What is muscle imbalance?

As physiotherapists, we need to be able to differentiate between what is considered a ‘normal’ (or ‘expected’) range of motion (ROM) and that which is deemed ‘abnormal’ – either hypo- or hypermobility – along with which structures may produce or restrict the range of motion. It must be noted that there may also be an underlying predisposition – or pathology – for hypo-/hypermobility, as in the case of connective tissue conditions, such as ankylosing spondylitis and hypermobility syndrome (see Figure 14.1) (as distinct from a joint demonstrating hypermobility), or neurological conditions, such as multiple sclerosis. However, it is outwith the scope of this chapter to discuss these specific pathological causes.

Muscle imbalance can be either ‘passive’ or ‘active’; passive being identified by muscle length and strength being either less or more than the ideal, and active being identified when one of a synergistic pair of muscles predominates during the movement (Sahrmann 1987). The resultant functional and structural changes in the muscle appear to be reversible, suggesting that exercise to facilitate muscle length changes will be useful in the management of movement dysfunction (Gossman et al. 1982).

Perhaps it is worth reviewing the general characteristics, function and roles of muscles first. Muscles can act as prime movers, or agonists, if they are primarily responsible for producing movement. Their direct opposites are antagonists, which do not normally oppose movement, but have the potential to do so if they are not inhibited; for example, when flexing the elbow, biceps brachii is the agonist whilst the triceps is the antagonist (relaxed, via reciprocal inhibition). Co-contraction of muscles is possible, which can assist movement and/or stabilise. When this occurs to assist the movement produced by the agonist, those muscles are said to be working as synergists (see the example of the scapular force couple in the shoulder section). When muscles contract to stabilise a joint and control the position of the origin of an agonist, they are known as fixators (or stabilisers, i.e. in the case of elbow flexion as above, the fixators would be those that stabilise, or fixate, the shoulder, such as the rotator cuff).

These descriptions are all well and good, but, unfortunately, prove rather inadequate when it comes to explaining more dynamic, complex movements. Therefore, further classification of the role of muscles has been attempted by various authors according to their anatomy, architecture, fibre type and function, as summarised in Table 14.1. To simplify, some muscles exhibit a tendency to be more stabilising (i.e. multifidius in the spine) or mobilising in their function (i.e. erector spinae), although there are also some that demonstrate characteristics of both and can ‘multitask’ their role depending on the demands placed upon them at the time. Examples of the latter include the vasti muscles of the quadriceps and soleus. Throughout this chapter, muscles will be discussed in relation to their functional role as local and global stabilisers, or global mobilisers.

Problems may occur when, for example, a predominantly stabilising muscle is injured or dysfunctional, leading to instability and altered joint biomechanics, increased strain on structures, such as joint surfaces, and pain. Muscles with a predominantly mobilising role can be used as temporary stabilisers, but as their anatomy and physiology does not lend themselves to this, this may lead to overuse, fatigue and pain. It has been suggested that myofascial trigger points (taut, irritable bands within muscles resulting from overuse) may develop as a result (Simons et al. 1999; Fernández-de-las-Peñas et al. 2006) and which can perpetuate the muscle imbalance through further pain and resultant inhibition.

Therefore, in short, if muscle imbalance is present and the muscles are unable to fulfil their role correctly, this can be through either being unable to stabilise or induce/permit movement because one or more are either too weakened and/or lengthened, or too over-active and/or shortened.

Stability

Additionally, the term ‘stability’, particularly ‘core stability’, has also become synonymous with approaches to dealing with muscle imbalance of the spine, especially in the lumbar spine. Confusion can arise with this term, particularly when used very specifically by one group of professionals to be more than merely a descriptive state; when is someone or something stable or unstable, what makes someone or something stable/unstable? For example, an orthopaedic surgeon may well be focussing on the bony congruency or ligamentous support at a spinal segment and any trauma or pathology associated with this (as in spondylolithesis) as the cause of instability. Conversely, a physiotherapist, unless assessment suggests otherwise, may be concerned with the quality of the spinal movement, any associated/compensatory movements and the support of the muscles to stabilise the movement. Therefore, the stability of the spine, in this example, is dependent on a number of factors. Figure 14.2 demonstrates a basic model of stability that considers the interplay of the principal systems involved (Panjabi 1992a, 1992b, 2003).

Panjabi (1992a, 1992b, 2003) additionally discusses control of the neutral zone: the area (or zone) around the segment’s neutral position where there is little resistance offered by the passive restraints in response to a small range of displacement (see Figure 14.3). Although originally related to the spine, this model can be applied equally to the appendicular, as well as the axial skeleton, when considering the interplay of the subsystems. This control of the neutral zone can be disturbed locally by the dysfunction of recruitment and motor control of the deep segmental stabilisers, and globally by an imbalance between the mono-articular stabilising muscles and the bi-articular mobilising muscles (Comerford and Mottram 2001). It is hypothesised that an increase in the size of the neutral zone (therefore decreased ‘stability’ or increased ‘instability’, if you like) correlates with pain and dysfunction (and possibly could be caused by either); correspondingly, decreasing the neutral zone may decrease pain and dysfunction (Panjabi 2003). However, it must be noted that the clinical reality is rarely this straightforward and is usually multifactorial (see Chapter 17)!

Motor control

Stabilisation requires automatic recruitment of the muscles surrounding the joint. This requires appropriate co-activation of muscles, the application of appropriate levels of force for the task in hand and appropriate timing of the muscles (Richardson 1992). Normally, the mono-articular stabilisers should activate earlier than the multi-articular mobiliser synergists – a feed-forward mechanism. This co-ordinated activity involves sensory strategies through feedback from the joint and ligament afferents, and muscle spindle activity, along with biomechanical, motor processing strategies and learned behaviour that anticipates change (Comerford and Mottram 2001).

Motor units (the motor neurone and the muscle fibres it innervates) contain the same type of fibre so that there are, pragmatically, two main types: slow (tonic, type I fibres) motor units and fast (phasic, type II fibres) motor units. Therefore, slow motor units have a slow speed of contraction, low contraction force and are fatigue resistant compared with fast motor units. Slow motor units are recruited primarily at low loads of less than 25% of maximum voluntary contraction (MVC) and fast motor units are recruited at higher loads (Gibbons and Comerford 2001). Therefore, the recruitment of slow motor units, and use of muscles with high proportions of these is necessary for optimal stabilisation. When mobiliser muscles, which contain high proportions of fast motor units are utilised as compensation for stabiliser dysfunction, degradation of the fine control results along with fatigue and potentially pain and spasm if then over-used.

However, biased recruitment of shortened muscles can be a problem. It is suggested that short muscles are recruited more easily than their lengthened synergists (Sahrmann 1987). This may be owing, mechanically, to the increased overlap of actin and myosin (as in the sliding filament theory, below) leading to an increase in the intrinsic ‘stiffness’ of the muscle and readiness for activation, and owing, neurologically, to the increased excitability of the alpha motor neurone pool facilitated by the increased tension and activity of the muscle spindle afferents (Comerford and Mottram 2001).

There is evidence to suggest that the reduction of proprioceptive input during sustained low-load contractions from the muscle spindle changes the recruitment order of the motor neurones and the normal dominance of the local stabilisers (Grimby and Hannerz 1976, cited in Comerford and Mottram 2001). Janda (as discussed by Comerford and Mottram (2001)), identified and quantified recruitment and sequencing differences between synergistic muscle groups in functional movement. From this, he was able to identify a consistent recruitment pattern in asymptomatic individuals and also characteristic abnormal patterns in symptomatic individuals. Similar evidence has been identified by several authors in relation to individuals with impingement symptoms of the shoulder (Ludewig and Cook 2000; Cools et al. 2003), cervicogenic headaches (Jull et al. 1999) or patellofemoral pain (McConnell 1996).

Muscle length adaptations

Several theories exist relating to the relationship between muscle length and strength (Sahrmann 1987), and are listed below.

Stretch weakness

It is suggested that stretch weakness occurs when a muscle is maintained in an elongated position beyond its neutral physiological rest position but not beyond the normal range of muscle length (Gossman et al. 1982). Examples of this may be weakness of the dorsiflexors in a bedridden patient when held in a lengthened position owing to the weight of the bed clothes holding the foot in a plantar flexed position. Equally, prolonged postural strain, such as drooping shoulders with elongation of the middle and lower trapezii, can lead to stretch weakness.

Positional weakness and length associated changes

When a muscle is immobilised in a lengthened or shortened position, the muscle adapts in order to either increase or decrease the number of sarcomeres respectively. This change in number allows for a change in sarcomere length to one that gives maximum overlap of actin and myosin for optimum cross bridge formation and the ability of the muscle to achieve maximum tension in the immobilised position (Williams and Goldspink 1978). These adaptations appear to differ with age, occurring primarily in the tendon in young people rather than muscle (Gossman et al. 1982), such that immobilisation in a lengthened position leads to elongated tendon and shorter muscle belly with a reduction in the number of sarcomeres in the muscle belly.

Williams and Goldspink (1984) also demonstrated changes in the connective tissue of the muscle when a muscle was immobilised in a shortened position. It is generally thought that muscle has a parallel elastic component (primarily from the perimyseum, but also the epimyseum) to the active contractile element. This parallel elastic component is thought to distribute forces associated with the passive stretch of the muscle and maintain the relative position of the fibres. In a muscle immobilised in a shortened position the increase in connective tissue is likely to result in an increase in muscle stiffness and reduced elasticity of the muscle.

Similar changes may occur when a muscle works at a shorter length (Williams and Goldspink 1984) and it should be noted that normal, transient changes in muscle length, as part of movement and positioning, will affect the tension that can be developed, as demonstrated by the sliding filament theory and the muscle length tension curve (Figure 14.4).

In addition, where a muscle is bi-/multi-articulate, then active and passive insufficiency can occur. Active insufficiency is the inability of a bi-/multi-articulate muscle to generate enough tension in a shortened position, where the position of one joint affects the tension of the muscle at the other. A classic example is the hamstrings: if you stand with your knees extended and your hips flexed (i.e. in a bow), the hamstrings are able to extend your hips/pelvis to raise your body upright, but if you do the same starting with your knees flexed, your hamstrings are disadvantaged and you rely on your gluteus maximus. The same occurs with the finger flexors if you try to flex the fingers to make a fist with your wrist fully flexed (although here you also encounter passive insufficiency), whereby the wrist extensors are fully lengthened across two or more joints (the wrist, metacarpalpharangeal and interpharangeal joints).

Relative flexibility and relative stiffness

‘Relative stiffness’ as described by White and Sahrmann (1994) in one segment will require flexibility in an adjacent area to gain functional movement. This relative stiffness can occur as discussed above in a shortened muscle, but also when the passive structures around the joint (capsule and ligament) or the joint surfaces themselves become restricted in their movement. An example of this might be an adhesive capsulitis of the glenohumeral joint; restriction of the capsule around the joint causes limitation of abduction resulting in hypermobility of the scapulo-thoracic joint to gain movement and hence lengthening of the stabilising muscles of the scapula on the chest wall. Similarly, ‘relative flexibility’ (White and Sahrmann 1994) can occur where mono-articular muscles are unable to adequately shorten, so are lengthened, strained or weak and allow excessive motion at the joint they act upon. This increase in mobility has obvious implications on initiating pathology. This relative stiffness and flexibility gives rise to the concept of ‘give and restriction’, as discussed by Comerford and Mottram (2001).

Treatment, intervention and management principles

As well as the theory described in this chapter, it must be noted that there are other factors to consider in order to determine the most effective and efficient intervention, such as psychosocial influences, age and comorbidities. Consideration also needs to be given to the patient’s expectations. Are the function and demands they expect to place upon themselves compatible with attaining/maintaining ‘muscle balance’?

The physiological parameters already discussed should inform your treatment decisions. Table 14.3 provides an overview of management principles.

In practice, there is an additional consideration and experiential, anecdotal phenomenon, which is important to consider for the life-busy (perceived or actual) patient who is at risk of non-compliance of rehabilitation if the programme is too time-consuming. Well-intended programmes have been known to be overloaded and discontinued if it becomes too much and so it may be prudent to withhold some lower priority rehabilitation for a later date and introduce as proven necessary.

The Lumbo-pelvic region

The lumbo-pelvic region has seen a significant amount of research and debate as to the role of the muscles in relation to lower back pain, which should not be surprising considering how common lower back pain is. However, it remains a complicated area and so it is beyond the scope of this chapter to consider all muscles and potential permutations of imbalance. As transversus abdominis (TrA) has received considerable interest both in the literature and clinical environment, this will be the focus as a template approach for the physiotherapist to consider in practice. Table 14.4 lists the main muscles acting on the lumbo-pelvis with their respective primary functional role.

Table 14.4

The main lumbo-pelvic mobiliser and stabiliser muscles

Muscle	Primary muscle role
Transversus abdominis	Local stabiliser
Multifidus	Local stabiliser (deep intersegmental fibres)
	Global stabiliser (superficial fibres)
Rectus abdominis	Mobiliser
External oblique	Global stabiliser
	Mobiliser
Internal oblique	Local stabiliser
	Mobiliser
Erector spinae	Mobiliser

The concept of ‘core stability’ and muscular stabilisation of the lumbar spine has derived from Panjabi’s (1992a, 1992b, 2003) model of the three subsystems described previously. With reference to the passive subsystem, the lumbar spine appears to be at a disadvantage, ‘sandwiched’ between the inherently more stable thoracic spine (via the rib cage) and pelvis (see Figure 14.5). Therefore, whilst the lumbar vertebrae and intervertebral discs are the largest and strongest in the spine, further support and control is required, but, as you will see in Figure 14.5, TrA, along with the multifidus, diaphragm and pelvic floor, appear to form a ‘box’ (or more aptly, a corset). The diaphragm and pelvic floor appear to contribute mainly through increasing intra-abdominal pressure and restricting the movement of the viscera (Richardson et al. 2004).

Transversus abdominis (TrA)

TrA is the deepest of the abdominal muscles (Figure 14.6). The direction of the muscle fibres runs horizontally medially from the lateral attachments of the internal surface of the six lowest ribs, the thoracolumbar fascia, internal surface of the iliac crest and the lateral third of the inguinal ligament to the sheath of rectus abdominis (Ombregt et al. 2003; Standring 2005). It can be seen from the attachments how contraction can mechanically increase intra-abdominal pressure and thus stabilise the lumbar spine, although it does not act alone, as co-contraction with multifidus is also thought to occur (Richardson et al. 2002, 2004). When considering this action, it is easy to understand how dysfunction may lead to pathological signs and symptoms, and subjects with low back pain have been shown to demonstrate delay and inhibition of contraction compared with asymptomatic subjects (Richardson et al. 2002, 2004).

It is widely accepted that TrA provides support for the abdominal contents and it has been demonstrated through research that it provides indirect stability for the lumbosacral spine and sacroiliac joints (Richardson et al. 2002, 2004). The associated levers of the pelvis and spine arising from these joints must be remembered together, with further consideration when relating TrA structure to its function and the stabilising of the pelvic postero-anterior lever in neutral; in other words, maintaining an antero-posteriorly neutral pelvic level.

Most of the literature explains how the pelvis is stabilised in the neutral position by the indirect stabilising role on the lumbo-sacral and sacroiliac joints, but it can be argued that the pelvis is stabilised in neutral on the spine and prevented from anteriorly tilting directly anatomically through the attachment to the pubis and indirectly via rectus abdominis.

Mechanically, transversus abdominis may have a direct role in maintaining pelvic neutral, producing a cephalic force on the anterior pelvis owing to the lower fibres of the muscle curving inferiorly and medially to attach to the pubic crest and pectineal line, along with the aponeurosis of internal oblique (Standring 2005). Further to this, if, on contraction, it places tension on the rectus abdominis, which in turn attaches to the costal cartilages and ribs superiorly and pubis inferiorly, it can be mechanically argued that transversus abdominis has an indirect role in stabilising and maintaining the pelvis in neutral relative to the spine. This, therefore, helps prevent anterior tilt of the pelvis. An anterior tilted pelvis can therefore present as a sign of transversus abdominis weakness and, from clinical experience, has been supported or accompanied by poor palpable contraction of the muscle. The same anterior tilted pelvis may be the causal link for increasing the lumbar lordosis and therefore be a source for causing mechanical back pain, for example through increased facet joint irritation from the resultant increased compression force production.

It is not only weakness that can lead to an anterior tilted pelvis. The lower fibres of TrA and all the fibres of rectus abdominis may adaptively lengthen over time, such as during pregnancy in women, for example. Also, through prolonged, repeated and sustained static posture in sitting there can be an over-compensatory posture with an anterior tilted pelvis and hyper-lordosis of the lumbar spine in an attempt to maintain a normal lumbar lordosis. This would be considered to be the adverse effects of the SAID principle (Selye 1951). In other words, unwanted adaptation to adverse imposed demand, such as lengthening of the abdominal muscle fibres and the anterior longitudinal ligament of the spine.

In the case of the former example, intervention would require, following confirmation through examination and analysis, recovery of the optimal length, contractibility and strength of the TrA muscle fibres; however, in the case of the latter, it would also require prevention in recurrence through changing postural habits. It has to be borne in mind that the above presentation may be asymptomatic initially and what transpires can be any other number of signs and symptoms of other secondary or tertiary problems, such as ‘knock-on’ cervico-thoracic or shoulder problems, but it is beyond the scope of this chapter to list or discuss all the potential problems that can arise from an anterior tilted pelvis through muscle imbalance.

Before considering further theory and research, the physiotherapist must also understand that it has also been argued in the literature (Richardson et al. 2002, 2004) that TrA can become non-functional as an inhibitory response to problems, such as mechanical low back pain. It is considered here that this may not be the order of events in all mechanical low back pain and it is difficult to research the order of events, as it would be necessary to have otherwise healthy subjects induce mechanical low back pain in order to determine if this is the point TrA switches off. Nevertheless, the physiotherapist can only treat what presents and in the presence of a non-functioning TrA the challenge is to rehabilitate the muscle.

As described above, the SOAPE process will be used for further illustration.

Subjective examination

The subjective reporting of pain may be evident and may be region specific over the lumbar spine with possible radiation into the glutei and lower limb, unilaterally or bilaterally.

Symptomology may occur in secondary areas both proximally and distally affecting the thoracic and cervical spine and upper and lower quadrants owing to the altered alignment of the lumbar spine posture and its knock-on effect on posture elsewhere. Signs and symptoms will need to be addressed but, equally, the other causations of an anteriorly tilted pelvis or associated and secondary lumbo-pelvic-hip complex problems would need investigating and correcting as necessary (see some examples in the non-exhaustive list in Table 14.5).

Table 14.5

Other contributors to the development of an anterior tilted pelvis and additional associated/secondary problems

Muscle	Problem	Additional associated/secondary problems
Iliopsoas	Too short/passive insufficiency causing anterior tilted pelvis	Increased lumbar lordosis and lumbar spinal dysfunctional restriction of lumbar flexion range of movement (ROM)
		Hip lateral rotational dysfunctional restriction of ROM, and shortening of internal rotators and adductors of the hip
		Hip extension dysfunctional restriction of ROM
		Shortening of other hip flexor, rectus femoris
		Shortening of other muscles of quadriceps femoris
		Medial knee joint stresses
Quadratus lumborum	Too short/passive insufficiency causing an increased lumbar lordosis and an anterior tilted pelvis	All of the above
		Plus, unilateral imbalance may cause rotation/torsion or lateral pelvic tilt
Multifidus	Weakness/lengthening or over-activity/shortening	Although acknowledged as segmental stabilisers, collectively they can contribute to the maintenance of abnormal posture if dysfunctional, such as hyperlordosis and therefore predispose to anterior tilt
NB: It should also be noted that muscles involving the lower limb, which also act on the pelvis need consideration, such as rectus femoris and the hamstrings (see Kendall et al. (2005) and others regarding postures such as the pelvic-crossed syndrome).

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