prime mover of the limb (9). This indicates that the contraction
of TrA may have been mediated by afferent input
from the movement and not as a component of the feedforward
postural response (9). The onset of TrA in our
long-standing groin pain population, although delayed, occurred
less than 50 ms after the onset of the prime mover of
the limb and, therefore, still occurred within the feed-forward
criteria. Thus, with a perturbation to the pelvic ring
caused by an ASLR, the contraction of TrA must still be
preprogrammed by the CNS, although delayed. This is consistent
with studies investigating the effect of a lower-limb
perturbation in an LBP population (9).
The findings are also consistent with O’Sullivan et al.
(17), who investigated motor-control strategies of individuals
with a diagnosis of sacroiliac joint pain. O’Sullivan et
al. (17) used the ASLR task to perturb the pelvic ring, and
found altered motor-control strategies in individuals with
sacroiliac joint pain. Although these authors did not specifically
measure TrA EMG activity, their finding that aberrant
movement of the pelvic floor was associated with sacroiliac
joint pain supports our findings of altered neuromotor control
of the lumbo-pelvic system in response to a perturbation
invoked by the ASLR task in individuals with long-standing
groin pain.
Due to the cross-sectional design of our study, it is not
possible to establish whether the delay in onset of EMG of
TrA in the long-standing groin pain population was present
before the onset of pain and could thus be seen as a causative
factor or, conversely, if the timing alteration has occurred
as a result of the presence of pain and dysfunction
associated with the condition. It is also not possible to
establish the mechanism of delay. There are a number of
potential mechanisms for the delay, including reflex inhibition
due to effusion (2,24), ligament stretch, or capsular
compression (3). At the sacroiliac joint, it has been demonstrated
in a porcine model that stimulation of joint afferents
affects lumbar muscle function (14). It is also possible that
the presence of pain resulted in the aberrant motor control of
TrA. Hodges et al. (7) demonstrated that acute experimentally
induced pain consistently impaired the feed-forward
response of TrA. Furthermore, it is important to note that the
consequence of such a delay in TrA activity cannot be
established from the present study.
The finding of a delay in TrA in long-standing groin pain
subjects is also important in that it provides support for
current physiotherapy management of long-standing groin
pain in Australia. The current treatment regime used by
physiotherapists at most Australian Football League clubs is
based on the work of Richardson et al. (21), and has been
adapted to long-standing groin pain by Hogan (11). This
program is based on restoring neuromotor control of the TrA
with the premise that it contributes to the stabilization of the
pelvic ring.