Active end-range

The active end-range is predominantly determined by the contraction forces generated by the muscles and the resistance from the antagonistic tissues. As movement approaches the end-range the agonist muscle’s contraction force tends to diminish progressively while, conversely, the passive resistance from antagonistic tissues tends to rise (Fig. 2.2).

In most joints, the passive ROM is a measure of the individual’s tolerance to discomfort or pain and not a true measure of range (Fig. 2.1). If you pull your index finger into extension the end-range will be determined by how much you can tolerate discomfort or pain (see stretch tolerance, Ch. 10). If a goniometer was at hand this position would be measured as the full extension range. However, the extension range would increase further if we were to anaesthetize the area and apply a greater force. So the painful range does not necessarily represent the full biomechanical range. This would apply to joints in which end-ranges are limited by soft-tissue resistance such as the spine, shoulder, hip and ankle, but not where there is bony apposition, such as in elbow extension.

So passive end-range is determined by stretch tolerance, which, by itself, can be highly variable and influenced by numerous factors. For example, sensitivity has natural variations during the day; a stretch performed with discomfort in the morning may be easier in the evening. An individual who stretches regularly will often complain of “good” and “bad” agility days. Sensitivity can change transiently simply as a result of repeating the same movement several times. Stretch the index finger into extension and then repeat it. On the second stretch you will find that it extends further with less discomfort (see creep deformation, Ch. 4). This means that the passive end-range is a vague clinical construct, highly variable and not an absolute measurement as we are often led to believe.⁶

ROM and sensitivity

End-ranges become even more blurred in conditions in which ROM losses are accompanied by pain and sensitization. In these conditions there is reduced tolerance to stretching and the experience of pain and stiffness determines the end-ranges. As a consequence, passive and active ROM losses can be due to elevated stretch sensitivity, but without physical changes in the length or stiffness of the tissues. For example, patients with low back pain often complain of increased spinal and hamstring stiffness in forward bending. However, they have the same flexion ROM as asymptomatic individuals.^7–10 Hence, stretching the back and the legs, a common exercise given to patients with chronic back pain, is unlikely to have any therapeutic value (since nothing is short, it just feels like it).

The variability of tolerance can complicate and add uncertainty to ROM assessment and treatment. We can never be sure how much of the ROM loss is due to “real” biomechanical limitations or is simply because the patient cannot tolerate the discomfort. Furthermore, because the end-range is experiential and not a mechanical phenomenon it provides inaccurate feedback during stretching; it can be difficult to determine how much force to use during stretching. If the area is highly sensitized the patient may terminate the stretching long before it reaches effective levels. Pain and sensitivity can also confuse the treatment progression. Unpredictable adverse reactions and fluctuating sensitivity can overshadow positive biological–adaptive ROM changes. A further discussion of this topic can be found in Chapters 9 and 10.