
Activation of muscle creates quick depolarization which induces ion movements
Elevating extracellular k
By adding lactate
Ionic imbalance of accumulation of inorganic phosphate
Interferes with ca binding to troponin
it blocks the Ryanodine receptor which controls the release of ca from the sarcoplasmic reticulum
Moves into SR and forms a precipitate with Ca - sequesters ca so it’s not available for cross bridge cycling
Hypoxia
Reduced oxygenation of hemoglobin units limit aerobic metabolism during high intensity aerobic exercise
More demand on anaerobic metabolism which leads to increased lactate and hydrogen
