Abstract

Low back pain (LBP) is one of the most common health problems, which in 10-15% of patients progresses to develop into a chronic low back pain (CLBP) condition, bringing enormous psychological and financial costs to the affected individuals, their families and society as a whole. There are many theories – pure bio-medical, bio-mechanical, psychological, as well as poly-modal ones, attempting to explain the pathology and aetiology of CLBP and guide its treatment. Although there is a general consensus that CLBP, as many other chronic pain conditions, is heterogeneous in nature, involving both organic (bio-mechanical and physiological) and psycho-social factors, there is still not a definite answer to the exact interactions and causative links between these factors. The present study employed a 15 minutes moderate treadmill exercise intervention in 10 CLBP sufferers and 10 healthy controls in order to further clarify the interactions between these physiological, bio-mechanical and psychological factors. The results from the present study, in accordance with previous research confirmed that CLBP participants are clearly identifiable according to their affective and cognitive profile - CLBP participants reported significantly higher levels of Pain Catastrophising (t = 3.81, p = .003), as well as Depression (t = 2.35, p = .03). Although both Pain Catastrophising and Depression were significantly correlated with the background pain (r = .755, p < .001 and r = .559, p = .010 respectively) in the CLBP group alone, contrary to previous CLBP studies, there were no significant associations between the background pain level and duration, Depression, Anxiety, Stress and even Pain Catastrophising. The Negative affective (NA) state was measured dynamically throughout the experiment and was reduced non-significantly by the exercise in both groups. Surprisingly, The NA was very low – 18 to 20 on a scale of 15 to 75, in both groups (even lower in the CLBP) and there was no significant difference between the NA of the CLBP and Control groups at any time-point of the experiment. The ES and MF back muscles activity was measured using a static standing and fully bent forward ratio, as well as flexion-relaxation ratio (FRR) pre- and post-exercise. The present study's results, although less robust than the results from previous research, confirmed that both standing and fully bent forward ES and MF measures, as well as FRR distinguished CLBP from control participants – CLBP had a higher level of static muscle activity (significant for the pre-exercise right MF in fully bent down position t = -2.48, p = . 044) and reduced FRR (significant for the pre-exercise left ES – t = 3.09, p = .013 and post-exercise left ES and right MF – t = 2.33, p = .038; t = 2.73, p = .032 respectively). Although the exercise produced non significant improvement of the ES and MF muscle activity, it also produced a divergent pain intensity (PPI) response between different CLBP participants – 5 (55.56%) had a decrease in PPI, while 4 (44.44%) had an increase. The pain decrease sub-group exhibited only a mild back muscles dysfunction, characterised by increased activity of the ES and MF in resting state (muscle tension), combined with a higher negative cognitive and affective mental set. The main characteristics of the pain increase sub-group was abnormal ES and MF flexion-relaxation, which pointed to compensatory increased activity of the superficial back muscles due to possible intrinsic spinal instability. In conclusion, the moderate treadmill exercise, utilised in the present study, was capable of identifying the existence of CLBP sub-groups, which were otherwise undistinguishable by the rest of their background pain, psychological or muscle activity characteristics. The low back pain of one of the sub-groups was associated with primary psychological top-down dysfunction of the 'active system' (muscles), while in the second sub-group the principal underlying factor identified was primary organic bio-mechanical dysfunction of the 'passive system'. The possible mechanisms and implications of this dichotomous nature of CLBP in respect to its aetiology, diagnosis, treatment and further research are discussed.

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