Drs Hart, Weltman, and Hertel are from the University of Virginia, Dr Beazell is from the University of Virgina-Healthsouth, Charlottesville, Va; Dr Ingersoll is from Central Michigan University, Mt Pleasant, Mich.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Joseph M. Hart, PhD, ATC, University of Virginia, 400 Ray C. Hunt Drive, Suite 330, Charlottesville, VA 22908-0159; e-mail: email@example.com.
Individuals with low back pain (LBP) tend to have weakness and imbalances in the muscles that surround the hips and pelvis1–3 and may absorb impact forces of running and walking less efficiently, which could allow impact forces to be transferred to the lumbar spine.1 The ability of the surrounding musculature to support the spine and pelvis may be hindered in individuals with LBP. Core stabilizing muscles such as the lumbar paraspinals and gluteals have been reported to be weaker and fatigue quicker compared with healthy controls.4 This is a concern during prolonged exercise, during which an otherwise pain-free person may experience neuromuscular adaptations that predispose to an episode of LBP or another dysfunction.
Postural control measures have been used to determine the effects of focal lumbar paraspinal muscle fatigue and in response to a trunk perturbation,5,6 indicating the important role of trunk musculature endurance in postural control. Deteriorated postural control has been reported following aerobic exercise7; however, it is not known how postural control in individuals with LBP will be affected following aerobic exercise. A magnified response to aerobic exercise may be due to the high fatigability of core musculature in individuals with LBP. This may lead to altered neuromuscular responses manifesting as deteriorated postural control during quiet stance and in response to an external perturbation. The neuromuscular responses leading to deteriorated postural control during prolonged, fatiguing aerobic exercises may contribute to the understanding of why an active person with a history of LBP is likely to experience a recurrent episode.
The active and passive structures that provide global and segmental stability to the lumbar spine as well as the hip joints and pelvis, collectively referred to as the “core,” must behave in a way that provides instantaneous responses to perturbations that occur during activity and sport. Individuals who maintain an active lifestyle experience excessive loads during dynamic activities in which they are continually required to adapt to changing postures and loading conditions. Active trunk musculature surrounding the core acts like a rigid cylinder while controlling spinal motion and returning the spine to a neutral position during postural perturbations.8 Inadequate response of core stabilizing muscles may increase the risk for recurring episodes of LBP.9 We hypothesize that if core muscles fatigue at quicker rates or experience a magnified response to aerobic exercise, postural control will be deteriorated when compared with healthy controls.
The purpose of this study was to compare changes in postural control in individuals with recurrent LBP and healthy controls following a standardized aerobic walking exercise protocol.
Thirty individuals volunteered to participate in this study. All participants reported no history of lower extremity surgery or ligamentous insufficiency, neuropathy, or recent muscle or joint injury (within the past 6 months), exhibited no radicular symptoms, and reported being recreationally active, defined as exercising for at least 30 minutes on 3 separate occasions per week. Fifteen participants (age = 25.7±7.2 years; height = 171.7±13.2 cm; weight = 80.3±17.1 kg) reported never experiencing LBP and 15 participants (age = 27.1±7.1 years; height = 179.3±9.1 cm; weight = 81.7±25.4 kg) reported at least 3 episodes (defined as pain severe enough to limit activities of daily living) in the past year. All participants who reported a history of recurrent episodes of LBP denied history of injury to bone, disc, or nerve and denied cancer diagnosis. Participants were excluded if they exhibited any of the following: bilateral asymmetry of the dermatome, myotome, or deep tendon reflex; self-reported pain which was >3/10 with standing lumbar extension; the inability to extend the spine at least 15°; or a positive straight leg test indicating pain and numbness. We measured hip-joint range of motion during the straight leg raise and lumbar forward flexion with a standard long-arm goniometer and calculated Oswestry pain and disability index score (Table 1). This study was approved by our university’s institutional review board and all participants provided written informed consent.
Table 1: Clinical Examination Findings and Participant Demographics
Prior to data collection, participants were screened for LBP history so they could be assigned to the appropriate group and to assess participant eligibility. We recorded baseline postural control while participants stood still on a force plate (AccuSwayPLUS; AMTI, Watertown, Mass) (sampling rate = 50 Hz) with eyes closed on the dominant limb (ie, the limb they felt most comfortable balancing on) and in double limb stance. We allowed multiple practice trials with single and double limb stances to acclimate the participants to the testing procedures. Once the participant felt comfortable, we recorded a 20-second trial of single limb stance followed by 2 trials of double limb stance. During one of the double limb stance trials, an examiner stood behind the participant and provided an unexpected vertical compression perturbation. This consisted of a light force (approximately 2 kg) applied manually to the participant’s shoulders and was directed downward and axially. This perturbation is similar to the vertical compression test that has been described previously10 and may be used to provide an estimate of postural control and spine stability where, if instability is present, spinal motion and buckling can occur. An athletic trainer (J.M.H.) who was experienced with applying the maneuver provided the vertical compression perturbations while standing on a step-stool.
Fatiguing Aerobic Exercise
Participants walked on a treadmill (Q65 series 90, Quinton Instrument Co., Bothell, Wash) at 3.3 miles per hour for 15 minutes. Each minute, the incline of the treadmill was increased and participants reported their perceived level of exertion using the Ratings of Perceived Exertion (RPE) scale.11 If a participant reported an RPE of 17 or above (17 corresponds to the perception of “Very hard: very strenuous and you are very fatigued”), the treadmill exercise was terminated and the participant was excluded from the analysis. Use of this exercise protocol has been reported previously as a method to study exercise-induced changes in neuromuscular function in individuals with LBP.12
Immediately following aerobic exercise, participants returned to the force platform and followed the same procedures as the baseline measurement. A grid on the force plate allowed for accurate reproduction of foot positioning for post-exercise measurements. A single trial for each testing condition was collected at both time points to minimize the effects of recovery time following the end of the aerobic exercise protocol.
Center of Pressure (COP) excursions were recorded during each trial. The COP data were low-pass filtered (10 Hz) and processed using Balance Clinic Software version 1.0 (AMTI) to calculate mean and standard deviation of the COP location in the medial-lateral (ML) direction (MLAVE, MLSD) and anteroposterior (AP) direction (APAVE, APSD). The mean and standard deviation variables were calculated from 1000 data points collected during each 20-second trial. The average COP velocity (VELAVE) and the area of a 95% confidence ellipse of COP excursions (AREA95) were also calculated.
A 2×2 factorial model with repeated measures was used in this study with the independent variables group (LBP) and time (pre- and post-aerobic exercise). The dependent variables were COP excursions during single leg stance, double leg stance, and a vertical compression perturbation while in double limb stance. The following variables were calculated from COP excursion data: the average location in the ML plane, AP plane, standard deviation of COP excursions in the ML and AP planes, area of a 95% confidence ellipse of COP excursions, and average velocity of COP excursions.
Three separate 2×2 (group × time) repeated measure ANOVAs were used for statistical analysis. Post hoc t tests were used where appropriate. The level of significance was set a priori at P ≤ .05 for all comparisons. All statistical tests were performed with SPSS version 17.0 (SPSS Inc., Chicago, Ill).
Means and standard deviations for all COP variables collected are presented in Table 2.
Table 2: Means (SD) of Center of Pressure Measures
Single Limb Stance
Participants experienced significant shift in APAVE (more negative or posteriorly located COP) following aerobic exercise (F1,28 = 4.5, P = .04). There were significantly increased values for APSD (F1,28 = 4.7, P = .04), VELAVG (F1,28 = 19.2, P < .001), and AREA95 (F1,28 = 4.4, P = .05). There were no group differences and no group × time interactions for any of the data collected during single limb stance.
Double Limb Stance
Participants experienced significant increases in MLSD (F1,28 = 13.6, P = .001), APSD (F1,28 = 10.7, P = .003), VELAVG (F1,28 = 11.0, P = .003), and AREA95 (F1,28 = 15.9, P < .001) after aerobic exercise. There were no group differences and no group × time interactions for any of the data collected during double limb stance.
Double Limb Stance with Vertical Compression Perturbation
There was a significant group × time interaction for APSD (F1,28 = 8.3, P = .007). Specifically, individuals in the control group experienced approximately 14.7% reduction in APSD (t14 = 1.7, P = .12) following aerobic exercise, whereas the LBP group experienced approximately 17.8% increase in APSD (t14 = −2.6, P = .02) (Figure). There were no differences for any of the COP variables, on average, over time or between groups.
Figure. Anteroposterior (APSD) Measures at Baseline and After Aerobic Exercise Separated by Group. Individuals with Low Back Pain Experienced a Significant Increase in APSD After Exercise.
In the current study, we compared the postural control response in individuals with recurrent episodes of LBP before and after a short bout of aerobic exercise. We hypothesized that individuals with LBP would experience a magnified response to aerobic exercise that manifested as deteriorated postural control during quiet stance and in response to an external perturbation. Our data do not support a magnified postural control response to aerobic exercise in participants with LBP during quiet stance; however, in response to a vertical compression perturbation, the LBP group experienced greater variation in AP COP excursions, suggesting deteriorated postural control.
We observed no differences between groups in postural control at baseline. However, after 15 minutes of aerobic exercise, individuals with LBP and healthy controls experienced deteriorated postural control in both single and double limb stances. This indicates that young, healthy, and recreationally active individuals experienced deteriorated postural control during single and double limb stances following a short bout of aerobic exercise, which appears to be uninfluenced by the presence of a history of recurring episodes of LBP.
The vertical compression perturbation performed on the participants in the current study elicited a postural control response in individuals with LBP that was different from that of healthy controls. This was not the case for postural control measures recorded during quiet stance (single or double limb). Clinically, it is important to understand how individuals with recurrent injury respond to postural perturbations because it is more applicable to active situations. The postural control response in individuals with recurrent episodes of LBP may be potentially deleterious during prolonged and fatiguing activities. In the current study, we observed an increase in the variability of COP excursions in the AP plane only in patients with recurrent episodes of LBP. Therefore, when fatigued, a person with recurrent episodes of LBP may experience a different response when making a sudden movement such as a quick change in direction, stepping off a curb, or landing from a jump. This may describe a postural control strategy in individuals who have recurrent episodes of LBP due to a magnified neuromuscular response after aerobic exercise. Postural control does not appear to be affected differently in individuals with a history of LBP unless a perturbation is applied. Whether the perturbation test used in this study is similar to perturbations experienced in sport activity or functions of daily living is unknown. However, these results provide evidence that individuals with a history of LBP may respond differently to perturbation events following a prolonged aerobic exercise. It is possible that participants anticipated the vertical compression perturbation and made a compensatory postural adjustment. We do not know whether or not this occurred; however, the vertical compression test was performed under the same conditions as it would during a clinical examination.
Panjabi13,14 proposed a hypothesis of core instability and dysfunction that can be characterized by an increase in the “neutral zone” of the spine due to factors such as pain or abnormal or increased spinal segment motion. The neutral zone has been described as the portion of spinal range of motion where there is minimal resistance to intervertebral motion.13 The goal of stabilization therapy is to improve neuromuscular control of the neutral zone, thereby improving stability and reducing pain. Efficient and coordinated activation of the muscles that act on the lumbar spine, hips, and pelvis provides stiffness at the trunk, making it act like a rigid cylinder and stable base for extremity movement.8 If trunk musculature is weakened following fatiguing exercise, the trunk may become less rigid, where greater oscillatory response would be experienced when the spine is perturbed in an attempt to restore the spine within a pain-free range of motion. The findings from the current study may indicate that individuals with recurrent episodes of LBP are experiencing decreased sagittal plane trunk control and potentially an increased neutral zone. The standard deviation of COP excursions describes the dispersion of the COP locations relative to the mean. Given that there were no differences observed in the mean AP COP location in response to a perturbation, the finding of increased COP standard deviation describes the possibility that after fatigue, individuals with LBP were experiencing sagittal plane trunk excursions within a larger neutral zone due to deteriorated core stability. Although the clinical importance of these changes is speculative, it is possible that along this continuum of exercise leading to exhaustion, individuals with neuromuscular insufficiencies may experience replacement strategies to maintain the desired level of functioning. This is concerning given that these adaptations may remain subclinical until tissue breakdown and injury occurs.
The fatiguing exercise protocol used in this study was short and relatively low intensity. The participants in this study were young, healthy, and all recreationally active individuals who may have been able to perform higher intensity and more prolonged bouts of exercise. Therefore, the aerobic exercise protocol may not have been sufficient enough to elicit a response that is detectable during static stance given that participants were well below the level of exhaustion. Changes in neuromuscular function or postural control may be magnified after more intense and exhausting activity in individuals with core instability and recurrent LBP. The response in less physically active individuals with a history or recurring episodes of LBP is not known and warrants further research.
We cannot be certain whether poor core muscle function or trunk neuromuscular control caused the changes in postural control following aerobic exercise in individuals with recurrent episodes of LBP. Altered ankle, knee, or hip neuromuscular control may also explain the observed post-exercise changes in AP COP deviations. Because we observed these changes during a provocative maneuver that is traditionally used to assess lumbar spine buckling, participants in our study may have been experiencing deteriorated lumbar spine stability following exercise. Individuals with recurrent episodes of LBP often experience muscle weakness, imbalances, and higher fatigability (ie, faster rates of fatigue).1–4,15
After prolonged exercise, the muscles surrounding the lumbar spine may fail to provide adequate spinal stability, resulting in altered postural control. In the current study, the aerobic exercise protocol did not cause diminished postural control during quiet stance; however, the exercise was sufficient enough to produce a change in AP COP variability when a perturbation was delivered in the participants with LBP. The results suggest a loss of lumbar spine stability during aerobic exercise in participants with LBP. We did not measure specific muscle weakness or fatigability; therefore, we cannot comment on which muscles could have influenced the observed exercise-related postural control response, nor can we be certain that muscle weakness or imbalances are the primary cause of LBP episodes in the experimental group. It is likely that the combined influence from abdominal wall muscles, posterior spine musculature, and more deeply located stabilizing muscles contributed to overall stability during a variety of dynamic tasks.16 It is unlikely that a single muscle can be identified as “most important” to maintaining core stability during exercise.16 Therefore, hypotheses regarding improvements in muscle function can be tested through translational and clinical research studies to better understand whether these responses to exercise can be mitigated with rehabilitation.
A potential limitation of this study is the use of only one 20-second trial of each stance condition. Traditionally, the average of multiple and longer trials are used for analysis. Previous research17 has shown acceptable reliability of force plate measures of postural control with trials lasting 20 seconds. Performance-based outcomes such as balance or muscle function after fatigue are inherently limited by recovery. There is a limited amount of time after an exercise protocol where outcomes are minimally confounded by post-exertional recovery. The time frame for post-exercise data collection is not well defined; therefore, post-exercise measures should be performed as quickly as possible. A previous study18 reported balance deficits persisting for 5 minutes after 20 minutes of continuous exercise protocol that were completely recovered after an additional 15 minutes of rest. To assure expedient post-exercise measurements, we provided participants with as many practice trials as they needed (prior to exercise only) to make sure they were familiar with the tasks. We allowed only one post-exercise trial of each outcome measure to minimize testing time. Prior to the start of data collection, the examiner rehearsed procedures extensively to complete in a timely manner.
Implications for Clinical Practice
Clinicians should be aware of the possibility of altered postural control both before and after exercise in active patients with recurrent LBP. Postural control adaptations when patients are fatigued may help clinicians identify potentially harmful deficits that can guide treatment and rehabilitation decision making.
In a rested state, individuals with a history of LBP behave similarly to healthy controls during static stance and in response to a perturbation. However, after a short bout of fatiguing aerobic exercise, individuals with LBP experience increased standard deviation of sagittal plane COP excursions during a vertical compression perturbation, which may be indicative of poor trunk control in this population.
- Nadler SF, Malanga GA, DePrince M, Stitik TP, Feinberg JH. The relationship between lower extremity injury, LBP, and hip muscle strength in male and female collegiate athletes. Clin J Sport Med. 2000;10:89–97. doi:10.1097/00042752-200004000-00002 [CrossRef]
- Nadler SF, Malanga GA, Feinberg JH, Prybicien M, Stitik TP, DePrince M. Relationship between hip muscle imbalance and occurrence of LBP in collegiate athletes: A prospective study. Am J Phys Med Rehabil. 2001;80:572–577. doi:10.1097/00002060-200108000-00005 [CrossRef]
- Nadler SF, Malanga GA, Bartoli LA, Feinberg JH, Prybicien M, Deprince M. Hip muscle imbalance and LBP in athletes: Influence of core strengthening. Med Sci Sports Exerc. 2002;34:9–16. doi:10.1097/00005768-200201000-00003 [CrossRef]
- Kankaanpää M, Taimela S, Laaksonen D, Hanninen O, Airaksinen O. Back and hip extensor fatigability in chronic LBP patients and controls. Arch Phys Med Rehabil. 1998;79:412–417. doi:10.1016/S0003-9993(98)90142-3 [CrossRef]
- Davidson BS, Madigan ML, Nussbaum MA. Effects of lumbar extensor fatigue and fatigue rate on postural sway. Eur J Appl Physiol. 2004;93:183–189. doi:10.1007/s00421-004-1195-1 [CrossRef]
- Madigan ML, Davidson BS, Nussbaum MA. Postural sway and joint kinematics during quiet standing are affected by lumbar extensor fatigue. Hum Mov Sci. 2006;25:788–799. doi:10.1016/j.humov.2006.04.004 [CrossRef]
- Fox ZG, Mihalik JP, Blackburn JT, Battaglini CL, Guskiewicz KM. Return of postural control to baseline after anaerobic and aerobic exercise protocols. J Athl Train. 2008;43:456–463. doi:10.4085/1062-6050-43.5.456 [CrossRef]
- Kibler WB, Press J, Sciascia A. The role of core stability in athletic function. Sports Med. 2006;36:189–198. doi:10.2165/00007256-200636030-00001 [CrossRef]
- Hammill RR, Beazell JR, Hart JM. Neuromuscular consequences of LBP and core dysfunction. Clin Sports Med. 2008;27:449–462, ix. doi:10.1016/j.csm.2008.02.005 [CrossRef]
- Johnson GS, Johnson VS. The application of the principles and procedures of PNF for the care of lumbar spinal instabilities. J Manual Manip Ther. 2002;10:83–105. doi:10.1179/106698102790819274 [CrossRef]
- Borg GA. Psychophysical bases of perceived exertion. Med Sci Sports Exerc. 1982;14:377–381.
- Hart JM, Weltman A, Ingersoll CD. Quadriceps activation following aerobic exercise in individuals with LBP and healthy controls. Clin Biomech. In press.
- Panjabi MM. The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis. J Spinal Disord. 1992;5:390–397. doi:10.1097/00002517-199212000-00002 [CrossRef]
- Panjabi MM. Clinical spinal instability and LBP. J Electromyogr Kinesiol. 2003;13:371–379. doi:10.1016/S1050-6411(03)00044-0 [CrossRef]
- Jones MA, Stratton G, Reilly T, Unnithan VB. Biological risk indicators for recurrent non-specific LBP in adolescents. Br J Sports Med. 2005;39:137–140. doi:10.1136/bjsm.2003.009951 [CrossRef]
- Cholewicki J, VanVliet JJ IV, . Relative contribution of trunk muscles to the stability of the lumbar spine during isometric exertions. Clin Biomech (Bristol, Avon). 2002;17:99–105. doi:10.1016/S0268-0033(01)00118-8 [CrossRef]
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Clinical Examination Findingsa and Participant Demographics
|LOW BACK PAIN GROUP||CONTROL GROUP|
|Oswestry disability index score (%)||6.9±6.3||N/A|
|Hip range of motion (°)|
| Left side flexion||67.0±9.7||72.9±15.5|
| Right side flexion||66.4±8.7||70.9±16.1|
|Trunk range of motion (°)|
Means (SD) of Center of Pressure Measures
|CONTROL GROUP||LOW BACK PAIN GROUP||COMBINED GROUPS|
| MLAVG (in)||−0.04 (0.36)||−0.06 (0.26)||0.02 (0.42)||0.04 (0.41)||−0.01 (0.39)||−0.01 (0.34)|
| MLSD||0.47 (0.14)||0.49 (0.10)||0.41 (0.09)||0.46 (0.13)||0.44 (0.12)||0.48 (0.11)|
| APAVG (in)||−0.05 (0.89)||−0.18 (0.78)||0.29 (0.95)||0.06 (1.10)||0.12 (0.92)||−0.06 (0.95)a|
| APSD||0.51 (0.19)||0.60 (0.15)||0.48 (0.10)||0.55 (0.23)||0.50 (0.15)||0.58 (0.20)a|
| AREA95(in2)||4.8 (3.1)||5.5 (2.2)||3.6 (1.4)||5.1 (3.4)||4.2 (2.4)||5.3 (2.8)a|
| VELAVG(in/s)||3.7 (1.5)||4.3 (1.2)||3.2 (1.0)||4.0 (1.6)||3.4 (1.3)||4.1 (1.4)a|
| MLAVG||−0.12 (0.24)||−0.08 (0.28)||−0.08 (0.25)||−0.10 (0.24)||−0.10 (0.24)||−0.09 (0.26)|
| MLSD||0.07 (0.02)||0.09 (0.24)||0.07 (0.04)||0.10 (0.06)||0.07 (0.03)||0.10 (0.04)a|
| APAVG||−0.87 (0.80)||−0.78 (0.94)||−0.63 (0.87)||−0.37 (0.94)||−0.74 (0.83)||−0.58 (0.95)|
| APSD||0.20 (0.08)||0.28 (0.16)||0.16 (0.05)||0.21 (0.08)||0.18 (0.07)||0.24 (0.13)a|
| AREA95||0.27 (0.13)||0.45 (0.32)||0.21 (0.15)||0.42 (0.33)||0.23 (0.14)||0.44 (0.32)a|
| VELAVG||0.59 (0.20)||0.75 (0.30)||0.56 (0.13)||0.68 (0.17)||0.58 (0.17)||0.72 (0.24)a|
|Bilateral stance with vertical compression|
| MLAVG||−0.08 (0.22)||−0.02 (0.28)||−0.01 (0.33)||−0.12 (0.27)||−0.05 (0.28)||−0.07 (0.28)|
| MLSD||0.14 (0.06)||0.13 (0.04)||0.12 (0.05)||0.13 (0.06)||0.13 (0.05)||0.13 (0.05)|
| APAVG||−1.2 (0.70)||−0.98 (0.75)||−0.93 (0.90)||−0.79 (0.83)||−1.0 (0.81)||−0.88 (0.78)|
| APSD||0.29 (0.10)||0.24 (0.08)||0.29 (0.14)||0.34 (0.18)a||0.29 (0.12)||0.30 (0.15)|
| AREA95||0.71 (0.39)||0.58 (0.27)||0.72 (0.62)||0.89 (1.0)||0.72 (0.51)||0.74 (0.74)|
| VELAVG||0.76 (0.14)||0.77 (0.18)||0.86 (0.29)||0.91 (0.30)||0.81 (0.23)||0.84 (0.25)|