To understand the concept of muscle imbalance and the implications of the alteration in muscle function, the neurophysiological components of muscle balance will be discussed first.

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 stabilizer 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). 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 immobilized position (Williams and Goldspink 1978). 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.


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