Muscle plasticity

Muscle plasticity where the muscle reaches the stage of plasticity. Its assessment and types are given in the slide show

1. Muscle Plasticity
By: Radhika Chintamani
Definition:
Plasiticity refers to dyanamic ability of a muscle to adapt when level of use is increased.
Skeletal muscle is the usual tissue in the human body which undergoes adaptation mostly.
Components of muscle which gets modified.
Architecture of the muscle.
Fiber type distribution.
Fiber diameter.
Fiber length.
Tendon length.
Myosin heavy chain profile.
Mitochondrial distribution.
Capillary density.
Adaptation to electric stimulation.
Once a muscle gets stimulated by electric current, there is contraction of muscle occurring in
response to electric stimulation. This current passed and the response leads to strengthening of
the muscle due to repetitive contraction of the muscle. But the strength attained is less than
that of minimal voluntary muscle contraction.
Hence electric stimulation induce repeatable quantifiable amount of exercise on muscle.
Experimental method for chronic muscle stimulation.
Slow twitch postural muscle = high amplitude electric stimulation.
Fast twitch muscle fibers = low amplitude electric stimulation.
Changes occurring in the muscle fiber during stimulation therapy.
Low amplitude electric stimulation
Metabolic changes
Circulatory changes

2. Morphological changes.
If a fast twitch muscle fiber is stimulated at 10Hz for 8-24hrs continusly for 8weeks then it gets
converted to slow twitch muscle fiber. The changes occurring in the muscle throughout the
course of conversion are as follows:
Contractile properties.
Metabolic changes
Circulatory density.
Morphological changes.
Assessment of changes in the muscle after stimulation therapy is achived by the following ways:
Ultrasound.
Histochemical properties.
Biochemical properties
Morphological properties.
Time course of muscle fiber transmission:
3hours following electrical muscle stimulation=sarcoplasmic retinaculum swelling.
2-12 days=
-Increase volume mitochondria.
-Increase in volume of oxidative enzymes.
-Increase in capillary density
-Total consumption of O2 increases.
Increased metabolic activity.
*Incraese in oxidative enzymes and capillary density is manifested by decrease in
fatigaebility.
14 days=
-Z band width increase.
-Decrease in amount and activity of calcium ATPase.
28days=
-Myosin profile is altered. [different myosin monomers incorporate into single
filament.]
-Muscle mass and fiber area decreases.
-Maximum tetatnic contraction that a muscle can build decreses.

3. -Z band is completely widened.
-T system density decreases.
Conclusion:
i.Muscle metabolic enzymes, oxidative enzymes, capillary density, oxygen consumtion, Z
band width are all increased.
ii.Muscle t system, fateagbility, maximum titanic contraction, muscle mass and area are
decrased.
Adaptation to intermittent electric stimulation:
Dr. Daniel conducted an expt on various stimulation frequencies and duration on both fast
twitch, slow twitch muscle fibers differently and together to observe which stimulation works
better;
Muscle fiber type Frequency Duration
F1 100 5
S1 10 5
S1F2 100+10 5+0.5
F2 100 0.5
Maximum titanic tension resulting from Intermittent electric stimulation
*Principle: muscle adaptation is based on the absolute meucle tension reached during
contraction and total number of muscle contarcting during stimulation.
Finding:
High tension were required for muscle strengthening.
Increase in muscle activity lead to reduce pain.
Groups that demonstrated strenghtehning were F2, S1F2.
S1 above didn’t produce any strengthening.
Twitch Kinetic fiber properties resulting from electric stimulation:
Twitch kinetic for all four groups for all the mucle fibers were significantly slow.
Increased activity caused muscle slowing.
Increased contraction time
Twitch fibers are mainly affected by rate at which the muscle fibers release and uptake
calcium.
Endurance of muscle affected to intermittent electric stimulation:
A fatigue test was done: muscle were stimulated for 40Hz for 33ms and allowed to rest
for 670ms. This cycle of activation and rest phase was continued for two weeks. The
fatigue level was assessed later.
Findings:
Endurance was increased.
Greater activity was associated with muscle slowing. [ increased endurance and
decrease strength]

4. High tension contraction are necessary for increasing muscle strength.
Adaptation to resistance training:
According to SAID principle:
Any soft tissue in the body when imposed with specific demands adapts itself to imposed
demands.
Skeletal tissue in the human body is highly responsive to the imposed demands on it.
But once these demands are removed out, the principle of reversibility takes place, which
suggests that once the specifically applied demands are removed and the attained level is not
maintained the soft tissue return back to its previous unaltered position.
This adaptation if occurs in response to strength training [resistance training], then it is called as
adaptive response to resistance exercises, nothing but muscle plasticity.
Within 3-6 months 25%-100% improvement can be seen in strength gains with resistance.
Two types of responses are seen with strength training:
Hypertrophy: increase In the size of the muscle bulk.
Hyperplasia: increase in the number of the muscle fibers.
these both occurs gradually and slowly.
Mechanisms of gain in strength in muscle:
Strength gains
Neural control of strength
gains
Fiber type alteration Muscle hypertrophy
i.Synchronization and
recruitment of
additional motor units.
ii.Autogenic inhibition
i. Fiber hypertrophy
ii.Fiber hyperplasia
A)Neural control of strength gains.
Eroka has made a statement that strength gains in the muscle can be achieved without
any structural changes, but not without any neural changes.
Motor unit recuritement is quiet important to strength gains.
i) Synchronization and recuritement of additional motor unit:
During volitional activity motor units are always recruited asynchronously. There
are different kinds of motor neuron which either stimulate or inhibit the muscle
fiber. Thus when a muscle is contracting the impulses from the motor must be
excitatory and the inhibitory impulses must be terminated. Even the agonist
muscle must be inhibited to produce the contraction orels, if both the muscle
activate at the same time then it will lead to isometric contraction.

5. The contraction reponse if assesd quantitatively, the summation of nerve
impulse matters. That is summating all the excitatory nerve impulse to individual
fiber increase the quantitative strength of the muscle contraction.
Electrical impulse induced on the muscle fiber may change the connection
between the muscle fiber and motor units which connects the spinal cord and
muscle, thus making muscle fiber to contact synchronously and increasing
muscle ability to generate more force.
ii)Autogenic inhibition: It is a negative feedback provided by muscle. The golgi
tendon organs situated in the muscle controls the amount of force exerted by
the muscle itself more than the bones and connective tissue. This inhibition of
force and control is called as autogenic inhibition. When the tension on the
muscle increase than the normal load it can take up, or load equal to the which
the bone can take up, the nerve excitatory impulses stimulate the golgi tendon
units, which through its autogenic inhibition principle inhibits this action. Even
the reticular formation in brainstem and cerebral cortex have an influence over
the autogenic inhibition principle.
Greater levels of strength can be attained once the autogenic inhibition principle
is reduced or the person gets adapted to this principle. This can be achieved by
repeated strength training of that particular muscle.
This theory can explain strength gains in the absence of hypertrophy.
iii)Other neural factors:
a)Coactivation of agaonist and antagonist: when both agonist and antagonist
contract simultaneously it leads to ismoteric contaction or static contraction.
This contraction is useful if the person or patient has problem with static
postural holds. But if to maximize force generated by agonist the antagonist
must be inhibited. The alpha motor neurons stimulate the agonist, whereas
gamma motor neuron inhibit the antagonist muscle fibers.
b)Rate coding: it’s the firing frequency or discharge rates of motor units.
Changes can be seen in morphology of the muscle with both increased or
decreased level of activity that might be directly related to the force
producing capacity of the muscle.
B)Muscle hypertrophy: two types of hypertrophy are generally seen as follows;
 Transient hypertrophy: this is the time limited hypertrophy of the muscle. It
occurs after single exercise bout, due to accumulation of the fluid in the
interstitial and intracellular spaces which is lost from blood plasma. This fluid
returns back to plasma once this pump-up is reduced back to normal.

6.  Chronic hypertrophy: it refers to increase in muscle size which refers to longterm
muscle resistance training.once the person gets adapted to the resistance
training, and repeatedly performs the training without skipping, the muscle gets
bulkier that is hypertrophied[increase in the size of the muscle] and the number
of the muscle fiber may also increase due to repeated movement[hyperplasia].
Recent studies: studies suggest that contant eccentric muscle training increase the cross-
sectional area of the muscle fibers.
Postulating mechanism:
i) Fiber hypertrophy: intensive resistance training significantly increases the cross-
sectional area of each fiber in that particular muscle being trained. Fiber trophy may
be caused by the following
Increase in myofibrils.
Increase in actin and myosin filaments.
Increase in sarcoplasm.
Increase in connective tissue or
Any combination of these.
Intensive constant resistance training.
Increase in muscle protein synthesis.
Increase in protein degradation[ during the eccentric training there may occur microtears of the
fibers leading to degradation of protein, while during the rest interval these tears are healed
which lead to lengthening of the muscle fibers. The energy utilized to heal this tears are
obtained from the muscle glycogen]
The provision of carbohydrate meal during the exercise and carbohydrate and protein meal
post exercise can reduce the degradation of protein, post-exercise.
Positive nitrogen balance.
Testosterone may be responsible for these damages as one of the function of this harmone is
muscle growth. Males experience greater increase in muscle size than in females, for the same
resistance training program.
ii)Fiber hyperplasia: once the resistance training performed continusly to gain the
muscle hypertrophy, hyperplasia occurs simultaneously due to repeated activity. It is
postulated that individual muscle fiber has the capacity of splitting to form two
separate muscle fibers. Satellite cells which are stem cells of musculoskeletal system

7. likely involved in generation of new muscle fiber may be the cause for fiber
hypertrophy.
Muscle injury ( particularly from eccentric training)
Satellite cells become activated
Migrate to damaged region
Fuse the existing myofibrils.
Integration of neural activation and fiber hypertrophy: neural factors make their greatest
contribution during first 2 to 10 weeks of training. Hypertrophy contributes very little in the
initial phase of training, which progressively increases its contribution after 10 weeks of training
as it takes time through decrease in protein degradation and increase in protein synthesis.
C)Fiber type alteration:
Muscle fiber alteration takes place following resistance training.
Mean % of FTb decrease significantly.
Mean % of FTc fibers increase significantly.
High intensity exercise training with resistance and short interval exercises lead
to conversion of ST to FTa fibers.

iii)Fiber hyperplasia: