HSE201 Lecture Notes - Lecture 12: Anaerobic Glycolysis, Sarcomere, Glycogen
Topic 4: Exercise & Fatigue
Neuromuscular Fatigue (1)
Fatigue
- A reduction in muscle force or power output during exercise, which is reversible during recovery
- Force criterion: 100% or 50% Maximal Voluntary Contraction (MVC)
May result from:
- Central Fatigue: > central neural activation
- Peripheral Fatigue: from muscle
- Can occur individually or combination of both
Central Fatigue
- Failure to recruit motor units
- Reduction in motor unit firing frequency: slowing of neural
stimulus frequency may not necessarily contribute to fatigue
- Fibre Fatigue: Slow twitch 50 – control, 25 – fatigue, Fast twitch:
100 control, 65 fatigue
- Stimulation with higher frequencies get a summation of force to
a tetanic contraction
- When experiencing fatigue stimulus frequency decreases
- Driven by 2 main factors
- Send feedback to the spinal cord to monitor the response coming out of the spinal cord
- Primary driver the brain, modified in the spinal cord
- Modification to reduce the ability for the CNS to activate muscle, arises from mechanoreceptors
that become desensitised during fatigue, thus amount of positive stimulation information coming
to the motor neuron is reduced: highly likely to reduce force
- Chemoreceptors: cause inhibition within the spinal cord to reduce the activity of the motor
neuron and thus force output
- Fatigue stops muscle damaging itself, or dying: protective mechanism
Motor Cortex
- Decreased central drive
- Transcranial stimulation: increased force during voluntary fatiguing exercise
- Mechanism is unclear: inhibitory input from muscle mechanoreceptors and/or chemoreceptors,
increased body temperature, circulating metabolities entering brain, decreased blood glucose
- If blood glucose is falling due to exercise it will fatigue and switch off exercise to protect the brain
Afferent Feedback
- Decreased excitatory input back to a-motor neurons: from muscle mechanoreceptors
- Increased inhibitory input back form a-motor neurons: from chemoreceptors K+, H+
- Inhibitory feedback decreases any excitatory input from mechanoreceptors
Lower or a-motor Neuron Activity
- Excitatory activity is depressed at the spinal cord: unknown mechanism
Action Potential Propagation
- Failure to conduct action potential along a-motor neuron or at neuromuscular junction: neither
are sites of fatigue in human skeletal muscle
- Action potential can disappear so the signal doesn’t get across the muscle
- Can be demonstrated in animals, but not in humans
Central VS Peripheral Fatigue
- Interpolated Twitch
- Fallen from where it was at the start, due to the exercise
bout causing fatigue in the middle
- Fatigue from central origins: can’t produce on own
- Fatigue has a central and peripheral origin: element of
peripheral fatigue more common
High intensity exercise
- Exercise of >10sec: fatigue PERIPHERAL
- Exercise <10sec: fatigue PARTLY CENTRAL: contribution may be ~30%
Endurance Exercise
- Knee extensor MVC (A) and maximal voluntary activation (B) before and after an ultra-marathon
Peripheral Fatigue
- Primarily factors that influence:
- Muscle force or tension
- Contraction Time
- Relaxation Time
Isometric Twitch
- Fatigue: increases in contraction & relaxation time & decreases in peak
tension
- When a muscle is fatigued: slower rate of tension, slower decrease
Isometric Tetanus
- Fatigue: decrease in peak tension
Isotonic Contraction
- Fatigue: decrease in shortening (contraction) velocity and
distance and decrease in relaxation velocity
- Shortened at a lower rate over time, and the relaxation rate is
also lower
- Slower rate of contraction & relaxation
Muscle Power
- In fatigue: decrease in power
- Force by distance over time
- Fatigue state: at any given force output not contracting the same
amount of power
Muscle Force determined by:
- Number of cross-bridges attached per CSA
- Force produced per cross-bridge
- Duration of cross-bridge attachment
- Fatigue is characterised by decreased force, therefore one or all of above must be altered by
fatigue
Contraction (shortening time) determined by:
- Rate of cross-bridge cycling
- Fatigue is characterised by decreased contraction (shortening time), thus rate of cross-bridge
cycling must be slowed with fatigue
Relaxation time determined by:
- Rate of calcium (Ca2+) re-uptake to sarcoplasmic reticulum (SR)
- Fatigue is characterised by decreased relaxation time, therefore
the rate of return of CA2+ to the sarcoplasmic reticulum must be
slower
Neuromuscular Fatigue (2)
Sites of Peripheral Fatigue
- A number of places fatigue might be generated
- Fatigue: can cause a reduction in force and contractibility
Sarcolemma and T-tubules: Sites 1 & 2
- Ability of muscle membrane to conduct an action potential
- An action potential block in t-tubules
- Probably caused by K+ loss from contracting muscle
- Ion concentrations across the sarcolemma
- Revolves around the loss of potassium ions from contracting muscle
- Ion concentrations (mM) across the sarcolemma change with fatigue
- During fatigue significant loss of potassium from the cell and rise outside the cell
- Effectively remove the gradient for potassium, with a large
change in potassium ions
- K+ loss causes sarcolemma and t-tubule resting membrane
potential to become depolarised
- Increasing in the membrane potential the closer to 0
- Depolarisation of resting membrane potential leads to de-
activation of voltage-sensitive Na+ channels: no muscle
action potential can be generated
Document Summary
A reduction in muscle force or power output during exercise, which is reversible during recovery. Force criterion: 100% or 50% maximal voluntary contraction (mvc) Can occur individually or combination of both. Reduction in motor unit firing frequency: slowing of neural stimulus frequency may not necessarily contribute to fatigue. Fibre fatigue: slow twitch 50 control, 25 fatigue, fast twitch: Stimulation with higher frequencies get a summation of force to a tetanic contraction. Send feedback to the spinal cord to monitor the response coming out of the spinal cord. Primary driver the brain, modified in the spinal cord. Modification to reduce the ability for the cns to activate muscle, arises from mechanoreceptors that become desensitised during fatigue, thus amount of positive stimulation information coming to the motor neuron is reduced: highly likely to reduce force. Chemoreceptors: cause inhibition within the spinal cord to reduce the activity of the motor neuron and thus force output.
