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SPINE Volume 29, Number 6, pp 628634 2004, Lippincott Williams & Wilkins, Inc.

Chronic Low Back Pain-Associated Paraspinal Muscle Dysfunction is not the Result of a Constitutionally Determined Adverse Fiber-type Composition
Kim Crossman, BSc, MCSP,* Mike Mahon, MSc, Paul J. Watson, PhD, MCSP,* Jacqueline A. Oldham, PhD, RGN, and Robert G. Cooper, MD, FRCP

Study Design. Investigative case control study. Objectives. To determine whether excessive paraspinal muscle fatigue in chronic low back pain results from a paucity of muscle type I ber content. Summary of Background Data. Paraspinal muscle function is vital for spinal protection. Prospective studies suggest that excessive paraspinal muscle fatigability may increase risk of rst-time low back pain. As contractile performance of the paraspinal muscles is governed by their constitutionally determined ber composition, the question arises whether a constitutionally determined adverse composition could predispose to low back pain through impaired spinal protection. Methods. Thirty-ve male patients with chronic low back pain were compared with 32 male control patients of similar age and anthropometry. During Sorensen and 60% of maximum voluntary isometric contraction fatigue tests, median frequency declines in the paraspinal muscle surface electromyograph signal were monitored and correlated with muscle histomorphometry. Results. Patients were weaker than controls during maximum voluntary isometric contractions (84.47 [28.44] vs. 98.74 [18.11] kg, respectively; P 0.02) and more fatigable during their Sorensen tests (endurance time 105.29 [28.53] vs. 137.50 [40.38] sec, respectively; P 0.01). There were no between-group differences in median frequency declines during the Sorensen (0.37 [0.16] vs. 0.36 [0.12]%.sec1) or 60% maximum voluntary isometric contraction (0.42 [0.31] vs. 0.51 [0.29]%.sec1) tests, for patients and controls, respectively. There were no between-group differences in the percent number of paraspinal muscle type I bers (64 [11] vs. 64 [9]%) or the percent area occupied by type I bers (67 [11] vs. 69 [9]%), for patients and controls, respectively. Type I and II muscle ber narrow diameters were similar for both groups. Conclusion. In the patients with chronic low back pain tested, their associated paraspinal muscle dysfunction

was not the result of a constitutionally determined adverse ber type composition. [Key words: low back pain, electromyography, paraspinal muscle, fatigue, histomorphometry] Spine 2004;29:628 634

From the *Musculoskeletal Research Group, School of Biological Sciences, and The Centre for Rehabilitation Science, University of Manchester, Manchester, and Rheumatic Diseases Centre, Hope Hospital, Salford, United Kingdom. Kim Crossman is supported by the Arthritis Research Campaign, UK. Acknowledgment date: March 21, 2003. First revision date: May 9, 2003. Second revision date: June 13, 2003. Acceptance date: June 13, 2003. The manuscript submitted does not contain information about medical device(s)/drug(s). Other funds (Arthritis Research Campaign) were received to support this work. No benets in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript. Address correspondence and reprint requests to Robert G. Cooper, MD, FRCP, Rheumatic Diseases Centre, First Floor, Clinical Sciences Building, Hope Hospital, Salford, M6 8HD, United Kingdom; E-mail:

Few clinicians would disagree that chronic LBP (CLBP) represents a major cause of disability and exerts detrimental socioeconomic effects on patients, their families, and society as a whole. The cause of chronic symptoms is often not apparent, despite careful clinical examination and detailed and appropriate modern radiology. The role of the paraspinal muscles has thus come under scrutiny, as these structures extrinsically stabilize the lumbar spine, thereby protecting the noncontractile spinal elements from potentially damaging stresses. Considerable evidence demonstrates that the paraspinal muscles of patients with CLBP are both weak1,2 and excessively fatigable,312 and in their discussions, these studies often suggested that, by impairing spinal stability, paraspinal muscle dysfunction had contributed to causing the LBP. Without saying so, these studies thus implied a primary role for paraspinal muscle dysfunction in LBP symptom generation. Indeed, the results of prospective population studies in normal patients appear to support this notion by demonstrating that poor paraspinal muscle endurance (assessed in terms of time to exhaustion during voluntary isometric back extensions) increases the risk for developing rst-time LBP.4,13 In none of these studies were any mechanisms offered up to explain how normal paraspinal muscle could dysfunction to predispose to LBP. Compressive or iatrogenic radicular damage, and reex inhibition of motor activation, could cause paraspinal muscle atrophy, but this would be expected to be severe and localized.14 However, in those radiologic studies conrming CLBP-associated paraspinal muscle atrophy, this appeared mild and symmetrical, and no greater than that observed in the psoas muscles of the same patients.15 Other studies demonstrated that patients with CLBP develop back, abdominal, hamstring, and quadriceps muscle weakness of a similar degree in all the muscles.16 Such results clearly suggested that CLBPassociated paraspinal muscle dysfunction is secondary rather than primary and the result of general deconditioning. An explanation of the discrepancies between the conclusions from these studies regarding the role of paraspinal muscle in CLBP may lie in the muscle assessment


Paraspinal Muscle Fatigue in Chronic LBP Crossman et al 629

methods used, i.e., voluntary contractions whose performance would have been inuenced by psychologic factors relating to volition. It is now possible to overcome such volitional difculties in the interpretation of voluntary performance tests by using electromyographic (EMG) methods of fatigue assessment. These monitor time-dependent changes in the EMG signal during brief submaximal isometric contractions5 rather than by endurance to exhaustion times. In particular, the median frequency (MF) decline rate has been validated as an objective measure of muscle fatigue.6 Many studies have demonstrated greater paraspinal muscle MF declines in patients with CLBP than in normal patients,7,8,10,11,17,18 and some authors speculated that this abnormality was the result of architectural differences within the muscle, e.g., of ber-type composition.7,9 Whether a muscle ber is phenotypically type I or II is dictated by the stimulation characteristics of its motor efferents,19 whereas muscle ber-type composition cannot be altered through voluntary activity alone. Neural drive characteristics and the ber-type composition thus appear constitutionally set parameters.20 It seems accepted that muscles with a high type II ber content are relatively strong, but they resist fatigue less well than those containing proportionally more type I bers.21 A recent paraspinal muscle study of normal patients also suggested that fatigueinduced MF declines correlated well with type I ber content, and demonstrated that the greater the type I ber content, the more fatigue resistant the muscle.22 An important question arising from these observations is whether the poor paraspinal muscle endurance times and rapid MF declines previously documented in patients with CLBP were due to a low type I ber content. If so, selective type I ber atrophy appears an unlikely cause because, to date, all histologic studies demonstrating paraspinal muscle ber atrophy in patients with CLBP conrm that it preferentially affects type II bers.23,24 If, in the absence of type I ber atrophy, CLBP-associated paraspinal muscle dysfunction is associated with a reduced type I ber content, it follows that this would be due to a constitutionally determined type I ber paucity. This would translate into an intrinsic liability to excess paraspinal muscle fatigue, and it is intriguing to speculate that this could have predisposed to spinal damage, and hence to the development of the LBP. In view of the discrepant conclusions highlighted, and such speculations regarding an etiologic role for the paraspinal muscles in LBP symptom generation, this study aims to determine whether the excessive paraspinal muscle fatigue seen in patients with CLBP reects a paucity in their paraspinal muscle type I ber content. Materials and Methods Overall Study Protocol. Patients attended 2 sessions with at least 3 days between each to ensure full recovery from testinduced fatigue. On the rst visit, anthropometric details were recorded. After familiarization with the test equipment and procedures, patients paraspinal muscle maximum voluntary

isometric contraction (MVIC) force was measured. After a 5-minute rest, patients then undertook an antigravity isometric fatigue test (Sorensen) to exhaustion. On the second visit, an MVIC was repeated, and after a 5-minute rest, patients then undertook a further 60-second upright isometric fatigue test set at 60% of MVIC (60% MVIC test). Paraspinal muscle EMG output was monitored during these fatigue tests. Patients underwent a paraspinal muscle biopsy at the end of the second visit.

Study Patients. As gender differences exist for paraspinal muscle performance tests,4,8 and to a lesser extent paraspinal muscle ber-type composition,2528 only male patients aged 18 55 years were recruited for this study. Thirty-ve males with CLBP (i.e., 6 months continual or recurrent LBP) were recruited through hospital and community physiotherapy departments and through a local newspaper advertisement. They were compared with 32 normal patients without signicant LBP, i.e., no episode lasting more than 3 days or of sufcient severity to cause work absence in the previous 12 months. Normal controls were recruited from hospital medical, nonmedical, and scientic staff. The patient numbers required for the study were derived from the results of a previous investigation.22 The power calculation assumed that, in the proposed study, fatigue-induced MF declines in patients with CLBP would be correlated with the underlying muscle ber-type area distribution in the same manner as was previously shown for normal patients,22 and that the ber type characteristics of patients muscles would be subject to the same relative differences from controls as for MF declines. It was thus calculated29 that comparison group sizes of 32 would have a 90% chance of detecting a signicant difference (at the 5% level) between the groups, if one existed. To ensure the patient group was pathologically homogeneous, patients were excluded if their clinical histories, examinations, and/or investigations suggested or conrmed specic pathologies capable of affecting muscle function, over and above the effects of LBP. These pathologies included: ankylosing spondylitis, idiopathic and degenerative kyphoscoliosis, malignant or metabolic vertebral disease, disc herniation, and spinal or exit foraminal stenosis. Patients with CLBP suffering simple sciatica, i.e., leg pain without objective clinical signs of radicular compression, were included. A previous history of lumbar spine surgery caused exclusion, as this could have caused covert nerve root damage. Ingestion of any drug with a potential to affect muscle function also caused exclusion. These criteria meant that included patients were suffering with nonspecic mechanical LBP. To minimize the potentially confounding effects of paraspinal muscle disuse atrophy on the EMG and morphometric results, signicantly disabled patients were excluded with the Von Korff Chronic Pain Grade (CPG). This is a simple method of grading the severity of patients chronic pain based on a classication of their pain intensity, disability, duration, and persistency.30 Patients are graded I if they score for low disabilitylow intensity pain, II if they score for low disability high intensity pain, III for high disabilitymoderately limiting pain, and IV for high disabilityseverely limiting pain. Only patients scoring Grade III or less were included. The study received local ethical committee approval before its onset. Maximum Voluntary Isometric Contraction. Paraspinal muscle MVIC force was determined using a custom-built test

630 Spine Volume 29 Number 6 2004 rig (Medical Physics Department, Manchester Royal Inrmary), with patients in a standing position, hips and knees slightly exed, and both supported against cushioned crossbars, facing a wall-mounted load cell. The use of this and similar equipment has been validated in previous studies.9,31,32 The extensor force generated was measured with a nylon harness secured across the shoulder region of the back. The harness was attached to the load cell via inextensible straps, which were adjusted to ensure that, at maximum force, the spine was held in a vertical position. During testing, patients were asked to rapidly generate their maximum extensor force and to maintain this force for 3 to 5 seconds. During this and subsequent efforts, patients were given vigorous verbal encouragement. Further maximal efforts were made, with a 2-minute rest between each, until 3 successive attempts produced measurements within 10% of each other, which is accepted as maximum in well-motivated and technique-acclimatized normal patients.33 The highest value obtained was taken as the MVIC. the skin was shaved where necessary, abraded with ne-gauge sandpaper, and cleaned with surgical spirits. A reference electrode for each recording pain was placed on the skin some distance away from the recording site (bipolar electrode technique). The electrodes were reapplied until the impedance between them was 10 kOhms.

Electromyograph Data Acquisition and Analyses. At the

commencement of both fatigue tests, patients were allowed 2 to 3 seconds to reach a steady state in respect of contractile effort and position before EMG monitoring began. The raw EMG signal was collected from the recording electrode sites (MP 100 WSW, BIOPAC Systems, CA), processed through a signal conditioning (SC-2043-SG) and data acquisition (AT-MIO-16E10) 12-bit card (National Instruments, TX). The EMG signal was band pass ltered between 8 Hz and 500 Hz (Butterworth lters) before amplication (10, CMRR: 110 dB minimum, SNR: 65 dB minimum) and analogue-to-digital conversion at a sampling rate of 1024 Hz. An additional 50 Hz notch lter was applied to remove the ambient noise from power sources. The digitized EMG signal was on-line analyzed by a graphical programming analysis system (LabVIEW 5.0, National Instruments) in order to continuously derive the MF of the power density spectrum for each second, using a Fast Fourier Transform (FFT) algorithm. Data epochs were normalized against their respective initial values (the average of the rst 2 seconds) and a linear regression was tted through the MF history to obtain a measure of the rate of MF decrease (slope of the regression). During the fatigue tests, there were no signicant between-side differences in the MF decline results, which were therefore combined to give overall values for lumbar paraspinal muscle activity. The reliability and between-days repeatability of this apparatus during these fatigue tests had previously been established, with intraclass correlation coefcient (ICC) values of 0.91 for the 60% MVIV test and 0.75 for the Sorensen test.31

Biering-Sorensen Test. For the Sorensen test, patients were placed prone on an examination couch with the lower body, (i.e., caudally from the anterior superior iliac spine) strapped rmly to the couch. Before and after the test procedure, the upper body was supported in the neutral position. During the test, patients were instructed to contract their paraspinal muscles, the upper body support removed, and they were instructed to hold their upper body horizontal. A sliding marker was lightly rested on the interscapular region of the thoracic spine to provide tactile feedback on the horizontal position of the trunk. With the hands touching the ears, elbows abducted and externally rotated to the side and level with the trunk, and the head in a neutral position, patients were asked to maintain this position against gravity for as long as possible. As soon as the upper body ceased to be horizontal, and the subject was unable to rectify the situation despite further vigorous verbal encouragement, the test was terminated. The endurance time was recorded to the nearest whole second. Upright 60% Maximum Voluntary Isometric Contraction Fatigue Test. Once strapped into the same apparatus
previously used to determine their MVICs, patients were instructed to generate extensor force until they achieved a target level set at 60% of their MVIC and to maintain this force for 60 seconds. During this test, patients received continuous verbal feedback, in respect of time progression, and visual feedback, in respect of target force maintenance. This target appeared on a wall-mounted computer screen placed in front of the subject. A computer-generated on-screen color change informed patients if their force fell 5% below the target level.

Surface Electromyograph Electrode Placement. Pairs of

disposable surface electrodes (Blue Sensor Ag/AgCl type M-00-S, Medicost, Denmark) were attached bilaterally over the muscle bellies at the L4 L5 level. The recording electrode pairs were aligned with their Ag/AgCl detection bars parallel to each other (with a center-to-center distance of 20 mm) and perpendicular to the direction of the underlying muscle bers (as determined by landmark-derived reference lines from cadaveric studies).34,35 These surface landmarks, reference lines and electrode locations, along with natural skin blemishes and distinctive marks, were plotted on the skin, copied to acetate, and used as a template for reapplication of the electrodes on the subsequent test session. Before application of the electrodes,

Muscle Biopsy Sampling and Analysis. Percutaneous paraspinal muscle biopsies were obtained using the conchotome technique36 modied for use in the paraspinal muscles, as previously described.22 All samples were transported within 1 hour to a histology laboratory where they were immediately inspected under a medium-power dissecting microscope to determine the orientation of the bers. With the muscle bers vertical, the specimen was placed in a hollowed-out space in a block of 1% agar gel, mounted on a labeled cork disc. The adherence of the cork to the gel was assisted with a viscous embedding compound (Optimal Cutting Temperature Compound OCT Tissue-Tek, Miles Elkhart, IN). The mounted, labeled block was then snap frozen in dichlorouoromethane (Arcton 12 ICI), suspended over liquid nitrogen, and stored at 80 C. Serial sections 10 m thick were cut in a cryostat at 22 C and then reacted for hematoxylin and eosin to allow inspection for myopathology and for myobrillar adenosine triphosphatase (ATPase) following acid (pH 4.3 4.6) and alkali (pH 10.2) preincubations to enable identication of individual muscle bers as type I (slow-twitch, acid stable ATPase) or type II (fast-twitch, acid labile ATPase). Images of these sections were captured and analyzed with a video camera attached to a microscope and interfaced to a microcomputer, using a Leitz-Kompira Imagan computerized image analysis system (Leica Microsystems Cambridge Ltd., UK). The mean ber size was quantied by a measurement of narrow diameter

Paraspinal Muscle Fatigue in Chronic LBP Crossman et al 631

Table 1. Anthropometric Characteristics of the Study Patients

Parameter Age (yrs) Body mass (kg) Height (m) Body mass index (kg/m2) Upper body length (cm) Leg length (cm) Percent body fat Fat free mass (kg) Skinfold thickness L3 (mm) Control Group (n 32) 38 (10) 79 (10) 1.78 (0.8) 24.95 (3.68) 79 (4) 94 (6) 17.66 (4.32) 64.53 (7.1) 12.46 (5.4) CLBP Group (n 35) 41 (11) 84 (12) 1.78 (0.8) 26.32 (2.99) 79 (3) 95 (6) 18.73 (3.77) 67.78 (8.8) 13.30 (5.31) Difference Mean (95% CI) 3.41 (8.431.62) 4.90 (10.380.58) 0.0015 (0.390.04) 1.38 (3.010.26) 0.67 (2.471.136) 0.41 (3.222.41) 1.07 (3.040.90) 3.23 (7.160.71) 0.84 (3.461.78) Signicance (P Value) 0.18 0.79 0.94 0.10 0.46 0.78 0.28 0.08 0.84

The % body fat was derived from skinfold thickness measurements made at biceps, triceps, suprailiac, and subscapular sites.38 CLBP chronic low back pain; CI condence interval.

(ND) (maximum diameter across the lesser aspect of the muscle ber), as this method overcomes the distortion that occurs when a muscle ber is sectioned obliquely.37 Determination of the relative number of type I and II bers and the mean ND of each ber-type within selected representative portions of the biopsy section enabled the calculation of the relative area occupied by each ber type (assuming circular-shaped bers). Spatial distribution assessment examined for evidence of ber grouping suggestive of denervation/renervation.

Statistical Analysis. The data were entered onto an SPSS for

Windows (Statistical Package for the Social Science, Version 10.0) database. As the anthropometric, MF, and ber type data were all normally distributed (Kolmogorov-Smirnov test, P 0.05), between-group comparisons were made using independent t tests. Linear correlations between MF declines and bertype characteristics were assessed using Pearson correlation coefcients. Signicance was set at the 5% level.

Results In all cases in the text and tables, results are given as means, with 1 SD in parentheses. There were no statistically signicant between-group differences for any of the anthropometric variables assessed, although there was an insignicant tendency for the patients to be heavier (Table 1).38 The self-reported duration of LBP ranged 0.5 to 21 years, mean 6.79 (4.73). Of the 35 patients recruited, 14 were graded I, 15 graded II, and 6 graded III on the Von Korff CPG. Of the 35, only 3 individuals were

unable to work because of their back pain, 3 were retired, and the remainder continued to work, despite their pain. The control group generated signicantly greater force than patients during their MVICs, i.e., 98.74 (18.11) versus 84.47 (28.44) kg, respectively (P 0.02), and demonstrated signicantly better endurance times than patients during the Sorensen test, i.e., 137.50 (40.38) versus 105.29 (28.53) sec, respectively (P 0.01). Despite these maximum performance differences, MF declines during the Sorensen test were similar, i.e., 0.36 (0.12) versus 0.37 (0.16)%.sec1 for controls and patients, respectively (mean difference 0.01 [range 0.06 0.07], P 0.845). During the 60% MVIC test, MF declines were slightly but insignicantly greater in controls than in patients: 0.51 (0.29) versus 0.42 (0.31) %.sec1, respectively (mean difference 0.09 [0.24 to 0.06], P 0.230). All muscle histology specimens demonstrated an admixture of type I and II bers, and no sample demonstrated any evidence for myopathology or ber grouping. There were no signicant between-group differences in ber types by percent number or in their mean ber narrow diameters, and it follows that there were no between-group differences in the relative area of the muscle samples occupied by type I bers (Table 2). Within both groups, type I bers were slightly larger than type II bers, and this difference was signicant for the patients

Table 2. Between-Group Comparisons of Paraspinal Muscle Fiber-Type Characteristics

Parameter % Type I bers by number ND Type I (m) ND Type II (m) MFND (m) CSA Type I (m2) CSA Type II (m2) MFA (m2) % type I bers by area CSA ratio I/II ND ratio I/II CLBP Group (n 35) 64 (11) 58.97 (10.95) 55.05 (10.46) 57.01 (9.52) 2820.63 (1033.70) 2461.94 (972.32) 2661.98 (904.32) 67 (11) 2.44 (1.30) 1.21 (0.41) Control Group (n 32) 64 (9) 61.60 (11.05) 53.50 (9.12) 57.55 (8.91) 3071.80 (1011.95) 2310.39 (758.09) 2763.41 (817.53) 69 (9) 2.60 (1.20) 1.40 (0.52) Difference Mean (95% CI) 0.7 (4.305.70) 2.63 (8.012.74) 1.55 (3.226.32) 0.54 (5.043.95) 251.16 (750.56248.24) 151.54 (271.91574.99) 101.43 (521.52523.74) 2.25 (7.092.58) 0.16 (0.770.44) 0.19 (0.420.04) Signicance (P Value) 0.778 0.331 0.518 0.811 0.319 0.477 0.631 0.355 0.597 0.100 t Value 0.284 0.979 0.650 0.240 1.004 0.715 0.482 0.931 0.531 1.668

CLBP chronic low back pain; CI condence interval; % type I relative distribution of type I bers; ND narrow diameter; MFND mean (regardless of type) ber narrow diameter; CSA cross-sectional area; MFA mean (regardless of type) ber area.

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(P 0.01). However, there were no between-group differences in type I or type II muscle ber size, as measured by narrow diameter (Table 2), suggesting that no significant atrophy of either ber type had occurred in the patient group. Although the mean type I ber results were similar for both groups, the individual results demonstrated large interindividual variations, the percent number of type I bers ranging from 47% to 83% and 43% to 84%, and the percent area occupied by type I bers ranging from 51% to 85% and 46% to 85% in patients and controls, respectively. When MF declines were correlated with the relative area of the muscle occupied by type 1 bers, there were trends suggesting that the lower the percent area occupied by type 1 bers, the more rapid the MF decline, i.e., the more fatigable the muscle. For the control group, this trend reached significance during the 60% MVIC test (r 0.369, P 0.038), but not quite so during the Sorensen test (r 0.329, P 0.066). For patients, both tests produced trends in the same direction, but with insignicant correlations (r 0.102, P 0.56 and r 0.271, P 0.0.115 for 60% MVIC and Sorensen tests, respectively). Discussion No histomorphometric differences were demonstrated between patients with CLBP and normal controls in this study, so it was not surprising that no between-group differences were observed in MF declines in either of the isometric endurance tests. However, the between-group MF decline similarities were surprising when the between-group differences in the MVICs and Sorensen test endurance times were considered. Moreover, the MF declines were less steep for patients than for controls during the upright 60% MVIC fatigue test. Such a nding has been reported,39,40 but the majority of previous studies reported greater MF declines in patients with CLBP than in controls.9 11,41,42 It is established in normal patients that paraspinal muscle MVICs are predictable from anthropometric parameters.43 As the patients in this study were of similar size and mass as controls and with similar muscle ber dimensions and ber-type compositions, they should have produced MVICs as large as those of controls. Indeed, it was crucial for the success of this study that test patients performed sincere MVICs, because the subsequent 60% MVIC test contraction level was set from this result. If patients with CLBP did, as a group, underperform during their initial MVICs, as seems likely from their results, then their paraspinal muscles would have been contracting at 60% during their supposed 60% MVIC endurance tests. This would explain why their MF declines were less steep than those of normal controls during this test. These results highlight the problems regarding CLBP patients motivation during voluntary testing and the interpretation of their results. The main objective of this study was to determine whether the paraspinal muscles of patients with CLBP exhibit a paucity of type I ber content. The results obtained clearly show that, compared to normal patients,

the patients with CLBP tested demonstrated no abnormalities of paraspinal muscle ber size, nor of ber type composition or content. Patients demonstrated no abnormalities of fatigue when monitored by MF declines, but did demonstrate signicantly impaired performance when motivational factors came into play during maximal voluntary force testing and when fatigue was assessed as time to exhaustion. What do these results mean regarding the notion that a constitutionally determined adverse paraspinal muscle ber-type composition could predispose to LBP? It appears unlikely that we have, by chance, sampled patient/control groups that just happen to have identical histomorphometry. This is because, although the type I and II ber dimension and distribution result ranges were large, they were very similar to those seen in several previous paraspinal muscle morphometric studies of normal patients.26,27,44,45 Our histomorphometry results are thus likely to be representative of general populations. It therefore seems reasonable to speculate that the normal interindividual variability of paraspinal muscle contractile function, expected due to the normal and constitutionally determined interindividual variability of ber size and type composition, plays no role in CLBP symptom generation. However, as this was a crosssectional case-control study, caution is required. It remains a possibility that normal individuals with the poorest (constitutionally determined) paraspinal muscle fatigue resistance are predisposed to develop LBP, but only a much larger prospective study combining EMG and histomorphometry could fully address this question. In view of our recruitment difculties for paraspinal muscle biopsies, such a study is unlikely to take place. In the control group, the correlation between MF declines and type I ber content by area during the 60% MVIC test reached a level of signicance similar to that seen in a previous paraspinal muscle study on normal patients.22 In this previous study, the correlation between MF declines and underlying ber-type distribution only became evident when the fatiguing challenge was of a sufcient degree. As a Sorensen test only demands around 45% of MVIC,18 this may explain why, during this test in the present study, MF declines failed to correlate signicantly with type I ber content in controls or patients. Poor volition in the patient group during the supposed 60% MVIC test may again have represented an inadequately fatiguing challenge, and hence explain the poor correlations between EMG-determined fatigue and histomorphometry in patients. Overall, these results suggest that current EMG methods are not sufciently accurate at predicting ber-type composition that they could be used without histology for the large prospective studies already discussed. It has been suggested that EMG is more discerning than lumbar mobility or maximum paraspinal muscle strength testing in identifying patients with CLBP.17 Indeed, MF changes during fatiguing isometric paraspinal muscle contractions have even been advocated as a

Paraspinal Muscle Fatigue in Chronic LBP Crossman et al 633

means of discriminating between those with and without healthy backs.5,11,40,46 Our ndings appear to refute this but support the possibility that paraspinal muscle EMG can discriminate between patients with CLBP.3 Patients with CLBP may be subclassied as avoiders or confronters, according to their responses to the Pain Behavior Checklist.47 Avoiders reduce their physical activity as a protective way of coping with LBP and would presumably tend towards deconditioning-induced atrophy, whereas confronters remain active despite LBP. The ambulant patients with CLBP used in the current study seem to conform to the confronter description.3 Paraspinal muscle EMG and histomorphometry have not been correlated in avoiders and confronters to date. However, our results suggest that, so long as patients with CLBP retain a high enough level of function, then paraspinal muscle ber atrophy does not occur. These results appear at odds with those of previous studies,26,48,49 which demonstrated paraspinal muscle ber atrophy. These studies did not, however, stratify patients with CLBP for their degree of disability. It may be that atrophy only affects the more severely disabled patients, whose results were responsible for the abnormal MF declines observed overall in these studies. In retrospect, it is a pity that we did not include a more severely disabled patient comparison group to explore this issue. Given the importance of the paraspinal muscles for spinal protection, minimizing paraspinal muscle atrophy appears a vital component of CLBP rehabilitation programs, in keeping with current guidelines recommending a rapid restoration of normal activity, despite back pain.50 Use of the Von Korff CPG in this study appears to have identied a degree of retained function sufcient to prevent CLBP-associated paraspinal muscle ber atrophy, and this information could theoretically be used to set functional target levels for rehabilitation.51 Key Points
In patients with CLBP remaining active despite their pain, paraspinal muscle maximum voluntary isometric strength is reduced compared to that of normal patients. Patients paraspinal muscle fatigue characteristics were normal when EMG assessed by MF declines, but excessive when assessed by time to exhaustion. Patients paraspinal muscle ber dimensions and ber-type composition were identical to those of normal patients. Excess CLBP-associated paraspinal muscle fatigue was due to poor performance and not the result of a constitutionally determined paucity of type I ber content In patients and normal controls, paraspinal muscle ber-type composition and contractile performance generally correlated poorly.

Acknowledgements The authors would like to thank the Arthritis Research Campaign, UK, who funded K.C. to undertake this study. References
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