STRENGTHENING
Years ago, there was some reluctance to strengthen hemiplegic muscles. Initially Bertha
Bobath avoided using strength training, as she felt that the muscles are not actually
“weak” but unable to generate strength due to exaggerated co-contraction of opposing
muscle groups with increased tone.1 This would then affect motor coordination and
timing.2 Any increase in effort against resistance would increase spasticity and would
therefore affect movement.1 The fear that strengthening will increase tone has been
shown to be unfounded.1,3,4
With the growing body of evidence surrounding neuroplasticity, where it has been shown
that motor practice and intensive training having positive effects on motor system
reorganization,5 we do need to take a look at strengthening and its effects on motor
recovery.
In the Evidence Based Review of Stroke Rehabilitation,6 the conclusion regarding
strength training was that “strength training is beneficial in improving outcomes in
hemiplegic stroke”. There is plenty of support in the literature that strengthening
increases strength, the issue is the lack of research looking at how strengthening
translates into improvement in functional activity.3,7,8,9 This is crucial when there is a
correlation between impairment of activity and strength.3
Strength
Strength is the ability to generate force and apply it to function.9 Strengthening
requires both the musculoskeletal attributes and the neural activation of the muscle.10
When we strengthen muscle, the muscle initially becomes more efficient in maximizing
voluntary contraction.11 Following which, hypertrophy occurs due to an increase in size of
the muscle fibers.11 In the healthy adult, neural factors have been found to initially
contribute to increasing strength for the first 4-8 weeks1, then changes occur at the
muscle level.11 In elderly men (60 and older) gains in strength have been found to be more
dependent on the neural factors.11
What are the components of strengthening?
To increase strength there must be an increase in muscle fibre size (hypertrophy) – as you
increase size you increase tension.11
Nervous system grades force by:
1. Recruitment - increase the number of active motor units = increased force of
contraction
2. Rate coding = increase frequency of activation of motoneurons and increase speed
of firing= increased muscle tension12
What are the neural and muscle level factors involved in strengthening?
The motor nerve innervates all muscle fibres of its motor unit. The muscle force is graded
by increasing the number of motor units activated, rate of activation and increasing the
synchronization of activation.10
The neural determinants of muscle tension are:
Motor unit size and recruitment order. To increase force you must increase the
number of motor units recruited. The order follows the Henneman’s size principle.
Smallest axon to largest = Slow oxidative→ Fast oxidative glycolytic→Fast
glycolytic fibres.10,12 Number of motor units firing
10,12
This is dependent on the amount of excitation to get the muscle to threshold.
Motor unit synchronization.10,12
Timing of muscle contraction.
Frequency of motor unit firing10,12
o
Dependent on the amount of motoneuron excitation.

The biomechanical determinants of muscle tension are:
Muscle fibre number
o
Fixed.
Muscle fibre arrangement
o
Alignment of fibre maximizes the muscle action at the joint. Muscle
migration can occur – fibres are no longer in the line of pull. Muscle
shortens/contractures occur and change alignment of fibres.
Muscle fibre type -can plastically adapt according to use. Slow fibres change to
fast due to disuse. Fast to slow with chronic use.11
Type I Slow Oxidative SO
Slow oxidative, small cell body, low threshold to fire, slow contraction, used for
endurance, fatigue resistant used in postural maintenance
Type IIA Fast Oxidative Glycolytic FOG
Fast oxidative, medium cell body, fast contraction, fast fatigue resistant, used in
sustained walking or running
Type IIB Fast Glycolytic FG
Fast glycolytic – large cell body, high threshold to fire, provides speed, fatigue
quickly, used for power
11,12,13
Muscle fibre size in cross section
o
Atrophy of fibres.
Muscle length – initial and velocity of length change
o
Muscles that shorten (lose sarcomeres) may be too weak to sustain
contraction. Muscle that lengthens (added sarcomeres) may not be able to
generate force. Velocity of change in length provides proprioceptive
information to muscles.
External load acting to oppose movement.
o
The muscle antagonist provides the primary external load to help control
acceleration, deceleration, provide stability.11
In order to generate a movement or perform a task, sensory input –
visual/tactile/proprioceptive is processed and integrated at higher centers , motor
commands then direct the muscles used, the timing of contraction, the coordination of
movement and adjustments based on updating feedback. The motivational system can also
contribute to stimulate interest to initiate and complete the task.
12
Initially post stroke, damage to the primary motor cortex, affects motor pathways such as
the corticospinal pathways9 as can occur in an middle cerebral artery infarct. This results
in the loss of descending central excitory drive to the spinal motor neuron pool and
reduced activation of motor units.3,10 The loss of movement is due to ”an inability to
recruit and/or modulate the motor neurons.”
10
What we see are the negative and positive
signs. Negative signs represent the loss of normal activities controlled by the
corticospinal system. These include paresis or decrease in strength, decrease in speed of
contraction, loss of fine motor control, impairment of muscle tone,9,12 fatigue with
repeated movements.9 The positive signs are the abnormal responses to stimuli, such as
the loss of inhibitory influences, increased muscle tone, presence of abnormal reflexes.10
Following which, with the factor of time, 6 months post stroke, you have the added effect
of decreased cross sectional area of muscle and reduced motor units.3
Strength deficits in stroke are due to morphological and neural changes in muscle tissue.
1
With an Upper Motor Neuron lesion or decreased use we find changes at the muscle
level:
 Muscle fibre transformation
o
Slow fibres transform into fast fibres
 Muscles with primarily slow muscle fibres atrophy to a greater extent than muscles
with mostly fast fibres
 Antigravity muscles atrophy to a greater extent than their antagonists
 Loss of sarcomeres and decrease in length of muscle fibre
 There is an increase in extracellular connective tissue – increases stiffness
 The most vulnerable muscles to change are those that are
o
Antigravity muscles
o
Muscles that cross one joint
o
Muscles with a large proportion of slow fibres
 Altered length tension and force velocity relationships occur causing impairment in
force production. 13
 E.g. if an ankle is in a sustained positioned of plantarflexion due to changes in tone ,
the soleus muscle will atrophy due to lack of muscle tension and the tibialis anterior
will hypertrophy due to the ongoing stretch.12
 In Miller and Light,1 the findings of the research on some of the changes in muscle
are outlined. The findings include: changes that occur on a neural level - decrease
in number of motor units, more severe atrophy of type II fibres (power), low firing
rates, abnormal patterns of discharge. This results in the reduced ability to recruit
and modulate agonist muscle where agonist recruitment is prolonged and the ability
to stop the movement is delayed. Studies have also found decrease in muscle fibre
diameter and changes in distribution of type II and type I fibres.
How can strengthening occur in a damaged CNS?
Reorganization of spared neurons and pathways may be assisting in recovery.9 Dobkin9
describes the corticospinal system as being designed to have some overlap of motor
neurons innervating muscles at one or multiple joints. This allows the neurons innervating
muscles at one or more joints to learn movement patterns together. This also provides the
corticospinal system the flexibility to relearn movement with damage to part of the
primary motor cortex and its descending tracts. Sparing of the corticospinal tracts is
necessary for good motor outcomes, particularly of the hand.9
Research
Resistance exercise may have a positive role in improving recruitment of agonist and
regular exercise has been shown to increase premotor times (cognitive aspects of
movement). 11
Strengthening interventions include electrical stimulation, biofeedback, muscle reeducation, mental practice and progressive resistance exercise. In all of these areas,
there are insufficient trials to provide good data on the effect of these interventions on
strength.3
Strengthening principles are the same regardless of the reason for weakness. To increase
muscle output, progressive resistance exercise is the method of choice.3,9
Engardt2 compared eccentric vs concentric training of knee muscles with isokinetic
maximal voluntary knee extension and flexion. Results indicated that eccentric and
concentric training significantly increased knee extensor strength. Interestingly, the
relative strength of the paretic leg with eccentric training improved both eccentric and
concentric strength. This did not occur with concentric training. Looking at sit to stand,
there was improved body weight distribution with only the eccentric training. Engardt 2
also found increased EMG activity indicating enhanced activation of the motoneurons, with
loading and voluntary effort, which are neural factors contributing to strengthening.
There have been studies looking at strength testing of both sides of the body with
findings indicating weakness on the non-paretic side in acute stages.10
As muscle post stroke, has the ability to respond to resistive exercise in the same manner
as normal muscle,” use of resistive exercise appears indicated in retraining for activities
that require coordination of motor units and power.”
1,9
The American College of Sports Medicine position on progressive resistance training for
healthy adults outlines the following protocol:
Use both eccentric and concentric muscle actions
Perform both single and multiple joint exercises
Complete large before small muscle group exercises
Multiple joint before single joint muscle exercises
High intensity before low intensity
Initially loads should correspond to 8-12 repetition maximum for novice training.
In Intermediate and advanced training, individuals use wider loading range from 112 repetition maximum, to heavy loading 1-6 repetition maximum with 3 minute rest
period between sets, performed at a moderate contraction velocity( 1-2 seconds)
2-10% increase in load can be applied when individual can perform the current
workload for one or two repetitions over the desired number
Training frequency 2-3 days/week for novice and intermediate and 4-5 days /week
for advanced training14
Can use elastic resistance bands instead of weights.9
What are some of other benefits of strength training?
 Important in maintaining bone density15.

It can affect limb loading ability as shown by Lomaglio and Eng.17 They found that
the strength and the ability to load the paretic limb are important factors in ability
to perform sit-stand in chronic stroke.

Harris18 found that strength of the upper extremity was a strong indicator of the
upper extremity’s performance in ADLs.
Recommendations
 Strengthening should be a part of stroke rehabilitation with in the first 6 months
post stroke.3
 If early strength changes are neural in basis, we need to emphasize neural
activation in treatment e.g. increased muscle fibre recruitment.11
 Much of the research has looked at strengthening per se and hasn’t looked at the
specificity of training with strengthening.7 Consider more task specific approach.9
 Strengthening should focus on the functional activities that are impaired. Not only
should the paretic limb be strengthened but the nonparetic and trunk as well.7
 Look at strengthening for both sides of the body10
 Optimize muscle length and position with stretching, splinting to optimize the
muscle biomechanically 12
 Consider using the recommended guidelines for strengthening outlined by the
American College of Sports Medicine. 3
 Using an isokinetic dynamometer (KIN-COM) allows controlled movement, at
controlled velocity and range of movement to encourage maximal voluntary
contraction.2 ,10
 Use eccentric as well as concentric training2
 More research is needed
References
1. Miller GJT, Light KE. Strength Training in Spastic Hemiparesis: Should it be
Avoided? NeuroRehabilitation 1997; 9:17-28.
2. Engardt M, Knutsson E, Jonsson M, Sternhag M. Dynamic Muscle Strength Training
in Stroke Patients: Effects on knee Extension Torque, Electromyographic Activity,
and Motor Function. Arch Phys Med Rehabil 1995; 76: 419-25.
3. Ada L, Dorsche S, Canning CG. Strengthening Interventions Increase Strength and
Improve Activity After Stroke: A Systematic Review. Australian Journal of
Physiotherapy 2006: 52:241-248.
4. Flansbjer UB, Miller M, Downham D, Lexell J. Progressive Resistance Training
After Stroke: Effects on Muscle Strength, Muscle Tone, Gait Performance and
Perceived Participation. J Rehabil Med 2008; 40: 42-48.
5. Boltes Cecatto R, Chadi, G. The Importance of Neuronal Stimulation in Central
Nervous System Plasticity and Neurorehabilitation Strategies. Functional
Neurology 2007; 22(3): 137-143.
6. Evidence Based Review of Stroke Rehabilitation 10th Edition.
7. Bohannon R W. Muscle Strength Training After Stroke. J Rehabil Med 2007;
39:14-20.
8. Taylor NF, Dodd KJ, Damiano DL. Progressive resistance exercise in Physical
Therapy: A summary of Systemic Reviews Phys Ther 2005; 85(11): 1208-1223. Can
be read online at pubmed.gov
9. Dobkin BH. Training and Exercise to Drive Post-Stroke Recovery. Nature of
Clinical Practice Neurology 2008: 4(20): 76-85.
10. Motor control: Theory and Practical Applications 2nd Edition. Constraints on Motor
Control. Anne Shumway-Cook and Marjorie H Woollacott. 2001 Lippincott Williams
and Wilkins, Baltimore Maryland.
11. Skeletal Muscle Structure and Function. Implications for Rehabilitation and
Sports Medicine. Richard L Lieber. 1992 Williams and Wilkins, Baltimore.
12. Principles of Neural Science 2nd Edition. Eric R Kandel and James H Schwartz.
1985, Elsevier New York.
13. Neurological Physiotherapy 2nd Edition. Susan Edwards. 2002, Churchill Livingstone
UK.
14. Kramer WJ, Adams K, Cafarelli E, Dudley GA, Dooly C, Feigenbaum MS, Fleck SJ,
Franklin B, Fry AC, Hoffman JR, Newton RU, Potteiger J, Stone MH, Ratamess
NA, Triplett-McBride T, American College of Sports Medicine. American College
of Sports Medicine Position Stand. Progression models in resistance training of
healthy adults. Med Sci Sports Exerc. 2002; 34(2):364-80.
15. Pang MY, Eng JJ. Muscle strength determinant of bone mineral content in the
hemiplegic upper extremity: implications for stroke rehabilitation. Bone 2005:
37(1), 103-11.
16. Lomaglio MJ, Eng JJ. Muscle strength and weight-bearing symmetry relate to sitstand performance in individuals with stroke. Gait Posture 2005: 22(2): 126-31.
17. Harris JE, Eng JJ. Paretic upper limb strength best explains arm activity in people
with stroke. Phys Ther 2007: 87(1):88-97.
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