Sage Journals: Discover world-class research

Abstract

Background:

Prolonged standing has been associated with an increased prevalence of low back pain (LBP) and is recognized as a potential workplace hazard for employees such as retail staff, assembly line workers, and healthcare personnel. Low back pain is more prevalent in women than in men, and disability due to LBP is worse in women with severe urinary incontinence. However, it is unclear whether pelvic floor dysfunction observed in stress urinary incontinence is a risk factor for LBP. The main purpose of this study is to determine whether co-activation patterns between the pelvic floor and abdominal muscles during a 2-hour prolonged standing task predict transient LBP in women with and without stress urinary incontinence.

Methods:

In this is prospective cohort study, 60 female volunteers will stand in a confined area for 2 hours (120 minutes) while performing tasks such as, ‘computer work’ and ‘small object assembly’. The primary outcome measure is transient LBP, which will be monitored every 10 minutes using a numeric pain rating scale. Surface electromyography (EMG) will be collected from the gluteus medius and internal oblique/transverse abdominis muscles, and an intravaginal electrode will be used to monitor pelvic floor muscle activity. The EMG signals will be divided into 12 10-minute blocks to assess changes in co-activation over time. Cross-correlation analyses will be used to quantify co-activation between the muscle pairs (e.g. pelvic floor and internal oblique/transverse abdominis), and the coefficient of co-activation will be expressed as a percentage for each block. A mixed-model regression analysis will be used to determine whether co-activation patterns can predict transient LBP during the prolonged standing task.

Discussion:

The primary objective of this research is to improve current understanding regarding the role of pelvic floor muscles in the onset of LBP and the potential association between stress urinary incontinence and LBP. These findings have the potential to inform prevention and rehabilitation programmes for women with stress urinary incontinence and LBP.

Trial registration:

ACTRN12618000446268 [Protocol Version 2].

Keywords

urinary incontinence prolonged standing low back pain pelvic floor

Background

Low back pain (LBP) is the most common, costly, and disabling musculoskeletal condition with a lifetime prevalence of up to 80%.¹ Low back pain is more prevalent in women than men with a mean prevalence ratio of 1.2:1.^2-5 Stress urinary incontinence (SUI) is also a common problem that disproportionately affects women,⁶ with a mean prevalence of 23.6%.⁷ Recent studies have highlighted an association between LBP and urinary incontinence (UI),^8-11 indicating that women with UI are more than twice as likely to experience frequent back pain as those without UI.¹² In addition, women with greater severity of UI also report an increased severity and greater disability related to their LBP.¹³

Standing for more than 30 minutes per hour has been identified as a significant hazard (hazard ratio: 1.9) for LBP in the workplace.¹⁴ In female-dominant occupations such as retail, teaching, assembly line work, and healthcare, prolonged standing for greater than 2 hours, is a significant risk factor for LBP.^14-17 Recent research indicates that prolonged standing might also lead to transient LBP in workers without previous history of back injury.^18-20 Transient back pain by definition exists solely during the exposure time and dissipates quickly once the standing ceases. Yet, during 2-hour prolonged standing laboratory trials, the development of transient LBP was found to be a positive predictor (3.33 OR for 12-month follow up) for future long-term and recurrent LBP.^21,22 Although the mechanism for the development of transient LBP is not well understood, the musculoskeletal characteristic most commonly linked with LBP is aberrant muscle activity.^23-25 Increased bilateral co-activation of the gluteus medius (GM) muscles has been specifically associated with transient LBP during prolonged standing trials.^19,26,27

Insufficiency of the pelvic floor muscles (PFMs) is a significant factor in SUI,^28-30 which leads to involuntary urine loss during abrupt increases in intra-abdominal pressure (i.e. coughing, sneezing, lifting, or laughing).³¹ Several PFM deficiencies have been identified in women with SUI, such as decreased tonic activity,³² PMF weakness,³³ and delayed onset of PFM recruitment.³⁴ Pelvic floor muscle and abdominal muscle synergies are a potentially important mechanism to promote continence by resisting increased intra-abdominal pressure.³⁵ Furthermore, the muscles of the pelvic floor when acting synergistically with those of the abdominal cavity, particularly the transverse abdominis (TA) and internal oblique (IO), are also important to lumbo-pelvic function and spinal stability.^28,36-39 Co-activation of the PFMs and abdominal muscles contribute to increased spinal stability through spinal column stiffening and increasing the intra-abdominal pressure.^40,41 It is possible that deficiency in the PFM activity alters the neuromuscular connection between the PFMs and abdominal muscles resulting in a disturbed muscle synergy, a mechanism observed in pregnancy and postpartum women.⁴² Putatively, this may be seen as a central nervous system (CNS) feedback mechanism to reduce intra-abdominal pressure in an attempt to maintain urinary continence; however, this mechanism may have a detrimental effect on lumbo-pelvic stability potentially increasing the risk for LBP in women with SUI. Partial support for this hypothesis comes from the works of Asavasopon et al⁴³ and Yani et al,⁴⁴ who identified common motor cortical areas associated with PFM and synergistic muscle activity in healthy participants.

The muscles of the pelvic floor are believed to play a duel role in lumbo-pelvic function.²⁸ The function of the PFMs in supporting continence is well known.^45,46 However, as they are also synergists with the abdominal muscles such as transverse abdominis, they may also play an important role in the mechanical function of the lumbo-pelvic complex.^36,47,48 It is reasonable to expect a relationship exists between PFM function, continence status and the development of LBP. The primary aim of this study is to determine whether co-activation patterns between the pelvic floor and abdominal muscles during a 2-hour prolonged standing task predict transient LBP in healthy women with and without SUI. The secondary aim is to determine whether transient LBP during prolonged standing is associated with changes in PFM activity and lumbo-pelvic stability after 2 hours of standing.

Methods

Experimental design

This is a prospective cohort laboratory design. All participants will provide written, informed consent before taking part in the study. Ethics approval (H18/009) has been granted by the University of Otago Human Ethics Committee (Health). This protocol has been developed in accordance with SPIRIT statement and guidelines.⁴⁹

Sample size estimation

The sample size was estimated for multiple regression analysis, using Pass software (NCSS^©, Kaysville, Utah, USA) considering 80% power, an effect size (f²) of 0.212 attributable to three independent variables using an F-test with a significance level (alpha) of 0.05. The variables tested are adjusted for an additional two independent variables. The calculations assume an unconditional (random X’s) model. Based on this, a minimum of 60 participants are required.

Participants

We will recruit a minimum of 60 participants, however, to ensure that our study sample is reflective of the population norm we plan to continue recruiting participants until we have at minimum sample proportion of 30% with stress UI symptoms.

Inclusion criteria

We will seek female participants over the age of 18 years who are free from LBP at the time of the study either with or without symptoms of SUI. All participants will be screened during initial phone interview for symptoms of SUI using the Questionnaire for Urinary Incontinence Diagnosis (QUID),⁵⁰ and if present, the severity will be examined with the Michigan Incontinence Symptom Index (M-ISI severity domain).⁵¹

Exclusion criteria

Participants will be excluded if they:

Have experienced any form of spinal/back surgery or have had recent abdominal or pelvic surgery (<12 months);

Have experienced any lifetime episode of LBP and/or pelvic girdle pain sufficient to cause >3 days of missed work/school/sport and to seek treatment from a registered health professional;

Have urge or mixed UI as determined from the QUID questionnaire;

Report a history of hip pathology that may cause pain with prolonged standing, including osteoarthritis, femoroacetabular impingement, and recent hip surgery (1 year);

Are currently pregnant or within 6 months postpartum;

Have been diagnosed with significant prolapse (Stage 2 or greater POP) or experience faecal incontinence;

Are currently experiencing severe allergies (e.g. hay fever) or upper respiratory infections.

Equipment

Surface electromyography (EMG) will be collected from the TA/IO, GM, and PFMs, using a 16-channel wireless EMG (Ultimum-EMG, Noraxon USA Inc, Arizona, USA). For monitoring the PFMs, surface electrodes will be inserted into the vagina (Periform Intra-Vaginal Probe, Patterson Medical Ltd, Huthwaite, Sutton-in-Ashfield, Nottinghamshire, England, UK). Raw EMG data will be sampled at 2000 Hz from electrodes adhered bilaterally as per international guidelines (SENIAM).⁵² Surface sites for TA/IO and GM will be prepped by first shaving and lightly abrading the area to remove any dead or loose surface skin cells, then the site will be cleaned with alcohol swipes. Electromyography signals will be normalized in the following ways; the TA/IO will be normalized to crook lying bent leg raise,⁵³ the GM to side bridge⁵⁴ and PFM signals will be normalized to muscle activity elicited during maximal voluntary contraction (MVC).

A force platform sampling at 1000 Hz with amplifier gain of 4000 (AMTI, Watertown, MA, USA) will be used to record postural sway. This will be assessed via centre of pressure (CoP) displacement in the anterior-posterior and mediolateral directions.

Experimental procedures

Demographic information will be collected including age, height, weight, number of prior pregnancies and births, and handedness. Participants will complete an assessment of general physical ability and fitness for the last 7 days with the International Physical Activity Questionnaire (IPAQ) and a Pain Beliefs Questionnaire.⁵⁵ Finally, assessment of lumbo-pelvic stability will be performed via the active straight leg raise (ASLR) test as per Mens et al.^56,57 Pelvic floor muscle EMG activity as well as the quality/ability of movement during the ASLR will be assessed for the evaluation of lumbo-pelvic stability. Quality of movement will be assessed using a six-point scale to rate the level of difficulty: ‘not difficult at all = 0; minimally difficult = 1; somewhat difficult = 2; fairly difficult = 3; very difficult = 4; and unable to do = 5’. To examine the effect of the prolonged stand on lumbo-pelvic stability, the ASLR outcomes will be re-assessed at primary time point at the end of the 120 minutes.

Standing protocol

Participants will be positioned on a 0.50 m × 0.46 m force platform and instructed to stand in their usual manner for prolonged standing of 120-minute duration. They must stay within the confines of the force platform borders and may not rest limbs on the tray in front of them. Participants will be given a set of tasks similar to those performed in prolonged standing occupations, such as, small item assembly or ‘computer work’.⁵⁸ Participants will be given the following set of instructions regarding their standing:

Stand in your usual manner, if standing for an extended period of time. You cannot lean on the table surface. Your feet cannot leave the grey area (force plate) on the floor or overlap one another, but you may move and reposition your feet within the grey surface.

Once collection starts there will be no opportunity for breaks; therefore, participants will be instructed to go to the bathroom if they require before data collection begins. This protocol has been established as a valid tool for predicting risk for long-term LBP in apparently healthy populations.^22,26

Outcome measures

Primary outcome measure

Pain scores will be used as the primary outcome and measured with a 11-point numerical pain rating scale (NPRS) with end-points of 0 “no-pain” (far left) to 10 “worst pain imaginable” (far right). The NPRS has good construct and predictive validity as a measure of pain intensity.^59-61 Pain scores during the stand will be normalized against baseline and scored as a continuous variable.

Secondary outcome measure

The secondary outcome measure will be pain outcome as assessed at the end of the primary time point (120 minutes) and represented as a dichotomous variable: pain-developer versus non-pain-developer. A change in NPRS score of 2 points or greater is considered a significant change in pain⁶²; thus, participants with scores increasing by 2 or more will be considered as pain-developers and those with scores less than 2 will be considered as non-pain-developers.

Time points

The study schedule of enrolment, interventions, and assessments is presented in Table 1. Outcome measures will be assessed at the following time points. Baseline, defined as the time before the start of the experimental protocol. Follow-up blocks, defined as 12 10-minute blocks occurring between the start of the experimental protocol (time = 0) and the end of the experimental protocol (time = 120 minutes). Primary time point, the end of the experimental protocol (time = 120 minutes). At baseline, we will assess pain using NPRS, demographic information (including physical fitness, pain beliefs, and UI severity questionnaires) and ASLR. During each of the follow-up blocks, we will assess the muscle co-activation and NPRS for primary outcome measure. At the primary time point, we will assess final NPRS to be used as the secondary outcome and ASLR.

Table 1.

Schedule of enrolment, interventions, and assessments for prolonged standing protocol.

	Enrolment	Baseline	Follow-up											Primary time point	Close out
Time point	−t₁	0	t ₁₀	t ₂₀	t ₃₀	t ₄₀	t ₅₀	t ₆₀	t ₇₀	t ₈₀	t ₉₀	t ₁₀₀	t ₁₁₀	t ₁₂₀	t _end
Enrolment
Eligibility screening Exclusion criteria	x
QUID questionnaire	x
Informed consent	x
INTERVENTION
Prolonged stand			x	x	x	x	x	x	x	x	x	x	x	x
Computer or small item task			x	x	x	x	x	x	x	x	x	x	x	x
ASSESSMENTS
M-ISI questionnaire		x
Measurement of height/weight		x
IPAQ questionnaire		x
Pain Beliefs questionnaire		x
Pain-developer/non-developer^a															x
Numerical pain rating (NPRS)^b		x	x	x	x	x	x	x	x	x	x	x	x	x
ASLR (lumbo-pelvic stability)		x													x
PFM muscle activity		x													x
Muscle co-activation		x	x	x	x	x	x	x	x	x	x	x	x	x	x

Abbreviations: QUID, questionnaire for urinary incontinence diagnosis; M-ISI, Michigan Incontinence Symptom Index; IPAQ, International Physical Activity Questionnaire; ASLR, active straight leg raise; PFM, pelvic floor muscle.

Secondary outcome measure.

Primary outcome measure.

Predictor variables

Muscle co-activation

We will assess co-activation between the PFMs and the TA/IO and the co-activation between the right and left GM muscles as predictors for the primary outcome variable (continuous NPRS score). Cross-correlation analyses will be used to quantify co-activation between the identified muscle pairs.⁵⁸ For each block, the normalized cross-correlation values R_xy will be calculated between the EMG signals using equation (1). R_xy(τ) is the normalized cross-correlation of the two muscle signals x(t) and y(t) at a phase shift τ having a value between +1 and −1. The mean cross-correlation value (R_xy), across all phase shifts, is calculated for each 10-minute block

R_{x y} (τ) = \frac{1}{T} \int_{0}^{T} \frac{x (t) y (t + τ) d t}{\sqrt{R x x (0) R y y (0)}}

(1)

This analysis will yield three co-activation coefficients; Right_PFM-TA/IO, Left_PFM-TA/IO, and Left_GM-Right_GM.

Pelvic floor activity during ASLR

Change in lumbo-pelvic stability related to the prolonged stand will be assessed via differences in PFM activity from baseline ASLR assessment to the end of the primary time point ASLR assessment. Change in PFM activity will be used as a predictor for the secondary outcome measure and pain development. To allow appropriate trial-to-trial comparison of ASLR activity, the height of the limb lift will be standardized using an ultrasonic sensor. The ultrasonic sensor (SICK AG^© Industrial Sensors, Germany model UM30-13113) has an analogue output for measuring the scanning distance with a resolution of 0.36 mm and accuracy of ⩽2% for limiting scanning distance (Sick, 2006). The sensor emits an auditory beep as soon as the participants attain the threshold height of 10 cm off the floor and the feedback signal sounds for as long as the threshold height is maintained. The EMG integral (PFM_integral) will be calculated for 3 seconds during the isometric portion of the ASLR task. To allow for trial-to-trial comparisons, the PFM_integral will be normalized to the MVC task. The variable will be stored as a continuous variable ΔPFM_integral (equation (2))

Δ \int P F M = \int_{b a s e l i n e} P F M - \int_{E n d p o i n t} P F M

(2)

PFM onset latency

Muscle onset latency will be assessed to determine if there is a change in motor control of the PFM that is predictive of pain development during prolonged standing. The timing of the PFM activation onset during the endpoint ASLR will be detected via computer algorithm as per Hodges and Bui.⁶³ Muscle onset is detected at the start of a 50-ms window during which the mean activity is greater than 2.5 SD more than the average EMG signal for the rest period.⁶³ The time of PFM onset will be normalized to the initiation of heel lift during the ASLR. The data will be stored as a continuous variable PFM_onset.

Michigan Incontinence Symptom Index

The baseline assessment of severity of UI symptoms scored from the Severity Domain of the questionnaire. This score will be recorded as a continuous variable and will be included as a covariate for the primary outcome measure and as a predictor for the secondary outcome measure.

Data processing and analysis

All questionnaire and demographic data, including the NPRS, will be collected using an electronic database (i.e. the participant will enter data directly) and verified as complete by the researcher before the participant leaves the laboratory. All data will be stored on a computer hard-drive and backed up on a second external drive. Raw EMG signals will be collected in LabChart (ADInstruments Pty Ltd, Bella Vista, NSW, Australia) and exported to MATLAB for postprocessing. The EMG signals will be divided into 12 10-minute blocks to assess changes in co-activation over time.⁵⁸ All EMG signals are processed using purpose written MATLAB scripts (version 2013b). Any electrical noise (50 Hz) will be removed with a 49.5 to 50.5 Hz band stop filter (fourth-order, dual-pass, zero-lag Butterworth filter). Low- and high-frequency noise is removed with a 10 to 500 Hz band pass filter (fourth-order, dual-pass, zero-lag Butterworth filter).⁶⁴ The signals are then full wave rectified and filtered through a 6 Hz low-pass filter (fourth-order, dual-pass, zero-lag Butterworth filter) to create a linear envelope.⁶⁵

Statistical analysis

The statistical analysis will be undertaken with R (Version 2.15.3, R core team, 2012). Demographic data (age, body mass index (BMI), parity, activity level, and Pain beliefs scores) will be assessed for comparisons between pain-developers and non-pain-developers using independent t-tests. The primary analysis will consist of mixed regression models to test the association between pain scores (the primary outcome and continuous variable) and predictors: (1) mean co-activation coefficient between PFM and TA/IO (Left-Right_PFM-TA/IO); (2) mean co-activation coefficient between Left and Right GM; and (3) time, with M-ISI UI score as a covariate. If required, the model may be adjusted for up to two demographic factors that may be revealed as significant in the independent t-tests comparing pain-developers with non-pain-developers.

A secondary analysis will include a logistic regression model to examine the association between pain event during the stand (pain-developer vs non-pain-developer) with a potential change in lumbo-pelvic stability with three predictors: (1) change in PFM activity during the ASLR test from baseline to primary time point (ΔPFM_integral); 2) muscle onset latency during endpoint ASLR (PFM_onset); and 3) M-ISI UI score.

Discussion

The primary objective of this research is to elucidate significant predictors of LBP related to PFM function during prolonged standing. Findings from this study can potentially improve work-related outcome for women presenting with PFM dysfunction.

Issues related to study design

Prospective study outcomes are considered high-level (Level II) evidence. However, large sample sizes are typically required, and they are prone to selection bias. Attrition bias is one problem with prospective studies due to the length of the follow-up period. We do not expect this to be a problem in our protocol due to the limited nature of the exposure time and confines of the laboratory setting. Another possible issue is the potential of systematic sample bias. While every precaution will be taken by way of exclusionary criteria to ensure sample homogeneity, there could be an underlying covariate within the population which may be associated with the outcome but is unknown to us at the start of the study. Therefore, we have allowed within the statistical design two possible adjustment factors which may arise from the analysis of the demographic data comparing pain-developers with non-pain-developers.

The strength and power of the statistical analysis is dependent on the incidence of LBP reported in the sample. Sample size was determined in part based on previous studies using the prolonged standing protocol to elicit transient LBP symptoms in healthy populations. These studies reported LBP incidence ranging from 39% to 70% in the exposed populations.^19,22,66,67 We expect our population incidence to be similar although we cannot be certain of these outcomes.

We are proposing the use of surface EMG for examining muscle activity in this study. Surface electrode placement for the IO muscle has been shown to have considerable crosstalk with the TA, which limits our ability to differentiate specific muscle fibre action from each of these muscle tissues independently.⁶⁸ In the case of this study, we are examining the effect of synergistic muscle action. Therefore, we are making an assumption that there will be some level of the co-activation of the TA and IO muscles that will be reflected in the activity measured using the described electrode placement. Depending on the findings of this study, future work may seek to separate the synergistic action of these two muscles.

Footnotes

Funding:

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study is supported by the University of Otago Research Grant [UORG – 0118-0319], New Zealand. D.C.R. is supported by The Sir Charles Hercus Health Research Fellowship – Health Research Council of New Zealand. There was no additional external funding received for this study. The funder did not have any role on the designing of the study and has not role on deciding whether the report can be submitted for publication.

Declaration of conflicting interests:

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Author Contributions

MDB was responsible for the design of the study and is the guarantor. SM, DCR, DA, SW, and NH provided guidance on the design and analysis planned for this study. MDB led efforts for securing funding, with the contributions from DA and DCR. All authors had input into revision of the manuscript for important content and approved the final version.

Availability of Data and Material

Final data used for statistical analysis will be made available on the Open Science Framework.

Data Availability

Final data will be made available on the Open Science Framework.

Ethical Approval and Consent to Participate

This study was approved by the University of Otago Ethics Committee (reference no.: H18/009). All participants will sign an informed consent prior to taking part in the study.

ORCID iD

Melanie Dawn Bussey

References

Andersson

GBJ

. Epidemiological features of chronic low-back pain. Lancet. 1999;354:581–585.

Bailey

Risk factors for low back pain in women. Menopause. 2009;16:3–4.

Wáng

J-Q

Káplár

Increased low back pain prevalence in females than in males after menopause age: evidences based on synthetic literature review. Quant Imaging Med Surg. 2016;6:199–206.

Schneider

Randoll

Buchner

Why do women have back pain more than men. Clin J Pain. 2006;22:738–747.

Bener

Dafeeah

Alnaqbi

Prevalence and correlates of low back pain in primary care: what are the contributing factors in a rapidly developing country. Asian Spine J. 2014;8:227–236.

Nitti

VW.

The prevalence of urinary incontinence. Rev Urol. 2001;3:S2–S6.

Serati

Ghezzi

The epidemiology of urinary incontinence: a case still open. Ann Transl Med. 2016;4:123.

Arab

Behbahani

Lorestani

Azari

Assessment of pelvic floor muscle function in women with and without low back pain using transabdominal ultrasound. Man Ther. 2010;15:235–239.

Bush

Pagorek

Kuperstein

Guo

Ballert

Crofford

LJ.

The association of chronic back pain and stress urinary incontinence: a cross-sectional study. J Womens Health Phys Therap. 2013;37:11–18.

10.

Cassidy

Fortin

Kaczmer

Shumaker

JTL

Szeto

Madill

SJ.

Relationship between back pain and urinary incontinence in the Canadian population. Phys Ther. 2017;97:449–454.

11.

Eliasson

Elfving

Nordgren

Mattsson

Urinary incontinence in women with low back pain. Man Ther. 2008;13:206–212.

12.

Smith

Russell

Hodges

PW.

Do incontinence, breathing difficulties, and gastrointestinal symptoms increase the risk of future back pain. J Pain. 2009;10:876–886.

13.

Kim

Kwon

Chung

et al . Age-sex differences in the hip abductor muscle properties. Geriatr Gerontol Int. 2011;11:333–340.

14.

Andersen

Haahr

Frost

Risk factors for more severe regional musculoskeletal symptoms: a two-year prospective study of a general working population. Arthritis Rheum. 2007;56:1355–1364.

15.

Yue

Liu

Neck/shoulder pain and low back pain among school teachers in China, prevalence and risk factors. BMC Public Health. 2012;12:789.

16.

O’Neill

. Standing problem. Hazards 91, August 2005:1.

17.

Parent-Thirion

Biletta

Cabrita

et al . Sixth European working conditions survey – overview report. https://www.eurofound.europa.eu/publications/report/2016/working-conditions/sixth-european-working-conditions-survey-overview-report. Up-dated 2016.

18.

Gallagher

Campbell

Callaghan

JP.

The influence of a seated break on prolonged standing induced low back pain development. Ergonomics. 2014;57:555–562.

19.

Marshall

Patel

Callaghan

JP.

Gluteus medius strength, endurance, and co-activation in the development of low back pain during prolonged standing. Hum Mov Sci. 2011;30:63–73.

20.

Callaghan

De Carvalho

Gallagher

Karakolis

Nelson-Wong

Is standing the solution to sedentary office work?

Ergon Des Q Hum Factors Appl. 2015;23:20–24.

21.

Callaghan

BJP

Carvalho

De Gallagher

Karakolis

Nelson-Wong

. Is standing the solution to sedentary office work? Ergonom Des. 2015;23:20–24.

22.

Nelson-Wong

Callaghan

JP.

Transient low back pain development during standing predicts future clinical low back pain in previously asymptomatic individuals. Spine (Phila Pa 1976). 2014;39:E379–E383.

23.

Danneels

Cagnie

D’hooge

et al . The effect of experimental low back pain on lumbar muscle activity in people with a history of clinical low back pain: a muscle functional MRI study. J Neurophysiol. 2016;115:851–857.

24.

Hodges

Holm

Hansson

Holm

Rapid atrophy of the lumbar multifidus follows experimental disc or nerve root injury. Spine (Phila Pa 1976). 2006;31:2926–2933.

25.

Hodges

Richardson

CA.

Transversus abdominis and the superficial abdominal muscles are controlled independently in a postural task. Neurosci Lett. 1999;265:91–94.

26.

Nelson-Wong

Callaghan

JP.

Is muscle co-activation a predisposing factor for low back pain development during standing? a multifactorial approach for early identification of at-risk individuals. J Electromyogr Kinesiol. 2010;20:256–263.

27.

Bussey

Kennedy

Gluteus medius coactivation response in field hockey players with and without low back pain. Phys Ther Sport. 2016;17:24–29.

28.

Sapsford

Rehabilitation of pelvic floor muscles utilizing trunk stabilization. Man Ther. 2004;9:3–12.

29.

Luginbuehl

Baeyens

J-P

Taeymans

Maeder

I-M

Kuhn

Radlinger

Pelvic floor muscle activation and strength components influencing female urinary continence and stress incontinence: a systematic review. Neurourol Urodyn. 2015;34:498–506.

30.

Nygaard

Barber

Burgio

et al . Prevalence of symptomatic pelvic floor disorders in US women. JAMA. 2008;300:1311–1316.

31.

Sultan

Monga

Lee

et al . An International Urogynecological Association (IUGA)/International Continence Society (ICS) joint report on the terminology for female anorectal dysfunction. Neurourol Urodyn. 2017;36:10–34.

32.

Deindl

Vodusek

Hesse

Schussler

Pelvic floor activity patterns: comparison of nulliparous continent and parous urinary stress incontinent women. A kinesiological EMG study. Br J Urol. 1994;73:413–417.

33.

Gunnarsson

Mattiasson

Female stress, urge, and mixed urinary incontinence are associated with a chronic and progressive pelvic floor/vaginal neuromuscular disorder: an investigation of 317 healthy and incontinent women using vaginal surface electromyography. Neurourol Urodyn. 1999;18:613–621.

34.

Stien

Kulseng-Hanssen

Kristofferson

Clinical and urodynamic assessment of nulliparous young women with and without stress incontinence symptoms: a case-control study. Obstet Gynecol. 1994;84:1028–1032.

35.

Junginger

Baessler

Sapsford

Hodges

PW.

Effect of abdominal and pelvic floor tasks on muscle activity, abdominal pressure and bladder neck. Int Urogynecol J. 2010;21:69–77.

36.

Pool-Goudzwaard

van Dijke

van Gurp

Mulder

Snijders

Stoeckart

Contribution of pelvic floor muscles to stiffness of the pelvic ring. Clin Biomech. 2004;19:564–571.

37.

Hemborg

Moritz

Lowing

Intra-abdominal pressure | trunk muscle activity during lifting. IV. The causal factors of the intra-abdominal pressure rise. Scand J Rehabil Med. 1985;17:25–38.

38.

Sapsford

Richardson

Maher

Hodges

PW.

Pelvic floor muscle activity in different sitting postures in continent and incontinent women. Arch Phys Med Rehabil. 2008;89:1741–1747.

39.

Sapsford

Hodges

PW.

Contraction of the pelvic floor muscles during abdominal maneuvers. Arch Phys Med Rehabil. 2001;82:1081–1088.

40.

Cholewicki

Juluru

McGill

SM.

Intra-abdominal pressure mechanism for stabilizing the lumbar spine. J Biomech. 1999;32:13–17.

41.

Cholewicki

Juluru

Radebold

Panjabi

McGill

SM.

Lumbar spine stability can be augmented with an abdominal belt and/or increased intra-abdominal pressure. Eur Spine J. 1999;8:388–395.

42.

Pereira

Botelho

Marques

et al . Are transversus abdominis/oblique internal and pelvic floor muscles coactivated during pregnancy and postpartum. Neurourol Urodyn. 2013;32:416–419.

43.

Asavasopon

Rana

Kirages

et al . Cortical activation associated with muscle synergies of the human male pelvic floor. J Neurosci. 2014;34:13811–13818.

44.

Yani

Wondolowski

Eckel

et al . Distributed representation of pelvic floor muscles in human motor cortex. Sci Rep. 2018;8:7213.

45.

Dumoulin

Hay-Smith

Mac Habée-Séguin

Pelvic floor muscle training versus no treatment, or inactive control treatments, for urinary incontinence in women. Cochrane Database Syst Rev. 2014;5:CD005654.

46.

Price

Dawood

Jackson

SR.

Pelvic floor exercise for urinary incontinence: a systematic literature review. Maturitas. 2010;67:309–315.

47.

Sapsford

Hodges

Richardson

Cooper

Markwell

Jull

GA.

Co-activation of the abdominal and pelvic floor muscles during voluntary exercises. Neurourol Urodyn. 2001;20:31–42.

48.

Hodges

Sapsford

Pengel

LH.

Postural and respiratory functions of the pelvic floor muscles. Neurourol Urodyn. 2007;26:362–371.

49.

Chan

Tetzlaff

Gotzsche

et al . SPIRIT 2013 explanation and elaboration: guidance for protocols of clinical trials. BMJ. 2013;346:e7586.

50.

Bradley

Rahn

Nygaard

et al . The questionnaire for urinary incontinence diagnosis (QUID): validity and responsiveness to change in women undergoing non-surgical therapies for treatment of stress predominant urinary incontinence. Neurourol Urodyn. 2010;29:727–734.

51.

Suskind

Dunn

Morgan

DeLancey

McGuire

Wei

JT.

The Michigan Incontinence Symptom Index (M-ISI): a clinical measure for type, severity, and bother related to urinary incontinence. Neurourol Urodyn. 2014;33:1128–1134.

52.

Hermens

Freriks

Disselhorst-Klug

Rau

Development of recommendations for SEMG sensors and sensor placement procedures. J Electromyogr Kinesiol. 2000;10:361–374.

53.

Dankaerts

O’Sullivan

Burnett

Straker

Danneels

LA.

Reliability of EMG measurements for trunk muscles during maximal and sub-maximal voluntary isometric contractions in healthy controls and CLBP patients. J Electromyogr Kinesiol. 2004;14:333–342.

54.

McGill

Childs

Liebenson

Endurance times for low back stabilization exercises: clinical targets for testing and training from a normal database. Arch Phys Med Rehabil. 1999;80:941–944.

55.

Edwards

Pearce

Turner-Stokes

Jones

The Pain Beliefs Questionnaire: an investigation of beliefs in the causes and consequences of pain. Pain. 1992;51:267–272.

56.

Mens

Vleeming

Snijders

Koes

Stam

HJ.

Reliability and validity of the active straight leg raise test in posterior pelvic pain since pregnancy. Spine (Phila Pa 1976). 2001;26:1167–1171.

57.

Mens

Vleeming

Snijders

Koes

Stam

HJ.

Validity of the active straight leg raise test for measuring disease severity in patients with posterior pelvic pain after pregnancy. Spine (Phila Pa 1976). 2002;27:196–200.

58.

Nelson-Wong

Gregory

Winter

Callaghan

JP.

Gluteus medius muscle activation patterns as a predictor of low back pain during standing. Clin Biomech. 2008;23:545–553.

59.

Jensen

Chen

Brugger

AM.

Interpretation of visual analog scale ratings and change scores: a reanalysis of two clinical trials of postoperative pain. J Pain. 2003;4:407–414.

60.

Jensen

Turner

Romano

JM.

What is the maximum number of levels needed in pain intensity measurement. Pain. 1994;58:387–392.

61.

Price

Bush

Long

Harkins

SW.

A comparison of pain measurement characteristics of mechanical visual analogue and simple numerical rating scales. Pain. 1994;56:217–226.

62.

Childs

Piva

Fritz

JM.

Responsiveness of the numeric pain rating scale in patients with low back pain. Spine (Phila Pa 1976). 2005;30:1331–1334.

63.

Hodges

Bui

BH.

A comparison of computer-based methods for the determination of onset of muscle contraction using electromyography. Electroencephalo Clin Neurophysiol. 1996;101:511–519.

64.

Merletti

Parker

Electromyography: Physiology, Engineering, and Non-Invasive Applications. https://books.google.co.nz/books?hl=enlr=id=SQthgVMil3YCoi=fndpg=PR15dq=related:xBmY9AE4i8EJ:scholar.google.com/ots=ooLtLtL-eZsig=c2fOrWu-XZ8fvm6U6foCnA_GfIg. Up-dated 2004. Accessed July 14, 2015.

65.

Winter

DA.

Biomechanics and Motor Control of Human Movement. New York, NY: Wiley; 2009.

66.

Gregory

Callaghan

JP.

Prolonged standing as a precursor for the development of low back discomfort: an investigation of possible mechanisms. Gait Posture. 2008;28:86–92.

67.

Viggiani

Callaghan

JP.

Hip abductor fatigability and recovery are related to the development of low back pain during prolonged standing. J Appl Biomech. 2018;34:39–46.

68.

Floyd

Silver

PHS

. Electromyographic study of patterns of activity of the anterior abdominal wall. J Anat. 1950;84:132–145.

Is Pelvic Floor Dysfunction Associated With Development of Transient Low Back Pain During Prolonged Standing? A Protocol

Abstract

Background:

Methods:

Discussion:

Trial registration:

Keywords

Background

Methods

Experimental design

Sample size estimation

Participants

Inclusion criteria

Exclusion criteria

Equipment

Experimental procedures

Standing protocol

Outcome measures

Primary outcome measure

Secondary outcome measure

Time points

Predictor variables

Muscle co-activation

Pelvic floor activity during ASLR

PFM onset latency

Michigan Incontinence Symptom Index

Data processing and analysis

Statistical analysis

Discussion

Issues related to study design

Footnotes

Funding:

Declaration of conflicting interests:

Author Contributions

Availability of Data and Material

Data Availability

Ethical Approval and Consent to Participate

ORCID iD

References