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Prolonged standing as a precursor for the development of lowback discomfort: An investigation of possible mechanisms

Diane E. Gregory, Jack P. Callaghan *

University of Waterloo, Waterloo, Ontario, Canada

Received 30 May 2007; received in revised form 14 August 2007; accepted 14 October 2007

Abstract

Low back discomfort (LBD) has been associated with prolonged periods of standing, yet research has shown that the magnitude of spinalloading during standing is relatively minimal. Therefore, the mechanism of this discomfort is not fully understood. Research has monitored

numerous variables during prolonged periods of standing; however the focus of this work has been primarily on the comparison of the effect of

different floor surfaces on these variables. No study to date has made an attempt to relate these changes to the development of LBD. The

purpose of this study was therefore to determine possible mechanisms for the development of LBD during standing by monitoring biological

variables. It was hypothesized that during a prolonged standing period, LBD would develop and the measured variables would change over

time. Sixteen individuals stood for 2 h while activation of torso and hip muscles, lumbar spine posture, back extensor muscle oxygenation,

torso skin temperature, and centre of pressure changes under the feet were monitored over time. Thirteen out of sixteen individuals developed

LBD as a result of the prolonged standing period, which significantly increased over the 2-h period ( p < 0.0001). Only three of the 37

variables measured were significantly altered over time. However, a generated regression model incorporating 15 of the 16 individuals (which

incorporated how each individual stood in the first 15 min) explained 78% of the variance in LBD at the end of the 2-h standing period.

Prolonged standing resulted in LBD, yet few significant changes in the measured variables were observed over time. It is possible that LBD is

not linked with alterations in standing over time, but rather associated with how an individual initially stands.

# 2007 Elsevier B.V. All rights reserved.

Keywords: Spine posture; Prolonged standing; Low back pain; Discomfort; EMG; Regression

1. Introduction

Research has shown that the actual compressive load on

the low back during standing is minimal [1], however

prolonged static standing has been associated with the

reporting of low back pain [2–8]. This is especially evident

in, but not limited to, the automotive industry where

automation has greatly reduced the prevalence of heavylifting and awkward postures experienced by the worker,

often resulting in reduced trunk motion and increased

repetitive upper extremity tasks. Jobs such as cashiers, bank

tellers, and casino dealers also spend the majority of their

workday standing.

Previous research has monitored numerous variables

during prolonged periods of standing; however the focus of

this work has been primarily focused on the comparison of

the effect of different floor surfaces on these variables.

Larger centre of pressure displacements while standing on a

hard surface as compared to a soft surface, whichparticipants rated as more comfortable, and larger displace-

ments following experimental pain elicitation have been

previously observed [9]. Further increases in the lower limb

skin temperature while standing on the hard surfaces and a

decrease in temperature while on the soft surfaces have also

been reported [9]. Higher perceived whole body and lower

limb fatigue [10] as well as increased back extensor

muscular fatigue [11] have been documented while standing

on a bare floor surface as compared to various footwear

www.elsevier.com/locate/gaitpost

Available online at www.sciencedirect.com

Gait & Posture 28 (2008) 86–92

* Corresponding author at: Department of Kinesiology, Faculty of

Applied Health Sciences, University of Waterloo, 200 University Avenue

West Waterloo, Ontario, Canada N2L-3G1. Tel.: +1 519 888 4567x7080;

fax: +1 519 746 6776.

E-mail address: [email protected] (J.P. Callaghan).

0966-6362/$ – see front matter # 2007 Elsevier B.V. All rights reserved.

doi:10.1016/j.gaitpost.2007.10.005

mailto:[email protected]

http://dx.doi.org/10.1016/j.gaitpost.2007.10.005

http://dx.doi.org/10.1016/j.gaitpost.2007.10.005

mailto:[email protected]



insoles and mats. Participants found mats and insoles to be

more comfortable during the standing period. Muscle

activation of the back and lower limbs has also been

examined during a prolonged period of standing, specifically

the tibialis anterior and the lumbar paraspinal muscles

during a 2-h period of standing on a concrete floor and a floor

mat [5]. This study found no differences in the mean muscleactivity of these muscles between the two floor types. It is

evident that extensive work has been conducted to assess the

effect of various floor surfaces on standing. However, to our

knowledge, there has been no reported attempt to associate

these changes with the development of low back discomfort

(LBD) over time. Therefore, the purpose of this study was

to examine variables that potentially contribute to the

mechanism of this discomfort as well as to determine if

trunk muscle activation, lumbar spine posture, centre of

pressure changes under the feet, skin temperature in the back

region, and erector spinae muscle oxygenation correlate

with the development of LBD during prolonged standing. It

was hypothesized that low back discomfort would increase

over the 2-h period of standing. It was also hypothesized that

the previously mentioned variables would change over time

as low back discomfort develops. Specifically it was

hypothesized that during the prolonged standing period,

the displacement/variability of centre of pressure, skin

temperature, and perceived fatigue and discomfort would

increase. These hypotheses were considered for several

reasons. It was hypothesized that due to the static nature of

prolonged standing, the discomfort perceived by the

individuals in the study would be a result of metabolite

buildup in the low back muscles. This accumulation of

metabolites has been shown to be a potential source of perceived discomfort, which individuals may try to alleviate

via increased movement. Further, due to the static nature of

standing, an increase in blood pooling in the low back, and

thus an increase in metabolite buildup, may be observed as

increased temperature at the skin.

2. Materials and methods

2.1. Participants

Sixteen individuals (Table 1) were recruited from the general

university population, eight males and eight females. All partici-pants were required to be free of LBD for at least 12 months prior to

data collection. Each participant was required to review and

consent to an outline of the experiment, approved by the University

Office of Research.

2.2. Data collection and analysis

Individuals were required to stand in a confined working space

(0.50 m 0.46 m, surface area of a forceplate) for 2 h while

performing four precision tasks, presented in random order, that

resemble jobs that often require periods of prolonged standing.

These tasks included small object assembly (retractable pens) to

mimic assembly line workers; currency sorting to mimic a bank teller; grocery store checkout to mimic a cashier; and card dealing

to mimic a casino dealer. No rest was given between the four tasks

such that each individual maintained the standing posture for two

straight hours. Individuals were not permitted to use anti-fatigue

devices (mats or footrests) but were allowed to adjust their posture

within the constrained space and rest their forearms on the work-

table without supporting their body weight. All participants were

required to wear their own athletic shoes. Fig. 1a and b depicts the

experimental and participant set-up.

2.3. Electromyography

Muscle activation levels from 10 muscle sites were measuredusing surface EMG with disposable pre-gelled EMG Ag–AgCl

electrodes (Blue Sensor, Medicotest, Inc., Ølstykke, Denmark).

These muscles included, bilaterally, thoracic erector spinae (TES),

lumbar erector spinae (LES), rectus abdominis (RA), external obli-

que (EO), andgluteus medius (GM). Electrode locationsfor the trunk

muscles were determined as per McGill [12], and thegluteus medius

electrodes wereplaced 15 cm inferiorand 5 cm posteriorof each iliac

crest. Raw EMG was collected at 2048 samples/s using a 16 bit A/D

card with a2.5 V range. Systematicbias wasremoved from theraw

EMG signal prior to signal full-wave rectification. The signal was

then passed through a second-order Butterworth filter, with a 2.5 Hz

cut-offfrequency [13], to produce a linear envelope foreachof the10

muscle groups recorded and then normalized to a maximum volun-

tary isometric contraction (MVC). Briefly, to perform a back exten-sor MVC, the participants were asked to extend against resistance,

whiletheirtorso wassuspendedover theedgeof a bench.Tocarry out

an abdominal MVC, the participants were asked to perform a

modified sit-up against resistance, while twisting about the waist

to ensure maximal contraction of the abdominal muscles. To carry

outeach hipabductorMVC,the participants were askedto lieon their

side (opposite of the leg performing the MVC) and abduct their leg

against resistance.

The total number of gaps (period of time when EMG levels drop

below 0.5% MVC for longer than 0.2 s [14]) and average activation

amplitudes for each 15 min time block were obtained for each

muscle. The number of shifts in EMG was also calculated for each

15-min block in order to determine if the activation of EMG

became more static or dynamic over the 2-h standing period. Shifts

were defined as a point in time when the level of muscle activation

exceeded a pre-determined threshold. The threshold was set as two

standard deviations above and below the mean, which was deter-

mined based on the first minute of standing. It was assumed that

individuals were standing quietly and were not fatigued during that

first minute of standing. The number of times the amplitude of

activation crossed the threshold, termed ‘shift’ (either above or

below the mean) was tallied and compared between time blocks to

determine if the level of muscle activation either became more

static or dynamic throughout the standing period. The mean about

which the thresholds were bounded was recalculated for each 15-

min block (while maintaining the same standard deviation) such

D.E. Gregory, J.P. Callaghan / Gait & Posture 28 (2008) 86–92 87

Table 1

Summary of participant parameters (age, height, mass) for males and

females

Male (n = 8) Female (n = 8)

Age (years) 25.1 (2.1) 23.5 (2.3)

Height (m) 1.83 (0.05) 1.72(0.1)

Mass (kg) 79.7 (9.3) 69.7 (12.3)



that if the EMG signals were to gradually increase/decrease over

time, it would not be perceived as one long shift.

2.4. Kinematics

Kinematics were measured using an active motion analysis

system (Optotrak Certus, NDI, Waterloo, Ont., Canada). IRED

markers were adhered to the skin at nine anatomical landmarks as

well as adhered to three rigid spine fins (additional nine markers)

shown in Fig. 1b. Three-dimensional lumbar spine posture was

calculated from marker locations on rigid fins (adhered over the

spinous processes of C7/T1, T12/L1, and L4/L5) using customsoftware, 3DBack (University of Waterloo, Waterloo, Ont.,

Canada). Average flexion–extension (FE), lateral bend (LB), and

axial twist (AT) angles were determined for each 15-min block and

were compared over time. Similar to the calculation of shifts in

EMG, shifts in lumbar posture about each axis were determined.

Joint coordinates were used to calculate reaction forces and the net

joint moment at L4/L5 using a two-dimensional rigid link segment

model (GOBER, University of Waterloo, Waterloo, Ont., Canada).

With the use of a simplified single muscle equivalent model, bone-

on-bone forces were determined at L4/L5. The single muscle

equivalent model incorporated a single extensor muscle equivalent

vector with a 5.38 angle of pull in the posterior direction with a

6 cm moment arm [15] and a single flexor muscle equivalent vector

anterior to the L4/L5 joint acting parallel to the joint compression

axis with a moment arm of 4.5 cm [16].

Centre of pressure under the feet in the medial–lateral (CoPML)

and anterior–posterior (CoPAP) directions were determined from

forceplate outputs (Advanced Mechanical Technologies Inc., New-

ton, MA, USA), which were sampled at 1024 samples/s. Indivi-

duals were permitted to change the location of their foot placement

providing both feet maintained contact with the forceplate.

2.5. Back extensor muscle oxygenation and skin temperature

Muscle oxygenation of the right TES was measured using near-

infrared spectroscopy (NIRS) (RunmanTM CWS-2000, NIM Inc.,

Philadelphia, PA, USA), and skin temperature (2100 Tele-Thermo-

meter, Yellow Springs Instruments, Yellow Springs, OH, USA) was

also measured over the right TES and right LES.

2.6. Rating of perceived low back discomfort

Participants were required to rate their level of perceived LBD

using a 100 mm visual analog scale (with end point anchors of ‘no

discomfort’ and ‘worst discomfort imaginable’). Ratings of dis-

comfort were conducted at the start of the 2-h standing period and

every 15 min until the end of the collection period (total of nine

ratings of LBD). The magnitude of LBD was determined bymeasuring the distance from the hatch mark on the scale to the

origin (in mm).

2.7. Statistical analysis

Ratings of perceived LBD, average muscle activation, average

gap number, shifts in EMG for each muscle, average lumbar

posture, shifts in lumbar spine posture, average L4/L5 joint load-

ing, shifts in CoP, muscle oxygenation, and average thoracic and

lumbar skin temperaturewere determined for each 15-min block. A

one-way repeated measure analyses of variance with blocks of time

was used to determine if anyvariable changed significantly over the

2 h duration. Tukey’s post hoc multiple comparisons were used to

examine any significant main effect finding.

Pearson’s correlations were used to determine thestrength of the

relationship between each of the previously mentioned variables

and the ratings of LBD. Three regression analyses were performed

with the ratings of LBD at the end of the 2-h standing period as the

dependent variable and the magnitude of the 12 most highly

correlated variables with LBD, measured in only the first 15 min

of standing, as the independent variables. These were performed in

order to determine if the level of LBD could be predicted by how

the participant stood during the first 15 min of the standing period.

Thethree regression models included onewhich incorporated all 16

participants; one which incorporated only the individuals who

developed LBD; and one which included 15 of the 16 individuals.

D.E. Gregory, J.P. Callaghan / Gait & Posture 28 (2008) 86–9288

Fig. 1. Experimental and participant set-up including Optotrak marker, electrode, NIRS (muscle oxygen sensor), and skin temperature sensor locations: (a)

posterior view and (b) sagittal view.



The removed individual in this regression model did not develop

LBD during the standing period but responded quite differently to

the other non-LBD individuals and was considered an outlier for

the third regression analysis.

3. Results

3.1. The effect of standing on LBD

Thirteen of the sixteen participants had some level of

LBD at the end of the 2 h of standing. When individuals

were examined based on whether they developed LBD, no

significant differences were observed in any single measured

variable between the two groups (those who developed LBD

and those who did not).

The rating of perceived discomfort in the low back was

found to be significantly affected by time ( p < 0.0001)

shown in Fig. 2 with a trend of increasing LBD over time. A

noteworthy point is that all participants had no perceivedLBD at the start of the standing period, but had an average

rating of 3.06 mm after the first 15 min and 19.00 mm after

the full 2 h. It is interesting to note the increased variability

in the perceived discomfort rating later in the standing

period as compared to at the start. While pain perception to

controlled stimuli has been shown to result in large inter-

individual pain rankings [17] there is evidence that the intra-

individual perception has strong test–retest reliability [18].

The subjective nature of pain perception would therefore

yield variability as the level of pain develops, yet has good

repeatability within individuals.

3.2. The effect of time

Only three variables significantly changed over the 2-h

period; the degree of lumbar spine FE, the magnitude of L4/

L5 joint shear, and skin temperature over the right TES site.

The degree of FE was significantly affected by time

( p = 0.0156), such that as time increased, individuals tended

to increase the degree of flexion in their lumbar spine from

an average of 0.358 (standard deviation (S.D.) 1.068) of

flexion after the first 15 min to 1.768 (S.D. 0.748) flexion

after the 2 h of standing. Time was also found to affect the

magnitude of bone on bone AP shear force at L4/L5

( p < 0.0001), such that posterior shear of L4 with respect to

L5 had a tendency to decrease over time. Theshear force was

calculated to be an average of 22.6 N (L4 posterior withrespect to L5) (S.D. 35.5 N) after the first 15 min, and 14.6 N

(S.D. 29.0 N) in the posterior direction after the full 2 h.

Last, skin temperature over the right TES was also affected

by time ( p < 0.0001). The skin temperature significantly

decreased over the 2 h from an average of 31.1 8C (S.D.

1.30 8C) after 15 min to 30.7 8C (S.D. 1.21 8C) after the 2 h.

3.3. Regression analysis—predicting the magnitude of

LBD

Pearson’s correlations were used to determine the

strength of the relationship between the magnitude of each

variable in the first 15 min of standing and the final rating of

LBD. Three step-wise regression analyses were performed

with the rating of LBD at the end of the 2-h standing period

as the dependent variable and the magnitude of the 12

highest correlated variables (determined using Pearson’s

correlations) in the first 15 min of standing as the

independent variables. These regressions were performed

in order to determine if the level of LBD after 2 h could be

predicted from how an individual stood in the first 15 min.

Model A incorporated all 16 participants ( R2 = 0.59), model

B incorporated 15 of the 16 participants; with one participant

(who did not develop LBD) removed ( R2 = 0.78), and model

C incorporated the 13 participants who developed LBD( R2 = 0.85). Model B could accurately predict the magnitude

of LBD at the end of 2 h of standing for all participants who

developed some level of LBD as well as predict minimal

LBD for two of the three participants who did not develop

LBD. Model B was thought to be the most functional as it

was able to distinguish between those who eventually

developed LBD from those who did not, and is therefore the

focus of the discussion. Coefficients for each variable and

the regression equation for each of the three models can be

found in Table 2.

4. Discussion

As originally hypothesized, the 2-h standing period

elicited low back discomfort in 13 out of 16 individuals. This

is a substantial finding as these individuals who developed

LBD during the 2-h period of standing had no history of

chronic LBD and were completely asymptomatic at the start

of the study.

It was hypothesized that the displacement in centre of

pressure, skin temperature, and perceived fatigue/discom-

fort would increase during the standing period. The results,

however, showed that few variables consistently changed


Fig. 2. The effect of time on the rating of perceived low back discomfort

over the 2-h standing period. Standard error bars are shown. Values grouped

under the same horizontalbar are not significantly different from each other.



over the 2-h period. The variables that did change over time

were the degree of lumbar flexion, L4/L5 joint shear, and

skin temperature over the upper back region. While the

drop in skin temperature may be directly due to the

participants’ back being exposed during the duration of the

collection, the moderate change in spine flexion and L4/L5

joint shear may be associated with the development of low

back discomfort. The moderate spine flexion developed

over the 2 h may have changed the facet separation and

ligament lengths. These passive tissues of the intervertebral

joint have been shown to be sensitive to length and pressure

changes and are highly innervated with type III and IV

nociceptors [19]. This altered loading of the passive

structures may have been one potential source of the

reported discomfort. Further, stadiometry research has

shown that prolonged standing results in disc height loss

[20,21]. This likely also occurred in the current study,

which creates several possible pain generating pathways.

The creep associated with the disc height loss in severe

cases may have altered the morphology of the neural

foramina resulting in nerve impingement, which has beenshown in an animal model to initiate pain with nerve root

compression of magnitudes as low as 8.4% [22]. More

moderate cases of creep changes could create strains in the

passive tissues in the intervertebral joint such as the disc or

articular capsule sufficient to generate pain from com-

pressive loading [23]. It should be noted that the significant

decrease in posterior L4/L5 joint shear over the 2 h was

expected as the model used to determine the joint loading

required lumbar flexion as an input. Given that the actually

observed change in spine flexion and L4/L5 joint shear was

small, these variables were not believed to be the source of

the discomfort. More likely the discomfort was related to

the initial postural and motor control conditions that each

individual self-selected at the start of the standing task, as

shown by the regression results. Based on these results, it

was possible to predict ( R2 = 0.78) the level of LBD after

2 h of standing in a model composed of 15 of the 16

participants by examining the magnitude of three variables

during the first 15 min of standing.

4.1. The ability to predict low back discomfort

As previously mentioned, regressions were performed

using the ratingof LBD at the end ofthe 2-h standingperiod as

the dependent variable and the observed variables in the first

15 min of standing alone as the independent variables, in an

attempt to determine if the level of eventual LBD was related

to how that individual stood in thefirst 15 min. When only one

participant was removed from the complete participant pool

(model B), an R2 of 0.78 was observed. Moreover,this high R2

value suggests that this model canpredict the rating of LBD at

the end of the 2 h in both individuals who did in fact develop

LBD and in those who did not,based onhow they stood in the

first 15 min. The single participant,who did notreport LBD in

the study, and who was excluded from model B was selected

as they were the only person who clearly did not fit the

eventual model. This was possibly due to either possessing a

much different strategy to aid in the prevention of LBD or an

altered perspective of perceived discomfort. When the

excluded participant’s variables were included in this model,

their predicted magnitude of LBD was 28.0 mm, with the

recordedvalue for this participant being 0 mm. Therefore, this

participant tends to stand similarly to those who develop a

substantial level of LBD at the end of 2 h, but did not report

LBD during the standing period.The variables included in both model B and C were shifts

in the CoPAP, gaps in the activation of left GM, and the

degree of axial twist. The coefficient for the number of

shifts in CoPAP is positive, suggesting that a higher number

of shifts was associated with a higher rating of discomfort.

In addition,the coefficient forthe numberof gaps in left GM

activation is also positive, suggesting that a higher number

of gaps in activation was associated with a higher rating of

LBD. These findings contradict previous findings that state

that an increased number of rest periods/gaps in the muscle

and dynamic postures, tracked by increased shifts in CoP,

potentially reduce discomfort and possibly prevent injury

[24,25]. The regression analysis and consequently the

generated model, suggest the opposite, implying that a

more static posture and continuous muscle activation is

associated with a reduced risk of the development of

discomfort.

Two possible interpretations exist that may explain the

direction of the observed relationships with LBD and the

potential mechanisms for the development of LBD. The first

is that the perceived discomfort is a result of the dynamic

nature of the aforementioned variables (increased CoP shifts

and increased muscle gaps). It is possible, according to the

regression model, for an individual to move too much (for


Table 2

Regression equations for each of the three models (coefficients for each variable are shown in parenthesis)

Model participants R2 Regression equation

All 16 participants 0.59 Low back discomfort = (0.028 number of gaps in LRA activation) +

(0.055 number of shifts in angle of axial twist) + (14.532)

15 of 16 participants 0.78 Low back discomfort = (0.062 number of shifts in CoP (AP)) + (0.113

number of gaps in LGM activation) + (1.678 degree of axial twist (8)) + (0.186)

13 LBD participants 0.85 Low back discomfort = (0.063 number of shifts in CoP (AP)) + (0.095 numberof gaps in LGM activation) + (1.424 degree of axial twist (8)) + (1.978)

Note that the dependent variable is the magnitude of low back discomfort at the end of 2 h in mm using a 100 mm visual analog scale.



example awkward twisting, bending and/or reaching) in the

first 15 min of standing, which may be the cause of the

development of discomfort. An alternative explanation is

that those who demonstrated increased shifts did so in an

attempt to prevent or reduce the expected LBD. In other

words, individuals who are more susceptible to developing

LBD may tend to stand with increased movement (example,increased number of CoP shifts) as a pre-emptive strategy.

The ability to potentially predict the development of

discomfort in the low back during standing based on the first

15 min alone is a substantial finding. Examining the

variables that have the largest effect on the generated

model provides information regarding which factors

potentially contribute to LBD. Based on this model, it

may be possible to decipher between individuals who will

develop LBD from those who will not based on how they

stand initially. Furthermore, understanding the character-

istics that possibly aid in reducing LBD during prolonged

standing may help to determine how an individual who

generally develops LBD can adopt these characteristics.

Caution should be taken when applying a generated

regression model to an entire population. The current model

incorporated a small sample group (15 participants), and

future work with a new sample group is required to

determine if the current regression model can be generalized

to and validated on a larger population. Therefore, the main

importance of this regression model is not the ability to

predict LBD development during prolonged standing but

rather to increase the understanding of LBD and the

variables that are associated with its development.

5. Conclusions

This study confirms the likelihood of developing LBD

during a prolonged period of standing, as 13 of the 16

participants developed LBD. Of the variables measured,

very few revealed differences between individuals who

developed LBD during prolonged standing and those who

did not. Additionally, few changes in the measured variables

were observed over time, despite the steady development of

LBD over time. However, there is strong potential in the

ability to predict the magnitude of the LBD developed after a

prolonged period of standing in the individuals monitored in

the current study, based on the first 15 min alone. This

indicates that individuals may adopt initial standing postures

that relate to the magnitude of LBD that they will develop

over time, possibly in an effort to minimize their eventual

level of discomfort. This sheds new light on the under-

standing of the variables associated with the mechanisms of

LBD development.

Conflict of interest statement

None.

Acknowledgments

The authors wish to acknowledge AUTO21—Network of

Centres of Excellence, Canadian Institute for the relief of

pain and disability, and Canadian Institutes for Heath

Research for financial support. Dr. Jack Callaghan is also

supported by a Canada Research Chair in Spine Biome-chanics and Injury Prevention. The authors also wish to

acknowledge Erin Harvey, University of Waterloo, for

statistical consulting.

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