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exercise
List of adaptations
-More efficient motor unit recruitment and
synchronisation
-Bone density
-Synchronisation of agonist and antagonist muscles
-Co-firing pattern
-Rate coding
-Autogenic inhibition
-Hormonal
-Strength, power or muscular endurance gains
-Hypertrophy functional and non-functional
-DOMS
Motor units
Increased training
Greater level of
MU
Increased force
-Increased motor
unit
firing
-Increase in number of motor
units effecting a muscular
contraction
-Enhanced ability to recruit
greater numbers of motor
units
-Increase in synchronisation
leading to a greater
production of force
MU synchronization
Why?
The synapses that the motor neurons make may become enhanced.
The characteristics of the these synapses are able to change as a
result of physical activity. The axon of the motor neuron may become
hypertrophic and as a result conduct impulses to the muscle fibres at
a greater speed.
Gabriel D.A et al. (2006)
Rate coding
MU recruitment
Hennamans size principle law states that the
order in which muscle fibres contract is small
and size principle
slow twitch fibres followed by the larger fast
twitch ones
Benefits
1) Minimizes fatigue by
recruiting the fatigue
resistant fibres first and
only using fatigable fibres
when high forces are
required
2) Permits fine levels of
control over force at all
level of output
Adaptation
Light load Type 1 fibres
(slow-oxidative)
Heavier load Type 2a fibres
(fast-oxidative)
Heaviest laod Type 2x fibres
(fast-glycolytic)
Studies
1. An
experiment by Conwit, RA et al. (1999) backs up the theory of MU recruitment in which they found that
motor units are in fact recruited in an orderly manner according the size principle. The study looked at
average motor unit size and firing rate in relationships with force productions of the quadriceps femoris by
using EMG. Results showed the size of motor units increased linearly with increased force production and
firing rate remained constant to 30% maximum force, increasing with greater generation of force.
2. Evidence
from Van Cutsem, Duchateau, and Hainaut (1998) provides substantial evidence for a neural
effect of training. In their study, they asked subjects to train their ankle dorsiflexors for 12 weeks (5 times
per week) by moving a load representing 30% to 40% of 1RM as quickly as possible. At the end of the
study, recruitment of motor units during ballistic contractions was examined using intramuscular
electrodes. The researchers found that ballistic contractions after the training program were faster, with a
more rapid onset of EMG. They also found that maximal instantaneous firing rates of motor units during
ballistic contractions were higher and showed less decrease in frequency after training. In addition, the
percentage of motor units showing incidents of doublets (two spikes of the same motor unit separated by
5 milliseconds or less) increased from 5.2% of the control units to 32.7% of the trained units. The authors
suggested that ballistic training causes increased motoneuron excitability that leads to the previously
described changes.
http://www.humankinetics.com/excerpts/excerpts/strength-training-results-in-measurable-changes-in-motor-unit-recruitment
3.
Autogenic inhibition
A sudden relaxation of muscle in response to high-magnitude tension
Controlled by GTO (Golgi-tendon organ) whereby a sudden stretch in a muscle
causes a reflexive activation of the antagonist muscle and relaxation of the agonist
Protects muscles against tearing
Muscle hypertrophy
Muscle hypertrophy
Sarcoplasmic hypertrophy (Transient)
Growth of sarcoplasm
Accumulation of fluid called Oedema
between the space of the muscle resulting
in temporary swelling
Non-contractile proteins that do not directly contribute to muscle force production
Non-functional
Fluid returns to blood circulation within couple of hours
More commonly known within typical bodybuilding athletes 60%+ 1RM, 8-12 reps,
30 seconds 2 minute rest
Myofibrillar hypertrophy (Chronic)
Muscle fibre grows more myofibrils and additional contractile protein units
Increased connective tissue as well as number of actin and myosin causing greater
strength
Functional
Higher number of active proteins within the muscle
Associated with Olympic weightlifting athletes due to more contractile protein gains
and therefore strength gains 80%+ 1RM, 1-5 reps and 2-3 minutes rest
Hyperplasia
The increase in the number of muscle fibres present
Studies evidencing the theory in animals however inconclusive for humans
There are two primary mechanism in which new fibres can be formed
1) Satellite cells can be activated cells generated to fuse with each other
after the damaging of muscles to form new fibres
2) Longitudinal splitting - large fibres can split into two or more smaller
fibres
Longitudinal splitting
-Suggested to occur
most frequently
during heavy weight
training
-Muscle fibres
divide and split into
two daughter cells
-These then can
each develop and
grow into a
functional muscle
fibre the same as
that of the parent
fibre
DOMS
Structural
tissue
Cell damage disruption of calcium homeostasis and
cellular respiration
This accumulation of calcium will break down and
degenerate muscle protein lead to inflammation and
pain due to accumulating histamines and potassium
outside the cell
Mostly caused by eccentric exercise
Gullick, DT et al. (1996) this type of exercise causes
the actin and myosin cross-bridges to separate prior to
relaxation, ultimately causing greater tension on the
remaining active motor units. This increases the risk of
broadening, smearing, and damage to the sarcomere
Microscopic ruptures in the muscle at the z-line of the
muscle sarcomere contractile units which make up the
muscle fibres and join them
These ruptures (microtraumas) enhance
Pre (left) normal muscle with regular repeating
the nociceptors within the connective
pattern of sarcomere
tissue to stimulate the sensation of pain
Post(right) severe disruption to the thick and
thin filaments within parallel group
Additional adaptations
Energy
system adaptations
Connective
tissue
Endocrine
system
Enhancement
hormones
Bone density
In
Reference list
Journals
Gabriel, D. A., Kamen, G., & Frost, G. (2006). Neural Adaptations to Resistive Exercise: Mechanisms and
Recommendations for Training Practices. Sports Medicine, 36(2), 133-149.
Conwit RA, Stashuk D, Tracy B, McHugh M, Brown WF & Metter EJ (1999). The relationship of motor unit
size, firing rate and force. Clinical Neurophysiology, 1270-1275.
Henneman, E., Wuerker, R. & McPhedran, A. (1965). Properties of motor units in a heterogeneous pale
muscle (m. gastrocnemius) of the cat. J. Neurophysiol. 28, 85-99
Cardinale, M., Newton, R., & Nosaka, K. (2011) Strength and conditioning biological principles and
practical applications. John Wiley & Sons, Ltd. Chapter 1.1, p.11.
Wilmore, J., Costill, D. & Kenney, W. (2008) Physiology of Sport and Exercise 4 th Edition. Champaign,
USA: Human Kinetics.
Poortmans et al. (1997) Long term effects of creatine monohydrate on strength and power. J strength
Cond Res 13: 187-192. 1999
Baechle, T and Earle, R (2008) Essentials of strength training and conditioning. Third edition. National
Strength and Conditioning Association, pg 103.
Gulick, DT; Kimura, IF; Sitler, M; Paolone, A; Kelly, JD (April 1996). "Various treatment techniques on
signs and symptoms of delayed onset muscle soreness.". Journal of athletic training 31 (2): 14552.
Internet
Freeborn, S (2012) Available at: http://intellectualfitness.org/?p=308 [Accessed online on: 21st February
2014)
Larry Kenney, W (no date) Physology of sport and exercise, Firth edition. Available at:
http://www.humankinetics.com/excerpts/excerpts/recent-research-provides-insight-into-muscle-soreness
[Accessed online on: 26th February 2014]