topic 9

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Topic 9: Muscle Fatigue (Comparability model)

• Fatigue = inability to generate required or expected force (maximal or submaximal)

• 2 general categories of fatigue: Central (nervous system) & Peripheral (muscle tissue)

Central: can result from alterations in motor neuron excitability, or failure of neuron to conduct impulse to nerve terminals to release neurotransmitter.

• intrinsic properties of motor neurons

• higher centers (brain)

• afferent feedback from muscle or tendon

• insufficient ATP supply to keep excitability

• depletion of neurotransmitter

Peripheral: alteration in excitation or contractile processes

→ Excitation: failure at sarcolemma, T-tubule, E-C coupling, SR

→Contraction: failure of regulatory proteins, contractile proteins, substrate metabolism, pH buffering, Pi increase

High frequency/intensity fatigue: onset of fatigue during high frequency (intensity) activation occurs sooner than with low frequency activation.

→ Recovery with high stimulation frequency is faster than with low stimulation frequency.

Potentials sites &mechanism:
→ Central drive/neuronal cells experience fatigue, also recieve afferent input
→ Failure at NMJ (depletion of neurotransmitter, changes in Ach metabolism at synapse, desensitization of Ach receptors)
→ Failure of sarcolemma (↓ excitability) Na⁺/H⁺ exchanger (antiprot), Na⁺/K⁺ pump , repolarization failure
→ Failure of E-C coupling (↓ pH alters efficiency by DHP receptor)
→ increased reliance on glycolytic metabolism (anaerobics)
→ Intracellular lactate (inc lactate production dec sarcolemmal transport)
→ Intracellular acidosis decrease Ca²⁺ affinity to troponin

• after fatigue stimulation, rate of tension recovery ghighly correlated with reestablishent of PH, correlation between decrease force production and dec pH during fatigue not as strong

→ low pH and high Pi affect x-bridge formation & force produced

Low frequency fatigue: onset of fatigue slower. recovry slower

Potential sites

• endurance exercise at intensity of ~60-85% VO₂max: limited by availability of CHO *rate of ATP synthesis with CHO is 3 – 6x faster than fatty acids, ATP synthesis must > utilization.

• ↓ Force at low frequency of activation, not accompanied by impairement of EMG (not problem of excitation)

• no apparent change in capacity of transsarcolemmal uptake of substrates

• low frequency fatigue greater during eccentric than concentric or isometric contrations at same relative intensity (%MVC) due to damaged fibers

  • because force/ fiber greater with ecentric

  • energy cost (Vo2/atp) lower with eccentric

• onset of fatigue much sooner during conditions of blood occlusions (↓ removal of metabolites, ↓ delivery of substrates & ocygen)

• can be due to “drop out” of FFR motor units

• at onset of low frequency stimulation (aerobic muscle) there is correlation between ↓ force produced and acidosos and increase pi, these reesatblished within `5 min, after this no furher ↓ in force but force remains low , due to ↓ ca++ releasee (EC coupling) and or faillure ca++ pump and ↓ sensitivty of troponin to Ca++

• recovery from low frequency fatigue not related to resolution of acidosis, unlike high frquency fatigue - does not recover ecen after pH recovers

Catastrophic Theory of Fatigue:

• built on mechanisms that cause fatigue exist to protect system from ireeprarable damage

  1. at cellular level (structural damage, dehydration, hyperthermia(excess heat), rigor (stiff due to lack of atp)

  2. at higher level (motor units) reflex fatigue - prevents further stress

  3. at even higher level (CNS) afferent feedback

**central governer model: brain prevents too much disturbance of body’s homeostasis