Our goal was to investigate gender differences in paraspinal reflex latency in an effort to improve our understanding of the gender disparity in LBP. Following trunk flexion perturbations, females responded with shorter latencies than males. They also exhibited a faster maximum trunk flexion velocity, which was not unexpected due to a smaller trunk mass in females than males. When controlling for this gender difference in maximum trunk flexion velocity, latency remained shorter in females than in males. Based upon the longer latencies reported in the injured lower back (Radebold et al., 2000
, Radebold et al., 2001
, Wilder et al., 1996
), these results do not appear to support the notion that gender differences in paraspinal reflex latency alone directly contribute to gender differences in LBP.
Our reflex latencies of 48 ms for females and 60 ms for males are comparable to previous studies. Paraspinal reflex latencies have been reported as 68 ms for females and 65 ms for males (Granata et al., 2005
) as well as 69 ms (Radebold et al., 2000
) and 63 ms (Radebold et al., 2001
) for healthy control groups including both males and females. While these values agree in a broad sense, some differences between studies are likely due to methodological differences. Granata et al. (2005)
, for example, had participants hold an extension preload and applied short stochastic force perturbations to flex the trunk using a motor. Radebold et al. (2000
suddenly released the resisting forces of isometric contractions, resulting in abrupt trunk flexion. In general, reflex responses are reported as having a monosynaptic stretch reflex ranging in latency from 30-50 ms and a functional polysynaptic reflex ranging from 50-80 ms (Matthews, 1991
, Schmidt and Wrisberg, 2008
). Although these ranges are generalized, our muscle activity was measured at the spinal level, so it appears that these reflexes are polysynaptic.
Our gender differences are inconsistent with previous investigations of paraspinal reflex latencies, but are consistent with gender differences in other muscles. Wilder et al. (1996)
reported longer paraspinal latencies in females, yet this was a main effect of gender and could be confounded by the statistical interaction between gender and rehabilitation. Specifically, males decreased their reflex latency more than females following a rehabilitation program, but gender differences prior to the rehabilitation protocol were not reported. Granata et al. (2005)
reported no gender differences in paraspinal reflex latency while participants held various trunk extension preloads. A preload exertion could reduce the need for quicker reflexes by stiffening the spine (Lee et al., 2007
) and potentially mask gender differences in reflex latency. In fact, longer paraspinal latencies have been observed within gender for a preload condition versus no preload prior to perturbation (Granata et al., 2004
). Despite the inconsistency between these two studies and ours, the 16.4% shorter reflex latency in females reported here is consistent with shorter reflex latencies observed in females in other muscles where experimental procedure did not appear to confound reflex measurements and perturbation kinematics were similar between genders. These include the posterior neck musculature during a whiplash movement where reflex latency was 8% shorter in females than in males (Siegmund et al., 2003
), as well as the medial/lateral quadriceps following internal/external knee rotation perturbations where reflex latency (i.e. of the medial quadriceps with external knee rotation) was 12% shorter in females than in males (Shultz et al., 2001
As described earlier, females are more prone to LBP than males (MacDonald et al., 1997
). Since LBP is associated with longer paraspinal reflex latencies (Radebold et al., 2001
), it would seem intuitive for females to exhibit longer paraspinal reflex latencies than males if longer latencies contribute to LBP. However, we found that females exhibited shorter
paraspinal reflex latencies than males. This suggests that something other than, or in addition to, reflex latency is contributing to LBP. It is possible that the shorter reflexes latencies in females, which would seem to be beneficial from a control perspective, could be compensating for or offset by some other factor within the control of spinal stability. For example, passive trunk stiffness could vary between genders, influencing reflex latency and/or other reflexive parameters. In response to a perturbation, decreased passive stiffness in the spine would cause the active tissues to stretch sooner and thus elicit a reflex earlier. This has been observed in the cervical spine with females exhibiting decreased passive stiffness (McGill et al., 1994
) and shorter reflex latencies (Siegmund et al., 2003
). Similar gender differences in passive stiffness could exist in the lumbar region. Such gender differences in passive trunk stiffness could involve gender differences in the “neutral zone” of the spine, i.e. the region of intersegmental motion with minimal passive resistance (Panjabi, 1992b
). A larger neutral zone would allow for greater trunk movement before passive (and active) tissues stretch. Additional research is necessary to clarify the roles of all factors contributing to spinal stability control, and to understand the causes for gender differences in LBP.
It is also possible that the longer paraspinal reflex latencies associated with LBP (Radebold et al., 2001
) may not have contributed to the development of LBP, but instead developed as a consequence to LBP. If so, it would be inappropriate to expect females, or any group predisposed to LBP, to exhibit longer paraspinal reflex latencies. The idea of longer reflex latencies as a result of LBP is supported by additional behaviors and characteristics that have been observed in LBP patients. For example, LBP patients have higher baseline EMG levels than healthy individuals in a normal upright stance (Wilder et al., 1996
). Based on these findings, the authors hypothesized this might be a mechanism constantly utilized to help stabilize the back by increasing muscle stiffness, but with the undesirable effect of increasing neuromuscular fatigue in the paraspinal musculature. Therefore, the characteristics seen in LBP patients’ such as decreased reflex magnitudes (Wilder et al., 1996
) and poorer performance in trunk balancing tasks (Radebold et al., 2001
), as well as delayed or longer reflex latencies (Radebold et al., 2000
, Radebold et al., 2001
, Wilder et al., 1996
), could be influenced by this constant fatiguing stabilization.
Several limitations of this study warrant discussion. First, this study focused on paraspinal reflex latency, which is only one component of multiple biomechanical mechanisms that contribute to spinal stability. Other mechanisms may have larger roles in the gender difference in LBP. Second, reflex magnitude can have a large influence on the contribution of reflexes to the control of spinal stability in addition to reflex latency. However, reflex magnitude was not investigated here due to potential habituation of reflex responses with repeated perturbations (reflex magnitude reduces following repeated perturbations (Siegmund et al., 2003
), yet reflex latency is unaffected (Blouin et al., 2003
, Siegmund et al., 2003
)). Third, maximum trunk flexion velocity was used to quantify the trunk kinematics that elicited paraspinal reflexes due to difficulties in determining the actual trunk flexion velocity (i.e. muscle stretching velocity). While the timing of maximum trunk flexion velocity lags reflex latency by about 80ms, we felt the use of this proxy was reasonable for quantifying trunk kinematics since the time span from perturbation impulse to maximum trunk flexion velocity did not vary between genders (P
=0.94). Fourth, trunk angle was measured at the T6/T8 level and used to determine trunk flexion velocity while reflexes were collected at L3/L4. Because of the motion of multiple spinal joints, subtle differences in flexion kinematics could exist between where the angular position was measured and where the reflexes were detected. Fifth, the pelvic angle in the initial testing position was not measured. As such, we cannot rule out slight differences between males and females in initial pelvic tilt during testing. Sixth, only right ES EMG was utilized because the task was sagittally-symmetric. Previous work reported symmetry in paraspinal reflexes using a similar perturbation protocol (Granata et al., 2004
). Lastly, our muscle activity threshold of two standard deviations above baseline that was used to detect the onset of the reflex response was relatively arbitrary, but has been used elsewhere (e.g. Granata et al., 2004
). While the choice of this threshold may have influenced our specific reflex latency values, it would not have compromised our comparison between males and females.