One could reasonably expect that if a muscle activation deficit was consistently contributing to pain or activity restriction in the broad population of people with LBP, improvements in pain and activity level would occur in conjunction with improvement in that muscle deficit.
This weakness is partly due to an ongoing muscle activation deficit characterised by an inability of supraspinal pathways to voluntarily drive the quadriceps muscle, known as arthrogenic muscle inhibition (AMI) (for a review see [ 1]).
Internal model deficits, combined with other known deficits such as postural muscles activation timing deficits, may exacerbate the balance impairment in children with DCD.
Clinical symptoms of impaired muscle function can either be related to an impairment of muscle activation, leading to both deficit (or negative) symptoms (e.g. paresis, loss of voluntary selective motor control) and excess (or positive) symptoms (e.g. spasticity), or to a change in biomechanical properties of muscles and connective tissues [ 4].
IntraMF has been correlated with deficits in central muscle activation [ 46], increased risk of future mobility loss [ 47, 48], and insulin resistance [ 49] in the elderly population.
Furthermore, in severe knee OA, deficits in volitional muscle activation contribute more to quadriceps weakness than muscle atrophy, and this may limit the effectiveness of volitional training programs [ 7].
Biofeedback studies focusing on inappropriate muscle activation and force adoption suggest that visual biofeedback of muscle activity can help to reduce excess muscle activation [23].
The analysis of the muscle forces showed realistic muscle activation with increased muscle synergy in the active pulley model.
There is limited work investigating neuromuscular deficits in the early stages of OA development; our data indicate that alterations in muscle activation patterns and postural sway do occur in these subjects when compared with age- and gender-matched control subjects.
