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fatigue presentation 5336 2010

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Fatigue

• Sensations

• = inability to maintain

a given workload, or

decrement in

performance

• Energy demand

exceeds ATP

production capability

• Cause is dependent on

intensity and duration

• Association or

causation

• Compartmentalization

• Environment

• Fiber type, training

status, type of activity

• Oxygen

ATP and fatigue

• Fatigue often

occurs without a

significant drop in

ATP levels

– Compartmentalization

– Protective effect

CP and fatigue

• CP drops in 2

phases

• Relative work

intensity affects

rate and extent of

depletion

Phosphocreatine and intensity









• After ~5 sec CP is ~80% depleted, and speed

decreases

• J. Hirvonen, European Journal of Applied Physiology, 1987. Vol 56; 253-259

• J. Hirvonen, Canadian Journal of Sport Sciences, 1992, Vol. 17:2; 141-144

Phosphate

• As phosphogens

deplete Pi ↑

– Inhibit PFK

– Displace Ca++ from

troponin

• f

Lactic acid

• Lactate anions vs.

H+ protons

• ↓pH

– Inhibit PFK

– Displace Ca++ from

troponin

– Pain receptors

– Free energy of ATP

– Inhibit FFA release

Calcium

• Ca++ uptake into mitochondria

– Increased O2 consumption for Ca++ removal

– Decreased Ca++ in SR

• Ryanodine receptor fatigue

– Lactate anion, H+

• Decreased responsiveness

Long distance aerobic exercise



• Glycogen depletion

associated with fatigue

• Prolonged

submaximal exercise

• > 60 minutes

Glycogen depletion and sensation

Selective glycogen depletion



• Intensity

determines FT

dependence and

glycogen usage

CHO during exercise

Central fatigue



• Central Nervous

System

–  Motor unit recruitment

–  Motor unit firing rate

• Evidence for and

against

• Neural stimulation

• Psyche (Arousal)

• Serotonin

Peripheral Neural factors

• Peripheral nervous system

• Neuromuscular junction

– neurotransmitters, synaptic

cleft, receptors

• Excitation-contraction

coupling; with repeated

stimulation there is a

possibility of blocking the

action potential through

the t-tubules, decreasing

Calcium release

Peripheral mechanical factors

• Cross bridge cycling

• disruption of actin &

myosin, sarcomere,

sarcolemma, SR

• Ca++ availability

• H+, Pi block troponin,

inhibit SR Ca++ release,

inhibit enzymes

• ATP availability; SR,

Myosin head



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