Unlike other studies reporting atrophy during LBP (Parkkola et al., 1993; Hides et al., 1994; Danneels et al., 2000; Barker et al., 2004), we were not able to reveal differences in total or lean muscle CSA during remission of recurrent LBP. We speculate that muscle size was not reduced, or, had recovered in this specific population. Support for recovery from atrophy is provided by associations showing that 62 and 64% (R2 = 0.623; R2 = 0.640) of the variance in lean and total CSA, respectively, can be explained by the time

selleck chemical elapsed between testing and previous LBP episode (mean: 64, min: 31, max: 144 days). This finding appears in contrast to Hides et al. (1996), who observed no alteration in localized MF asymmetry after about 42 pain-free days. In addition to the methodological differences discussed above, our association was irrespective of pain side, muscle or selleck level and observed in a wider timeframe. Further longitudinal research

of the natural course of lumbar muscle morphometry during resolution of LBP is needed. Below, several hypotheses for decreased lumbar muscle size in relation to LBP are discussed in view of our lack of atrophy during remission of LBP. First, atrophy may result from muscular disuse e.g. general deconditioning and local disuse (altered recruitment) (Hides et al., 1994; Danneels et al., 2000; Hodges et al., 2006). With regard to conditioning status, both groups had similar scores for physical activity, comparable to scores from young adults filipin (Baecke et al., 1982). Altered recruitment of muscles cannot be discounted as there is evidence for decreased (Macdonald et al., 2009), unchanged (Macdonald et al., 2010) and increased (Macdonald et al., 2011; D’Hooge et al., in press) MF recruitment during remission of recurrent LBP. Second, experimentally-induced spinal injury

(disc and nerve root lesion) has been shown to cause specific patterns of muscle wasting in the porcine MF within 3 days of the lesion (Hodges et al., 2006). It is not known what muscular replications can particularly be expected from non-specific LBP, 64 days at average after LBP resolution. Third, if peripheral nociception would reduce muscle CSA directly, this could contribute to marked differences observed during LBP compared to less conclusive evidence during LBP remission. Further research that investigates the isolated effect of nociception on lumbar muscle size may be able to confirm this hypothesis. MFIs in lean muscle tissue were increased during remission of LBP, which reflects increased relative amounts of intramuscular lipids (Elliott et al., 2010). The extent of lean fatty infiltration was generalized rather than localized (multiple muscles and levels, both previously painful and non-painful sides). The main causes of fatty infiltration are muscular disuse and spinal injury, similar to the causes of atrophy (Elliott et al., 2006; Hodges et al., 2006).