The document discusses muscle imbalance as a pathological condition characterized by an inequality of muscle length and strength between agonist and antagonist muscles, impacting normal posture and movement. It outlines intrinsic and extrinsic approaches to muscle function, details the continuum and paradigms of muscle imbalance, and provides insight into the biomechanical and neurological factors contributing to such imbalances. Treatment methods and the interaction of various muscle and sensory systems in maintaining balance are also explored.

1. Muscle Imbalance
By: Radhika Chintamani Ref: Janda’s Approach
Definition: It is the relative inequality of muscle length or strength between an agonist and an
antagonist: this balance is necessary for normal posture or movement.
Muscle imbalance is the pathology which happens to be seen when either one muscle overacts
compared to the opposite muscle or due to an overuse. Here the dynamic and static balance
between the muscles is disturbed, such that either the movement or the range of motion or both
may be affected.
Musculoskeletal approaches of structure and function of muscle:
It has two different approaches for muscle function:
1. Intrinsic:
a. Physiological function: response of the tissue to dysfunction and damage as well as the
healing process itself.
b. Biomechanical function: involves osteo- and arthrokinematics involved in human
body movements and the resulting force vectors imparted on human tissue.
c. Neuromuscular function: relates to sensorimotor aspects of movement with
proprioception and reflexes.
2. Extrinsic: made up of specific, purposeful and synergestic movement that integrates the
three intrinsic system.
There are two basic types of muscle imbalance:
Functional Imbalance Pathological Imbalance
Atraumatic With/Without trauma
Adaptive changes Adaptive changes
Activity specific Associated with dysfunction
No pain With/without pain
When muscle imbalance impairs function, it is considered to be pathological which is typically
associated with dysfunction and pain.
The muscle imbalance continuum: As described by Janda muscle imbalance continuum stated
as follows
Tissue damage
Muscle Imbalance (tightness or weakness)
Altered movement

2. The muscle imbalance continuum may progress in either direction.
Burnhm et al 1993: suggested that shoulder impingement is associated with rotator cuff tear and
Cools et al, 2003:scapular stabilizer weakness,
While
Barden et al 2005: suggested that shoulder instability is associated with muscle imbalance.
Page stewart reported that patients with knee joint dysfunction demonstrated hamstring weakness
on involved side.
LBA has also been associated with decreased range of motion in hip extension (Van Dillen et al,
2000) and internal rotation (Ellison et al, 1990).
Muscle Imbalance Paradigms:
Janda described two schools of thought of muscle imbalance.
1. Biomechanical Paradigm.
2. Neurological Paradigm.
Biomechanical Paradigm:
Constant stress that the muscle experience form prolonged posture and repetitive movement.
Saharmann suggests that prolonged, sustained posture or repetitive movements leads to
adaptation in muscle length, strength and function, which in turn may lead to movement
impairments. Muscles grow either longer or shorter according to the demands imposed and the
daily activities, hence depending on these demands number of sarcomeres increase or decrease
respectively.
 If the muscle fiber is constantly maintained in the shortened position for prolonged period
of time, the sarcomeres move closer together and may even overlap, this overlap leads to
decrease in the space for actin myosin coupling which leads to decreased and painful
contraction of muscle, hence leading to weakness of the muscle.
 If muscle fiber is maintained from shortened to lengthened position then the muscle fiber
can be lengthened permanently on sustained maintenance. Inducing lengthening methods
of muscle fibers, eg: stretching has the same principle, that is lengthening leading to
increase in the distance between actin and myosin and also number of sarcomeres, also
increased blood supply, leading to stimulation of GTO (Quick stretch has property of
fascilitatory which acts on GTO), leads to increase in length. Eccentric training leads to
increase in length by the same principle except that Willmore also suggested that
eccentric training leads to microtear of muscle fiber, leading to separation of the actin and
myosin, and training being fasciltatory increases number of sarcomeres too, which leads
to lengthening.
 If the muscle fiber is maintained constantly in a lengthened position for a prolonged
period of time, then there is increase in the distance between each actin and myosin
bonding, leading to no bonding at all because of the increased distance between each of
them, leading to no contraction and hence muscle weakness sets in.

3. Muscle kept in prolonged shortened position
Tightness of the synergist
Contracture of the synergist
Weakness of the synergist
Bergmark 1989, described a classification scheme that divides muscle systems equilibrating the
lumbar spine into global and local. Global muscles are superficial, fast twitch muscles, have
tendency to shorten and tighten. Local muscles are slow twitch and deep stabilizers that are
prone to weakness.
Neurological Paradigm:
Here the neural control circuit which controls the motor function of the muscle is damaged
which may alter the strategy of recruitment of the AHC’s leading to temporary or permanent
weakness or dysfunction of the muscle. This change in recruitment alters the muscle balance,
movement patterns, ultimately the motor program.
Janda described that predominantly static or postural muscles have tendency to undergo
tightness. He also stated that the muscle lies between the CNS and PNS, that is it is controlled by
both CNS and PNS. Any damage to any structure leads to muscle imbalance. Muscle imbalance
can be locally or globally depending on the site of damage. If the site of damage is local that is
any part of muscle of nerve innervating it ( PNS) leads to local muscle weakness leading to
imbalance, whereas any damage to CNS, that is central damage to the pre-motor area leads the
global muscle weakness, leading to imbalance of the muscles.
Prolonged stretching of the antagonist
Weakness of the antagonist
Disturbed joint stability

4. Janda’s Neurological Paradigm of Muscle Imbalance
Comparison of Janda’s and Scharmann’s approaches to
muscle imbalance
Sr. No Concepts Scharmann’s approach (Biomechanical) Janda’s approach (Neurological)
1. Basic
concept
Repeated movement, and prolonged posture
can cause tissue changes and movement
pattern.
Joint develops directional susceptibility to
movement (DSM) in a specific direction, this
DSM becomes the cause of pain due to
microtrauma due to movement in that specific
direction.
Deviation of path of center of rotation in the
kinesiological system leads to movement
impairment.
Musculoskeletal system lies between
CNS and PNS, hence proper stimuli
from both these system leads to proper
activation of synergist and inhibition of
antagonist. If one of the system is
damaged leads to muscle imbalance.
Proprioception a part of sensorimotor
link, also has a important role here.
2. Etiology of
imbalance
Muscles maintained in
lengthened position->shift of length tension
curve to rt->increase in tension generating
capacity->stretch weakness.
Shortened position->shift of length tension
curve to lt->decrease in tension generating
capacity->active insufficiency.
Extrinsic and Intrinsic factors
Structural Pathology
Pain and pathology
 Inflammation.
 Fatigue and stress
Functional Pathology
Altered proprioceptive input
 Abnormal joint motion or
position.
Muscle imbalance response:
hypertonicity and inhibition
Altered movement patterns and
adaptive changes.

5. 3. Movement
impairment
In a multijoint system, movement occurs at
one joint with least resistance, and the
compensatory movement occurs at the other
joint. This compensatory movement occurs in
other direction leading to laxity of muscle,
ligaments on that side.
Muscle prone to tightness are approx.
1/3rd
stronger than those prone to
weakness. Tight muscles are readily
activated during various movement.
4. Evaluation Identifying all impairments.
Identifying mechanical cause
Identifying painful tissue
Correcting the problems
Posture analysis
Gait analysis
Muscle length assessment
Most coordination
Most pattern (evaluates timing and
sequence of firing of motor unit and
also degree of activity of synergist)
5. Treatment Shortening long muscle
Decreasing load on weak or long muscle
Supporting weakened or strained muscles.
Correct usage taught
Normalize function of all peripheral
structures.
Restore muscle balance to tight and
weak muscles.
Improve CNS control and
programming by increasing
proprioceptive flow.
Activate system that regulate
coordination, posture and equilibrium.
Improve endurance in coordinated
movement patterns.
Sensory motor system:
Sensory information
Panjabi 1992 described a model of spinal stabilization similar to Janda’s philosophy which
consisted of 3 subsystems, skeletal, muscular and CNS. A dysfunction in any of the one
component leads to one of the following three conditions:
1. Successful compensation from the other system, or normal adaptation.
2. Long term adaptation from one more subsystems.
3. Injury to one or more components of any subsystems, or pathological adaptation.
Three levels of control for the sensorimotor system
Sr. No Location Speed Control Awareness
CNS processing
Joint position and motion sense
Motor response
Afferent Efferent

6. Brain
Spinal
cord
1. Spinal Fastest Involuntary Unconscious
2. Subcortical Intermediate Automatic Subconscious
3. Cortical Slowest Greatest Conscious
Structural and functional components of the sensorimotor system
A. Structural
Afferent Central Efferent
Mechanoreceptors Spinal tracts Peripheral nerves (alpha and
gamma motor neurons)
Muscular Receptors Subcortical (brainstem) ------do--------------
Exteroceptors Cortical Muscles
B. Functional
Proprioception Processing
Motor programming
Stabilization (postural stability
and joint stabilization)
Most
Postural stabilization loop:
Visual Input
Vestibular
Input
Somatosensory Input
Muscles, joints, and
cutaneous receptors

7. Muscle activation in weight shift:
Weight shifts Muscle activation for stabilization
Anterior Gastro, Hams, Lumbar Paravertebrals
Posterior Tibialis anterior, Quads, Abdominal muscles
Medial Peroneals, Lateral HAMS, Hip abductors
Lateral Tibialis posterior, medial Hams, Hip adductors
Ankle strategy: This strategy is used when small shift of COG needs to be corrected to stay
balanced. When a person is standing on an unstable surface his body stabilizes himself on the
ankle, with activation of various muscles distal to proximal in the respected direction of the
sway. This is also called as inverted pendulum.
Hip strategy: This strategy is used when large shift of COG needs to be corrected to stay
balanced. The person stabilizes himself by activating muscles proximal to distal direction
asynchronously.
Step strategy: when a person is unable to reposition the COG with ankle or hip strategy alone,
then the person takes a step to reposition the COG in the BOS so that he becomes stable.
Chain reactions:
The chain system is nothing but the interaction between the skeletal, muscular and the CNS in
order to perform movement perfectly and in a well coordinated way.
Interaction of three different systems in body for chain reactions:
Primary chain Secondary chain Types of chain
Articular Muscular
Neurological
Postural
Kinetic
Muscular Articular
Neurological
Synergist
Muscle slings
Myofacsial chains
Neurological Articular
Muscular
Primitive reflexive chains
Sensorimotor system
Neurodevelopmental
locomotor chains
I. Articular chain
Postural Chain: position of one joint in
relation to another when the body is in an
upright posture
1. Structural: influence of static skeletal
system on the adjacent structures. This
chain are influenced by static position
of the joint. The most recognized
Kinetic chain: usually recognized as a concept
of CKC and OKC in which focus is on
movement of joint as the distal extremity
whether fixed or not.
 Lower extremity Closed Kinetic chain
can be observed by gait assessment,
what position the foot goes in every

8. structural postural chain occurs in the
spine. Postural position of cervical
thoracic and lumbar is often assessed
when the patient complains of
musculoskeletal pain.
***Cogwheel chain mechanism of poor
posture explained by Brugger A. 2000.
2. Functional: dynamic influence that the
position of keystone structures has on
muscles attaching to those structures.
This chain is influenced by muscle
activity around joint structure.
Keystone structures here are referred to
skeletal structures that serve as
attachment points of group of postural
muscles, most notably pelvis, rib, and
scapulae.
sub-phase of stance, while open kinetic
chain can be assessed by what position
the foot goes in every sub-phase of
swing.
 Upper extremity closed kinetic chain
can be assessed by pushups, weight
bearing and weight shift on upper
extremity, quadripod position,
crawling. Whereas open kinetic chain
can be also assessed while gait with
parameter called arm swing, and also
by free movements of the entire upper
extremity including all the joints
separately.
II. Muscular Chain:
Synergist: Muscle which
works with the prime
mover is called as
synergist. These help the
prime movers of the joint
for that particular action to
complete the muscular
action with good strength.
Eg: during shoulder
rotation rotator cuffs are
active, however the scapula
is stabilized by rhomboids,
serratus anterior and
trapezius for the
completion of movement in
a painless way.
Muscle sling: these are the
muscles which provide the
movement and stabilization
across multiple joints. These
also provide stabilization and
movement in the reciprocal
and contra lateral movements
in locomotion. Typically
muscle slings are connected as
one muscle insertion and the
next muscle origin on the same
keystone structure. Eg:
Rhomboid, serratus
anterior=scapula;
rhomboid, triceps=scapula;
trapezius, biceps=scapula;
biceps, pect minor=scap;
biceps, pect major=humerus;
lat dorsi, triceps=humerus
SA, EO=ribs
Pect major, IO=ribs
IO, EO=linea alba
IO, Glut med=pelvis
IO, sartorious=pelvis
EO, adductors=pelvis
Hams, glt max=pelvis
Glt max and C/L lat dorsi=
Myofacsial chain: Fascia
integrates the joint motion. It can
either exert tensile force via
attachment between muscle and
bone, or can exert compressive
force via muscles contracting
within facial envelopes. Serves
as a link between various
muscles acting together to
produce movement, or for
stabilization.
 Abdominal fascia:
attaches EO, IO, TrA,
pect major, and serratus
anterior. Contains the
links to form a dynamic
muscle sling with pect
major, serratus anterior,
and EO.
 Thoracolumbar fascia:
attaches EO, IO, TrA, Lat
dorsi, and glut max. plays
an important role in
proprioception. Yahia
and colleagues in 1992
found that this fascia
consists of

9. pelvis and thoracolumbar
fascia
Glt max, quads=femur
Hams, hip flexors=femur
Hams, tibialis anterior=tibia
Quads, plantar flexors=tibia.
*****Extremity flexor and
extensor sling
*****Trunk sling
mechanoreceptors that
help in sensorimotor
control of the lumbar
spine.
 Superficial back line
 Superficial font line
 Deep back line
 Deep front line
 Lateral line
 Spiral line
Extremity flexor and extensor sling:
Extremity slings are designed for compound movements of the limbs. A) LE:
Extensor sling
Hip=glut max,
Knee=rectus femoris
Plantar flexion=Gastrocnemius
Flexor sling
Hip=iliopsoas
Knee=hamstring
Dorsiflexion=tibialis anterior
During gait swing phase activates flexor sling in LE, while the stance phase activates extensor
sling in LE. Throughout the gait, these two phase alternatively activate and inhibit and
reciprocate between each lower extremity such that, when one leg is in stance (extension sling)
the other leg is in swing phase (flexion sling), hence reciprocal, rhythmic co-activation of muscle
in contra lateral LE’s produce a balanced gait.
When both slings are activated simultaneously LE’s are stabilized. Such that in upright standing
position both LE’s have activated extension sling in them making an individual stable in his
BOS.
UE-
Extensor sling
Rhomboids
Posterior deltoid
Triceps
Hand extensor
Flexor sling
Pect major
Anterior deltoid
Trapezius
Biceps brachii
Hand flexors
These extremity slings are activated along with lower extremity sling to form a reciprocal gait.
During swing phase- Rt UE= flexor sling coupled with
Lt LE=flexor sling.
Trunk muscle sling:
These slings are necessary for fascilitating the reciprocal pattern of the gait between both the
upper and lower extremity for rotational trunk stabilization. There are total 3 slings:
1. Anterior
2. Spiral

10. 3. Posterior.
Anterior:
Biceps
Pect major
IO
Contra lateral hip abductors
Sartorious
Spiral: (wrapping from posterior
to anterior)
Rhomboids
SA
EO
Contra lateral IO
Contra lateral Hip adductors
Posterior
Hamstrings
Glut max
Thoracolumbar fascia
Contra lateral lat dorsii
Triceps.
Importance of posterior sling:
Vleeming and collegues 1995, demonstrated that posterior dynamic stabilization sling provides
stabilizing force for the ipsilateral SI joint. They noted that ipsilateral glut max. and contra lateral
lat dorsii. are connected functionally via thoracolumbar fascia.
Mooney et al in 2001 found that ipsilateral glut max and contra lateral lat dorsii. activated
simultaneously during gait and trunk rotation.
This chain can be key structure for indicating for any dysfunction in glut max and SI joint.
Extension of posterior chain: connection of hamstrings to the ipsilateral glut max and erector
spinae via sacrotuberous ligament. During gait the body often compensates for weakness of glut
max (i.e. hip extension) via activation of erector spinae (i.e. lumbar extension)
Hungerford. Et al demonstrated that SI joint dysfunction patients had early activation of biceps
femoris incase of glut max weakness in order to stabilize the SI joint, which shows that biceps
can stabilize SI joint via sacrotuberous ligament.
III. Neurological chains:
a. Protective reflexive chain: two fundamental protective reflexes are, crossed extensor and
withdrawal reflex which are triggered by sensory receptors.
 Flexor Withdrawal reflex:
Excessive heat or noxious stimulus
Activation of flexor and inhibition of extensor
Pulling of the limb away from the stimulus.
 Crossed extensor reflex:
Cutaneous noxious stimuli
Flexor activation on the same side and extensor activation on the contra lateral
side.
Pushing the noxious stimuli away from the contra lateral limb.
Janda’s additional reflexes:
 Locomotion: in lower extremity, a combination of extension, adduction and
rotation provide basic gait pattern to avoid danger.
 Prehension: in upper extremity, flexion, adduction and IR is performed to bring
the food to mouth.

11.  Mastication: Adduction of the jaw (closure of the jaw) is necessary to chew food.
 Breathing: Not easily influenced by voluntary action for longer duration.
b. Sensorimotor chains: linked neurologically through afferent and efferent systems in
controlling feedback and feed-forward mechanisms. Provides both local and global
dynamic stabilization of the joints through muscle activity.
 Reflexive stabilization: on contraction of one muscle the other muscle has to
contract to provide stability of that particular joint.
[ Eg: Horak and Nashner in 1986 in their study demonstrated that on giving
perturbation on the human body in one direction say, anterior direction the
opposite side muscle contract to maintain the balance of the body in the distal to
proximal way( ankle strategy) to maintain smaller perturbation and proximal to
distal way (hip strategy) against a larger perturbation. ]
The most important stabilizing sensorimtor chain in human body is the pelvic
chain, consisting of the TrA, multifidus, diaphragm, and the pelvic floor. These
four muscles are coactivated in the pelvis for its stability and force transmission.
Pelvic weakness has shown both proximal and distal pathologies such as LBP,
groin strains, IT band syndromes, anterior knee pain, ACL tears, Ankle sprains.
The sensorimotor chain depends on proprioception. Joint dysfunction often disrupts the
dynamic stabilization of the chain.
[Eg: a study by Falla et al, demonstrated delayed activation of deep cervical flexor on
upper extremity tasks in whiplash injury patients.
Delayed activation of middle and lower traps in patients with shoulder impingement.
Cools et al.2003]
 Sensorimotor adaptation chains: these adaptation takes place when dysfunction
such as pain or pathology within the sensorimotor system occurs. The adaptation
may be in the form of systemic and predictable pattern. Janda described the
adaptation as follows:
i) Horizontal adaptation: occurs when impaired function in one joint or
muscle creates reaction and adaptation in the other joint segments.
Commonly seen in spine, eg; LBA often leads to cervical syndromes.
[Horal et al, suggested that after 6y of first episode of onset of LBA, the
individual develops cervical syndromes.]
Muscles conform to horizontal adaptation creating a predictable pattern.
Can be either proximal to distal or either way.
ii) Vertical adaptation: occurs between CNS and PNS. Adaptation of one part
of sensorimotor system leads to impairment in the function of entire motor
system. May progress from PNS to CNS or either way. It is seen as change
in motor programming that is reflected in abnormal movement pattern.
Demonstrated in global movement pattern or postural control.
c. Neurodevelopmental locomotor patterns:
There are two groups of muscles in phylogenetic origin: tonic and phasic.

12. i. Tonic system: older in origin, dominant, involved in repetitive and rhythmic
activities and also involved in withdrawal reflex in UE and LE. Predominant
action is flexion.
ii. Phasic system: younger in origin, typically work against gravity, mainly for
postural stabilization, predominant action is extension.
Study of movements in infants as they mature is called as developmental kinesiology.
Innate reflexes seen in infants such as ATNR and STNR integrate into the
musculoskeletal system and become the function of the human being. These primitive
reflexes may reoccur if any injury is seen globally in CNS.
Tonic and phasic muscles do not function individually, rather they work through co-
activation for posture, gait and coordinated movements. This co-activation occurs in
particular chains to achieve the desire movement or action to be achieved synchronously
in a well balanced way.
These chains are as follows:
Tonic and Phasic chains of the upper and lower quarter:
Co-activation chains Upper quarter Lower quarter
Functional movements Prehension, grasping,
reaching.
Creeping, crawling, gait
Tonic chain Flexion
IR
Adduction
Pronation
Plantar flexion
Inversion
Flexion
IR
Adduction
Phasic chain Extension
ER
Abduction
Supination
Dorsiflexion
Eversion
Extension
ER
Abduction
The proper balance between two chains in both and upper lower quarter is demonstrated
by normal gait and posture. This combined integration between both the chains in upper
and lower quarters, specifically co-activation of contra lateral UE and LE leads to
reciprocal arm and leg movements during gait.
Imbalance in one of the system leads to postural compensation and adaptation of any of
the system in compensation to another.

13. Chronic musculoskeletal
pain cycle
Pathomechanics of musculoskeletal pain
and muscle imbalance
Janda believed that pain is only way that the musculoskeletal system can protect itself.
Pathology of musculoskeletal pain:
Muscle imbalance can develop from both acute or chronic pain.
Acute pain
Localized muscle response
Change in movement pattern to protect or compensate for injury
This altered movement becomes centralized in CNS
Pain persist via the altered movement due to impact on the structures
Spasm occurs.
Again pain persists.
Muscle imbalance
( tightness and
Impaired
movement
patterns and
Faulty motor
program/motor
learning
Altered joint forces
and altered
proprioception
Joint degeneration
and postural
changes
Pain and
inflammation

14.  Muscle imbalance: According to Graven et al. Chronic pain is associated with a
protective adaptive response, in which agonist decreases in tone whereas
antagonist increases in tone. According to Janda this neurologically mediated
response is seen tonic and phasic system. Muscle imbalance presenting with
fascilitation of an agonist inhibits the antagonist leads to greater risk for the joint.
 Impaired movement patterns and postural changes: Postural responses to pain are
common. Mechanism for all this is basically adaptive response of musculoskeletal
system towards the pain so that, the posture causing the pain is inhibited by the
person, and the posture without pain i.e. compensatory posture is attained and
maintained by the individual. Hence there is altered posture and movement
pattern in response to pain. Once the imbalance sets in the altered posture and
movement is maintained for avoiding pain. This makes further imbalance within
that specific joint. Tightness of antagonist subsequently inhibits the agonist on the
basis of Sherrington’s law 1991. This further leads to muscle imbalance around
the joint, ROM restriction, and further risk for that particular joint.
 Faulty programming and motor learning: reemergence of primitive reflexes
affects the normal movement pattern. Constant repetitive movement performed in
an abnormal way, dominates the normal way it is usually performed because of
the effect on motor learning. This faulty program attained by the individual due to
pain becomes new motor program which becomes fixed in the motor cortex.
 Altered joint forces and altered joint proprioception: altered movement patterns
change the normal stress placed on the joint in different position. Muscle
imbalance alters joint position, which further alters the stresses placed on the joint
in different direction, which alters the amount of stress produced, leads to
improper distribution of joint stress force on joint articular surfaces, articulating
capsule, and muscles and ligament around the joint.
 Joint degradation: altered stress placed on the articulating surfaces and the capsule
and muscle and ligaments around that particular joint lead to degeneration of the
joint. Poor proprioception may be ultimately responsible for joint degeneration.
 Chronic pain: inflammatory mediators such as histamine and bradykinin, cause
pain and send impulse to the brain via mechanoreceptors. Efferent impulses alter
the position or movement pattern which reduces the pain. This may further cause
muscle imbalance.
Pathomechanics of muscle imbalance
Depending on the tonic and phasic classification of the muscle, usually the muscles undergo
imbalance. Before starting muscle imbalance read about tonic and phasic systems of muscle
Tonic system Phasic system

15. Phylogenetically older Younger
Generally flexor or postural muscles Generally extensor
Tendency towards tightness, hypertonia,
shortening, and contractures
Tendency towards weakness, hypotinia,
lengthening
Readily activated in movement, especially with
fatigue or novel or complex movement patterns
Delayed activation
Less likely to go atrophy More likely to go atrophy
Less fragile More fragile
Typically one joint muscles Two joint muscles
Eg: back muscles Eg: extremity muscles
Janda’s classification of muscle prone to tightness or weakness:
a) UPPER QUARTER
Tonic system prone to tightness Phasic system prone to weakness
Suboccipitalis Middle and lower traps
Pect (major and minor) Rhomboids
Upper tarps SA
Levator scapulae Deep cervical flexors (longus colii and capitis)
SCM
Sclenes*
Scalenes
Lat dorsii UE extensors and supinators
UE flexors and pronators
Masticators
Digastric
Scalenes may be tight or weak
b) LOWER QUARTER
Tonic system prone to tightness Phasic system prone to weakness
Quadratus lumborum Rectus abdominis
Thoracolumbar paraspinals TrA
Piriformis Glut max
Illiopsaos Glut med, min
Rectus femoris Vastus med, lat
TFL-IT band Tibialis anterior
Hamstrings Peroneals
Short hip adductors
Triceps surae ( particularly soleus)
Tibialis posterior
Causes of muscle tightness and weakness:
Muscle tightness Muscle weakness
Contractile and neuroflexive
components
Limbic system
TrPs
Reciprocal inhibition
Arthrogenic weakness

16. Muscle spasm Deafferentation
Pseudoweakness
TrP weakness
Fatigue
Viscoelastic property Adaptive shortening Stretch weakness
Tightness weakness
I) Muscle tightness:
Key factor in muscle imbalance.
Muscle prone to tightness are 1/3rd
stronger than those prone to weakness. (Janda 1987)
Tightness of a muscle reflexively inhibits its antagonist causing its weakness leading to
muscle imbalance.
Leads to abnormal distribution of forces across the joint.
Joint dysfunction
Compensation.
Altered movement patterns.
Early fatigue.
Finally overstress of activated muscles and poor stabilization leads to injury.
Janda believed that there are 3 important factors leading to muscle tightness as follows:
1. Muscle length: tight muscles are shorter in length.
2. Irritability threshold: easily irritated by stretching them.
3. Altered recruitment: usually during movement tight muscles are recruited first. But if
the necessity to control movement is very high then these muscles behave weaker
than the normal muscles.
Neuroreflexive factors for increased tension:
1. Limbic system activation: stress, fatigue, pain, and emotional disturbance activates limbic
system, which activates the muscle tension. Muscle spasm due to limbic system
activation are not painful but tender on palpation. Frequently seen in shoulder, neck, low
back and in tension type headache.
2. Trigger points: focal area of hypertonicity that are not painful during movement but are
painful with palpation. These are localized hyperirritable nodules found within the taut
bands in the muscle.
3. Muscle spasm: muscle spasm causes ischemia or an altered movement pattern.

17. a) Overuse of muscle
Deposition of waste metabolites
Further overuse of the same muscle
Metabolites persisting in the muscle not washed away by lymphatics
Triggers the pain on palpation
b) Any injury to the nearby structures
Inflammation
Guarding response seen by the muscle
Muscle spasm
c) Repeated use of muscle
Muscle spasm by overuse phenomenon
Continued use of muscle spasm
Muscle ischemia
Muscle spasm leads to reflex arc of inhibitory response to any stimuli which causes arousal of
pain within that muscle.
II) Muscle weakness:
a) Neuroreflexive factors for decreased tension: many contractile factors contribute
to decreased muscle tension, as follows;
i) Reciprocal inhibition: Muscle becomes inhibited reflexively when its
antagonist is stimulated. Weakness is often reflex mediated inhibition
secondary to increased tension in antagonist.
ii) Arthrogenic weakness: Muscle becomes inhibited via AHC’s due to joint
swelling or dysfunction. This weakness also leads to selective atrophy of
type II muscle fibers.
iii) Deafferentation: It is decrease in afferent information from neuromuscular
receptors.
Damage to mechanoreceptors
Loss of articular reflexes
Altered motor programs

18. De-efferentation
Loss of efferent signals to alpha motor neurons
Decreased muscle strength
iv) TrP weakness: Hyperirritable nodules in taut bands of muscle fibers leads
to decrease in the pressure pain threshold. (Simon’s 1999) leading to
overuse, fatigue and ultimately weakness. Muscles with active TrP fatigue
early than the normal muscle do, and they also have less number of firing
motor unit and poor synchronization (Janda 1993).
v) Fatigue: caused by metabolic or neurologic factors.
Often pain is experienced before muscle undergoes fatigue.
Once the fatigue sets in the muscle, the person develops abnormal faulty
posture before experiencing pain.