KP322 Lecture Notes - Lecture 26: Golgi Tendon Organ, Muscle Contraction, Hyperplasia
19 Mar 2020
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Neural changes:
1) increased muscle activity
-Ability to recruit MU
-Altered MN firing rates
-Enhanced MU synchronization
2) Reduced neural inhibition
-Decrease coactivation of antagonists
-May be between acute and chronic
-Increase activation of synergist muscles
-May between acute and chronic
Neural changes:
-Muscle contraction involved innervation of MU stimulating many muscle fibres to contract in
order to perform physical activity
-We can record this activation with EMG
-Thus, we can use EMG to measure some of the neurological changes that occur
-The size of the EMG single varies depending on the muscle force output
-Control of muscle force is determined by the interplay in MU recruitment and MU firing
-MU recruitment
-Is when more muscle fibres are required to produce the desired force output to another MU
is recited
-MU firing rate
Practical explanation:
-During a typical RT set;
-A specific pool of MU are active and firing at a constant rate to generate enough force to
perform the desired contractions
-As the reparations continue, and fatigue begins to occur, MU recruitment and/or FR increase
to overcome this loss in force production
-Fatiuge = increase MU recruitment and MU FR
-Can we overcome the size principle —> No
Neural adaptations to training
-Basically
-Body learns to use the force it already has
-seems impossible
-Autogenic inhibition - muscle prevents its self from causing serious damage
-Uses Golgi tendon organs as sensor
-Maybe not if you think closely about the neural adaptations to training
Muscular changes:
-Hypertrophy vs hyperplasia
-Hypertrophy
-Increasing muscle fibre size (myofilaments)
-Definitely a results of proper training (and diet)
-Hyperplasia
-Increasing muscle fibre number
-Mixed evidence so far
-Not likely in humans
Document Summary
Enhanced mu synchronization: reduced neural inhibition. Muscle contraction involved innervation of mu stimulating many muscle bres to contract in order to perform physical activity. We can record this activation with emg. Thus, we can use emg to measure some of the neurological changes that occur. The size of the emg single varies depending on the muscle force output. Control of muscle force is determined by the interplay in mu recruitment and mu ring. Is when more muscle bres are required to produce the desired force output to another mu is recited. A speci c pool of mu are active and ring at a constant rate to generate enough force to perform the desired contractions. As the reparations continue, and fatigue begins to occur, mu recruitment and/or fr increase to overcome this loss in force production. Fatiuge = increase mu recruitment and mu fr. Can we overcome the size principle > no. Body learns to use the force it already has.
