Investigating women’s chest size,trunk muscle co-contraction and back pain during prolonged standing

Abstract

BACKGROUND:

Chest size is a known factor in the development of back pain for women. However, the neuromuscular mechanisms associated with chest size and back pain are poorly understood.

OBJECTIVE:

The purpose of this study was to investigate chest size and its association with back pain development and muscle activity patterns during prolonged standing.

METHODS:

Twenty university-aged women were divided into two groups: small chest size ( $n=$ 10, $\sim$ A/C cup) and large chest size ( $n=$ 10, $\sim$ D/E cup). Participants completed a 2-hr standing protocol, where eight channels of bilateral trunk electromyography were collected. Muscle activity, specifically co-contraction, was compared between chest size groups, pain developers, and time.

RESULTS:

The large chest size group reported higher amounts of pain at the upper, middle, and low back. Women in the large chest group sustained higher levels of co-contraction for muscles involving the thoracic and lumbar erector spinae compared to those in the small chest size group during prolonged standing.

CONCLUSIONS:

Thoracolumbar co-contraction determined in this study may be a potential mechanism contributing to increased back pain development for women with large chest sizes during prolonged standing. This pain mechanism could be targeted and addressed in future non-invasive musculoskeletal rehabilitation to improve back pain for women.

Keywords

Anthropometry low back pain occupational standing muscle co-contraction

1. Background

Prolonged static postures, such as standing, are considered contributors to health concerns including low back pain (LBP). Approximately 40% to 70% of asymptomatic individuals will report clinically relevant pain ratings as a result of transient LBP throughout bouts of prolonged standing as short as 2 hours [1, 2]. This exposure, therefore, serves as an accessible protocol to investigate musculoskeletal and anthropometric factors contributing to the development of LBP [3]. Previous research has identified neuromuscular responses of the trunk that are contributors to the pain developed by previously asymptomatic individuals when exposed to prolonged standing [1, 4, 5, 6, 7]. Specifically, in asymptomatic individuals, muscle co-contraction involving the trunk (i.e. erector spinae, abdominals, and gluteal muscles) has highlighted stabilizing, adaptational, and predisposing neuromuscular mechanisms contributing to back pain [5, 6, 7]. One such example, bilateral co-contraction of gluteus medii was identified as a predisposing mechanism for LBP for asymptomatic individuals, that could be successfully reduced through therapeutic exercise intervention, resulting in lower reports of transient LBP development during prolonged standing [4, 5, 6, 8]. Therefore, the interpretation of anthropometric and musculoskeletal factors contributing to co-contraction patterns provide direction for future interventions for non-invasive treatment of prolonged standing induced LBP.

While investigation into standing exposure and neuromuscular responses has been well quantified, the impact of anthropometric characteristics, specifically sex-specific characteristics has received little attention [1, 2]. Chest size, specifically for females, is as a known factor influencing LBP that has not been well quantified [9]. Research regarding chest size and pain has been predominantly retrospective in nature, with the majority of research stemming from reduction mammoplasty or breast cancer studies [9, 10, 11, 12]. These studies report that pain is common for women with larger chest sizes specifically in the neck, shoulder, and low back regions and often surgical intervention or bra support proves successful in the reduction of reported symptoms [10, 11, 12, 13]. In addition to pain, quantified postural differences such as increased thoracic kyphosis and lumbar lordosis have been measured for women with larger chest sizes which in turn may result in muscular adaptations [10, 13, 14, 15, 16]. With positive correlations between muscular activation of erector spinae and chest size it is understandable that there may be additional muscular responses that are necessary for postural support for these women [12]. Chest size specific muscular responses, such as trunk co-contraction, during prolonged standing are unknown and as a result may be a mechanism in LBP for women with larger chest size.

Prolonged standing protocols present a method of interpreting muscular mechanisms in transient low back pain development, as such anthropometric factors, such as chest size, influencing these mechanisms could be investigated using these protocols [1, 9]. With prolonged standing as a common exposure in many occupations, and a lack of non-invasive solutions to back pain for large chest size women, there is an ergonomic, therapeutic, and rehabilitative need to understand the role of muscular contribution to back pain for this population and exposure. An analysis of localized muscle co-contraction specific to chest size has not been previously investigated, therefore, the objective of this study was to establish trunk muscular co-contraction patterns for women based on the factors of chest size and pain development during prolonged standing. It was hypothesized that women with larger chest sizes would exhibit higher LBP development and higher trunk co-contraction patterns over time.

2. Methods

The aim of this study was to quantify the neuromuscular and pain responses to prolonged standing in women with small and large chest size. A 2-hr prolonged standing exposure performed in laboratory was used to investigate the factor of chest size on trunk muscle activation, muscle co-contraction, and self-reported back pain in a mock standing workplace environment. A definition of transient low back pain (LBP) was used to guide the measures of pain in this study, which was retrieved from Sorensen et al., (2015). This protocol was approved by York University’s Office of Research Ethics.

Table 1
Participant characteristics and average 2-hr thoracic and lumbar angle represented as mean (SD). *Significant difference between groups

	Small sized chest ( $n=$ 10)	Large size chest ( $n=$ 10)	$P$ -value
Age (years)	23 yr (3)	20 yr (2)
Pain developer (PD)	6	10
Mass (kg)	60.7 kg (11.4)	61.9 kg (7.25)
BMI (kg/m ${}^{2}$ )	21.8 kg/m ${}^{2}$ (2.39)	22.2 kg/m ${}^{2}$ (2.56)
BIA (%)	20.3% (4.84)	21.9% (6.01)
Waist circumference (cm)	70.5 cm (8.1)	70.6 cm (4.1)
Chest circumference (OBCC – UBCC) (cm)*	7.4 cm (2.1)	14.0 cm (1.8)	$p=$ 0.021
Cup size	A-C	D-E
Thoracic angle ( $\theta$ )*	19.7 ${}^{\circ}$ $\pm$ 6.85	22.0 ${}^{\circ}$ $\pm$ 4.08	$p=$ 0.007
Lumbar angle ( $\theta$ )	$-$ 20.0 ${}^{\circ}$ $\pm$ 8.68	$-$ 23.3 ${}^{\circ}$ $\pm$ 13.8

2.1 Participants

Twenty female participants aged 19–30 years were recruited from a university community setting. Descriptive anthropometric measures included weight, body mass index (BMI), body fat percentage (BIA), wait circumference, and chest size. Chest size was the main independent variable used to classify the participants into small and large chest size groups (Table 1). Chest size was measured as the difference between two chest circumferences: the widest portion of the breast (OBCC) and the circumference just beneath the mammary fold (UBCC). Each 2.54 cm incremental difference corresponds to the common terminology of 1 cup size, i.e. a difference of 2.54 cm is equal to an A cup, 5.08 cm is equal to a B cup and so forth [17]. Participant exclusion criteria included any previous back pain (upper, middle, or low back) where medical care was sought or resulted in absence from work/occupation/school within 12 months prior to the data collection, previous chest surgery (i.e., breast reduction or augmentation), and/or current or prior pregnancy.

2.2 Instrumentation

Electromyography (EMG) was recorded bilaterally from eight muscles: rectus abdominis (RA) external oblique (EO), internal oblique (IO), upper-thoracic erector spinae (T ${}_{4}$ ES), lower-thoracic erector spinae (T ${}_{9}$ ES); latissimus dorsi (LAT), lumbar erector spinae (L ${}_{3}$ ES); and gluteus medius (GLT). Placements were made according to SENIAM guidelines for collection of surface electromyography [18]. The skin surface was cleansed first through shaving removal of hair and rubbing alcohol prior to the application of disposable surface electrodes (Ag/AgCl Ambu Blue Sensor N, Ambu A/S, Denmark). The EMG signals were collected and differentially amplified (AMT-8: Bortec, Calgary, CAN) with the following parameters: 10–10000 Hz frequency response, 115 dB at 60 Hz common mode rejection, 10 G input impedance, and 2400 Hz sampling rate. Pain was measured using subjective report on an unanchored 100 mm visual analog scale (VAS) for the low back regions [3, 19, 20]. In addition to the previously validated measure of transient LBP, transient pain was also measured at the upper and mid back to represent the thoracic region. An unmarked VAS scale was completed for each collection point during the study to mitigate participant bias.

Trunk kinematics through three-dimensional motion capture, were collected at 32 Hz using NDI motion capture system (3D Investigator™, Northern Digital, Ontario, Canada) and analyzed in Visual3D Professional™ Software version 5.02.30 (C-Motion Inc., Germantown, MD, USA). However, this study directly answered the research question related to muscular adaptations.

2.3 Maximum voluntary contractions (MVC)

Maximum voluntary contractions (MVC) were performed using manual resistance. The MVC protocols for the RA, EO, and IO were performed with the participant in a modified curl-up, with flexion, lateral bend, and axial twist motions respectively [21]. A back extension, with strapped legs and manual resistance applied to the scapular region was performed for ES (T ${}_{4}$ , T ${}_{9}$ , L ${}_{3})$ [21]. The MVC for the LATs was performed by a lat pull down [22]. Side lying hip abduction was performed bilaterally for the GLTs [5]. The maximum MVC value recorded for each muscle from three trials (5 minutes rest in between) was used for post collection EMG normalization processing.

Table 2
Normalized average muscle activation over 2-hour prolonged standing for small (NPD: non pain developers, PD: pain developers) and large chest groups, no significant differences for time ( $p=$ 0.08), therefore reported are mean (SD) for the entire prolonged stand

	Mean (%MVC)	(SD)	Mean (%MVC)	(SD)	Mean (%MVC)	(SD)
Muscle	Small NPD		Small PD		Large PD
Left
RA	3.24	(2.28)	4.38	(3.73)	5.26	(1.91)
EO	3.70	(3.13)	4.90	(4.01)	3.18	(2.11)
IO	5.98	(6.54)	6.79	(7.15)	7.89	(3.94)
$T_{4}$ _ES	4.59	(4.05)	3.67	(1.52)	5.26	(3.91)
$T_{9}$ _ES	5.08	(3.70)	4.54	(2.01)	5.90	(3.35)
L_ES	2.19	(1.34)	3.55	(3.15)	3.64	(1.82)
LAT	1.75	(1.13)	2.92	(2.84)	3.63	(2.09)
GLT	2.69	(1.72)	3.34	(2.48)	3.07	(1.74)
Right
RA	3.28	(3.19)	6.39	(6.10)	3.26	(1.74)
IO	4.93	(2.84)	3.77	(2.77)	4.51	(3.20)
EO	2.57	(1.91)	3.15	(1.45)	2.60	(1.66)
$T_{4}$ _ES	3.07	(1.95)	4.81	(2.99)	4.83	(3.11)
$T_{9}$ _ES	4.38	(2.93)	5.39	(3.28)	5.52	(4.61)
L_ES	2.43	(1.51)	5.72	(4.96)	2.94	(2.18)
LAT	3.30	(6.56)	2.16	(2.83)	5.55	(1.67)
GLT	5.02	(4.46)	2.92	(2.01)	4.21	(6.24)

2.4 Protocol

Before the protocol, participants completed three trials of upright quiet standing (reference baseline posture). Participants stood at a mock-up workstation completing various randomized 30 minute blocks of tasks including card shuffling, small object assembly, small object sorting, and keyboard typing at a table surface, standardized to participant height as previously described in prolonged standing protocols [7]. A resting baseline of electromyography (participant lying supine) was taken prior to commencing the prolonged standing protocol. The 2-hr time period was blocked in 15-minute epochs, with continuous collection of EMG. Pain (VAS rating) was collected for the upper, middle, and low back (3 measures) at baseline, the start of every 15 minute, and at the end of the 2-hr protocol. For this study, the VAS measure for the low back was used to categorize pain developers (PD) and non-pain developers (NPD) using a change in VAS was greater than 10 mm between any successive epoch [23].

2.5 Data processing and analysis

Postural data (angles) were calculated in the sagittal plane (flexion-extension) for the thoracic (C7 cluster relative to T12 cluster), and lumbar regions (T12 cluster relative to L5 cluster). Angle data were low-pass filtered with a dual-pass, fourth-order Butterworth filter (residual analysis cutoff frequency: 2.5 Hz [23]. The EMG signals were processed post collection using a customized MATLAB program (The MathWorks, Inc., Natick, USA). A Butterworth high pass, dual-pass filter with a cut-off frequency of 30 Hz, was applied to remove heart rate contamination [24]. The linear envelope of the signals was performed by full-wave rectification, and smoothing with a 2.5 Hz cut-off dual pass Butterworth filter. Each signal was normalized to %MVC, averages over the 2-hr protocol are reported in Table 2. Data were down-sampled from 2400 Hz to 50 Hz.

A co-contraction index (CCI) was used to quantify the co-contraction level (simultaneous contraction of any pair of muscles) of the trunk and back muscles throughout the stand [8, 25, 26]. The CCI provided an indication of the degree to which a pair of muscles had concurrent activation based on the linear envelope of their EMG signals (expressed as %MVC) magnitudes for a given time interval between any pair of muscles Eq. (1).

$\displaystyle\text{CCI}=\sum^{N}_{i=1}\left(\frac{\text{EMG\_low}(i)}{\text{% EMG\_high}(i)}\right)[\text{EMG\_low}(i)+\text{EMG\_high}(i)]$ (1)

Higher values represent scenarios when a pair of muscles are activated for similar timing for a long period of time or one or both muscles have high activation levels. Therefore, two muscles with similar timing of high activation levels results in the highest CCI output. CCI was calculated for each minute of data in the 15-minute epochs. An average for each epoch was then calculated, reducing the data to 8 CCIs per pairing for data analysis. A combined flexor-extensor measure was characterized by the pairings of abdominal muscles with the lumbar erector spinae (12 in total) [1, 21].

An a priori sample size analysis was conducted using G*Power3 to determine group differences using a general linear model with repeated measures with a medium effect size ( $\alpha=$ 0.5), and a significance level of ( $\alpha=$ 0.05) to achieve a power of 0.95 [27, 28]. The sample size yield was 18 participants. The main outcome variable of muscle co-contraction, reduced to an average for 8 time points during the 2-hr stand, was analyzed using a general linear model with between effects of chest size (2 groups), and pain developer (2 groups) and a within effect of time ( $\alpha=$ 0.05). For within effect violations of Mauchly’s test for sphericity, Hyunh-Feldt corrections were applied. Post hoc analyses using Tukey corrections were applied for significant main effects and interactions.

3. Results

3.1 Participant characteristics and pain development

The small group ( $n=$ 10) average chest size measure was 7.4 $\pm$ 2.1 cm ( $\sim$ A-C cup size), compared to the large group ( $n=$ 10) 14.0 $\pm$ 1.8 cm ( $\sim$ D-E cup size). The two groups did not differ in any other anthropometric measure; Table 1. Using the VAS method of classifying transient pain developers 4 participants in the small group were classified as NPDs, and 6 were classified as PDs. All women in the large group developed clinically relevant levels of LBP (average $\Delta$ VAS $=$ 35 mm); Fig. 1. Additionally, 80% of this group developed clinically relevant pain at the upper and mid back regions (average $\Delta$ VAS $=$ 32 mm and 33 mm, respectively). The magnitude of reported pain was greater for all PDs, regardless of chest size, than the small NDPs ( $p<$ 0.001); Fig. 3. For all PDs, there were significant linear associations between pain and time for the upper ( $R=$ 0.95, $p<$ 0.001), mid ( $R=$ 0.97, $p<$ 0.001), and low back ( $R=$ 0.97, $p<$ 0.001) respectively; Fig. 2.

Figure 1.

Percentage of participants reporting a given ( $<$ 10, 10–20, 20–40 mm) change in VAS from baseline. Clinically relevant levels are greater than 20 mm, darkest shade in the charts.

Significant correlations between co-contraction and pain were found for 44 bilateral and 35 ipsilateral of the total 120 trunk muscle pairings. Sixty-eight of these associations occurred between the bilateral and left-side pairings, coinciding with the pairings in which CCI was highest for the large chest group. LATS, $T_{4}$ and $L_{3}$ were found to have the strongest correlations to all three VAS ratings (upper, mid, and low back). The correlations for the thoracic ( $T_{4}$ and $T_{9}$ ES) held moderate positive associations with upper and mid back pain (range of Pearson $R$ values $=$ $+$ 0.260 through $+$ 0.559, $p<$ 0.001), but had moderate negative associations with the low back VAS (range of Pearson $R$ values $=$ $-$ 0.256 through $-$ 0.595, $p<$ 0.001).

Whole-body kinematics were not integrated in the analysis of the outcome variables in this study; however, the average trunk posture of the thoracic and lumbar region was calculated. There was a significant difference in posture between chest size groups, with no effect of pain group. On average, the large group displayed greater thoracic kyphosis, with no significant postural changes over time, compared to the small group. No significant differences were found for the lumbar angle between groups, nor were any changes in posture calculated over time (Table 1).

Figure 2.

Linear association between pain and time between groups (VAS Analogue Scale 100 mm), PDs both large and chest size reported significantly greater levels of pain at all timepoints compared, except baseline compared to NDPs in small chest group ( $p<$ 0.05).

Figure 3.

Average co-contraction for pairings of involving the thoracic and lumbar erector spinae, displayed as CCI $\pm$ SEM as calculated by CCI equation using %MVC. All pairings: significantly greater CCI for the large chest size group (all PDs) compared to small chest size group, regardless of pain development (PD and NDP) ( $p<$ 0.043 to 0.001).

3.2 Muscular responses

A low level of muscle activity was required throughout the stand with no statistical differences in average muscular activation ( $<$ 10 % MVC) during any of the 15-minute epochs between the small NPDs and PDs and large chest PD groups (Table 2).

The main muscles of interest involved the thoracic ( $T_{4}$ , $T_{9}$ ) and lumbar ( $L_{3}$ ) erector spinae pairings, however, a full analysis was completed to investigate all 120 possible muscle pairings. Over half of the measured trunk muscle pairings ( $n=$ 71) displayed significantly higher co-contraction for the large chest size group. For bilateral co-contraction of the same muscle group (i.e. Right muscle: Left muscle), chest size was a significant main factor on co-contraction level: RA: 356 $\pm$ 75 %MVC, EO: 436 $\pm$ 75 %MVC, IO: 129 $\pm$ 108 %MVC, $T_{9}$ ES: 1260 $\pm$ 143 %MVC, L ${}_{1}$ ES: 995 $\pm$ 23 %MVC, GLT: 588 $\pm$ 0 %MVC ( $p<$ 0.005 to 0.001). Specific to the bilateral co-contraction of LATs and $T_{4}$ ES, pain developer group and chest size group had a significant interaction, where all three: 1) large chest PD 2) small chest PD and 3) small chest NPDs were significantly different from one another ( $p=$ 0.001, respectively). For LATs, the average CCI for each group was: Large PD (2110 $\pm$ 129 %MVC) $>$ small PD (812 $\pm$ 182 %MVC) $>$ small NPD (145 $\pm$ 21 %MVC). For $T_{4}$ ES, the average CCIs for each group, where significant differences were found between all 3 groups were: Large PD (2110 $\pm$ 129 %MVC) $>$ NPD (145 $\pm$ 21 %MVC) $>$ small PD (812 $\pm$ 182 %MVC). Displayed in Fig. 3 are the bilateral thoracolumbar pairings that were significantly greater for the large chest group ( $p<$ 0.043 to 0.001). For the large chest group, CCIs involving ES and LATs were significantly higher (two-fold magnitude) compared to all other bilateral pairings ( $p<$ 0.005). For ipsilateral left side pairings, the large group displayed higher levels than both PDs and NPDs of the small group ( $p<$ 0.001) for all possible pairings. Where chest size was a main factor, the large chest group maintained higher CCI levels consistently over time ( $p>$ 0.05). The average values for all possible pairings are accessible in the supplementary data.

Figure 4.

Global flexor-extensors CCI during prolonged standing for large, small PD and NPD respectively. Interaction effect of chest size and time, shaded area denotes main effect of chest size where large PD $>$ small PD and small NPD ( $p<$ 0.05), * denotes time differences for large chest group only where 90 min. $>$ 15 min. 105 min, and 120 min ( $p<$ 0.05). $\blacktriangle$ denotes difference between both large and small PDs $>$ small NPDs. ( $p<$ 0.05).

An interaction effect between chest size and time ( $p=$ 0.023) was found for the global measure of flexor-extensor; Fig. 4. Presented as a combined measure of lumbar ES with core muscle antagonists [8, 29], the large group had significantly higher CCI during the first 90 minutes of standing (1955 %MVC $\pm$ 720), compared to PDs (1400 %MVC $\pm$ 411) and NPDs (1254 %MVC $\pm$ 811) of the small group ( $p<$ 0.001, respectively). For the large chest size group only, post-hoc comparisons reported significantly higher flexor-extensor CCI at the 90-minute epoch compared to the first baseline and 105 and 120 minutes of the standing ( $p<$ 0.001), there were no differences across time for the small chest PDs or NPDs. Upon completion of the stand, at the120-minute timepoint, both PD groups small and large chest size exhibited significantly higher CCI values than the small NPDs.

4. Discussion

Throughout a 2-hr prolonged standing protocol, differences in transient pain development and muscular co-contraction existed between women with small and large chest sizes. During the protocol, 100% of women categorized as the large chest group, and 60% of the small chest group developed transient LBP. No differences were determined in average muscle activation, with relatively low levels of average %MVC required for upright prolonged standing. However, significantly higher levels of co-contraction were sustained throughout standing for the large group, predominantly for pairings involving the thoracolumbar erector spinae ( $T_{4}$ , $T_{9}$ , LES regions). Moderate positive linear associations between co-contraction and pain in the thoracic region were determined during standing. Heightened co-contraction levels, specifically those involving the thoracic and lumbar erector spinae, were associated with chest size, and may be a mechanism contributing to transient back pain development during prolonged standing. The implications of thoracolumbar trunk muscle co-contraction are discussed to position muscular pre-habilitation or rehabilitation, as non-invasive solutions, for back pain during standing in women.

Transient LBP, companied by pain in the upper and mid (thoracic) back regions, occurred for most women in this study. A similar proportion (40% to 70% of asymptomatic individuals) of PDs to that of previous prolonged standing research was reported in the small chest group, however, 100% of the large group presented as PDs [1, 5, 7, 30]. Previous literature has demonstrated significant pain reporting of the neck, shoulders, and back regions as a result of large chest sizes [9, 15, 31]. This study adds to the understanding that chest size is a factor in back pain, demonstrating that prolonged standing of greater than 90 minutes results in clinical reporting of back pain for women with large chest sizes. The fact that all of the participants in the large chest size group developed pain within 2-hr of prolonged standing warrants further investigations into musculoskeletal mechanisms of pain for this group.

Similar to previous studies, LBP was investigated as a transient measure developed from during the protocol [3]. In addition, this study did not localize solely LBP but instead recorded VAS pain for the upper and mid back regions as well. Non-specific to chest size, 2-hr prolonged standing transient LBP was further complicated by the superior regions of the back as demonstrated by high upper and mid back VAS ratings for small and large chest PDs. While trunk co-contraction involving low back stabilizers (i.e. lumbar ES, multifidus) have known associations with pain [30, 32], these findings further supported the implication of these muscle stabilizers, but in addition emphasize the thoracic region of the extensor grouping during standing. Considering the continuation of the erector spinae grouping throughout the length of the spine, the musculoskeletal responses of the entirety of the spine are important in the targeting solutions for LBP. Given the respective muscular contribution to both trunk and upper limb stability required for completing tabletop tasks while standing, transient prolonged standing back pain may not just be related to maintaining sagittal plane postural stability but to frontal plane stability as well, specifically when completing prolonged standing tasks [33]. The thoracic region in conjunction with the lumbar region and their combined role in transient prolonged standing back pain should be considered when attempting musculoskeletal rehabilitation or treatment strategies.

Factoring in the anthropometric measure of chest size for women in a prolonged standing protocol demonstrated muscular contributions to the burden of back pain associated with large chest size. The large chest size group entered the standing protocol with higher levels of thoracolumbar co-contraction bilaterally (CCI levels greater than 2000 %MVC) and sustained these levels over time, in comparison to women in the small NPD and PD groups. It is possible that large chested women consistently employ co-contraction as an extensor stiffening to account for the greater anterior load while standing, as positive relationships with average ES muscle activity and chest size have been previously established [13, 14, 15, 16]. Thoracolumbar co-contraction as a postural support, may also be required to account for the increased thoracic kyphosis experienced by women with larger chest sizes [9, 10, 15, 34]. While a small difference, the large chest group stood over time, on average, with greater kyphosis. Recognizing that with increased anterior mass there are resultant postural changes, the required demand of the thoracolumbar musculature implicates itself in the responses to prolonged standing and subsequent transient LBP development.

In addition to the sustained high levels of thoracolumbar co-contraction displayed between bilateral and core muscle comparisons, antagonistic co-contraction as measured by the global co-contraction of the combined flexor-extensors (average of 12 pairings of lumbar ES) displayed chest-size effects in the results [8, 25]. There was a chest size and time interaction found, in which the large chest size group displayed significantly higher co-contraction than the small chest groups and displayed a marked increased after 90 minutes This increase returned to baseline in the remaining 30 minutes of the stand, where both small and large chest PDs completed the stand with higher antagonistic co-contraction than the small NPD group. As established biomechanical models have proposed antagonistic co-contraction as a means of increasing spinal stability [33, 35, 36]; it is possible that increased antagonistic contraction was required balance the trunk moment for the large chest group, reflecting the higher sustained levels in the initial 60 minutes of standing. However, the marked increase for the large chest group after 90 minutes might suggest this antagonistic co-contraction shifting from a stability mechanism to a postural bracing mechanism [8, 33, 35] Despite an attempt to mitigate pain, the marked increase in antagonistic co-contraction for the large chest PDs returned to baseline in the final 30 minutes, with continual transient pain increases. It was important to note that upon completion of the stand at the 2-hr mark, both small and large chest PDs had higher antagonistic co-contraction than small NPDs. As all PDs had greater antagonistic flexor-extensor co-contraction at the end of the stand, the fine line between stability and bracing for posture in prolonged standing appears to be linked to transient pain. While the timing of this bracing was later in this prolonged stand than previous research, where flexor-extensor co-contraction increased after 60 minutes (1); it nevertheless highlights the temporal consequences of prolonged standing, specifically for larger chested women with no initial baseline low back pain. As the participant population was a younger, active cohort they may have held greater tolerance to prolonged standing lasting beyond the initial 60 minutes determined in other studies [6, 35, 36]. Nonetheless, it is still necessary to further investigate the biological and psychosocial factors that influence the temporal considerations in stabilizing and bracing trunk co-contraction for maintenance of spine stability during prolonged standing.

The limitations that should be considered when applying these findings are as follows. While the findings warrant caution to prolonged standing bouts up to two hours, due to the cross-sectional nature of the study, inference to longer occupational standing (i.e., full workdays), or repeated bouts of prolonged standing requires further investigation. Only university aged females completed this study, which limits its generalizability. Breast size variation, such as those early in puberty, throughout development, pregnancy, and aging were not represented by the cohort or the circumferential measurement method of measuring chest size. However, despite this measurement as a representation of chest size, there were still clear size differences found in the muscular responses. Transient pain development, as measured by VAS, classified all of the large chest size group as PDs, therefore, there was no NPD comparison group for the large group. Correcting for the unbalanced design, interpretations and comparisons were made with the small chest NPDs in combination with findings of previous studies investigating co-contraction in asymptomatic university aged populations. Finally, only select superficial muscle groups were recorded due to surface EMG measurement, deep muscles and individual motor unit synchronization were not collected. While these thoracolumbar co-contraction mechanisms were significant, there are potentially other muscle groups, and additional mechanisms of pain contributing to back pain development in standing for women.

5. Conclusion

In conclusion, chest size influenced muscular co-contraction patterns and transient back pain development in prolonged standing for women. Thoracolumbar co-contraction was, on average, two times higher for women with large chest size compared to small chest size during the 2-hour standing protocol. High pain ratings in all three regions of the back and high co-contraction levels throughout standing demonstrate harmonized co-contraction – back pain mechanisms. Reported are chest size specific thoracolumbar co-contraction patterns that highlight where interventions, such as extensor strengthening, intermittent walking, sitting, or standing breaks may be investigated in the future as non-invasive solutions for back pain in this population.

Availability of data and materials

The datasets analyzed during the current study are not publicly available as this was not captured in the consent form. Participants agreed to have their data anonymized and analyzed for the purpose of this study but did not have the option to make the dataset publicly available.

Consent for publication

Consent forms, highlighting publication as a potential dissemination, were completed by all participants.

Ethics approval and consent to participate

Human research ethics was approved by the Human Research Ethics Review Committee at York University.

Funding

Doctoral (Johnston) and Discovery Grant (Drake) funding support from the Natural Sciences and Engineering Research Council (NSERC).

Supplementary data

The supplementary files are available from https://dx. doi.org/10.3233/BMR-200090.

Footnotes

Conflict of interest

The authors declare that they have no competing interests.

References

Nelson-Wong

Howarth

Callaghan

. Acute biomechanical responses to a prolonged standing exposure in a simulated occupational setting. Ergonomics. 2010; 53(9): 1117-28. doi: 10.1080/00140139.2010.500400.

Coenen

Parry

Willenberg

Shi

Romero

Blackwood

, et al. Associations of prolonged standing with musculoskeletal symptoms – A systematic review of laboratory studies. Gait Posture. 2017 June; 58: 310-8. doi: 10.1016/j.gaitpost.2017.08.024.

Sorensen

Johnson

Callaghan

George

Van Dillen

. Validity of a Paradigm for Low Back Pain Symptom Development During Prolonged Standing. Clin J Pain. 2015; 31(7): 652-9. doi: 10.1097/AJP.0000000000000148.

Viggiani

Callaghan

. A hip abduction exercise prior to prolonged standing increased movement while reducing cocontraction and low back pain perception in those initially reporting low back pain. J Electromyogr Kinesiol. 2016; 31: 63-71. doi: 10.1016/j.jelekin.2016.09.005.

Nelson-Wong

Gregory

Winter

Callaghan

. Gluteus medius muscle activation patterns as a predictor of low back pain during standing. Clin Biomech. 2008; 23(5): 545-53. doi: 10.1016/j.clinbiomech.2008.01.002.

Marshall

PWM

Patel

Callaghan

. Gluteus medius strength, endurance, and co-activation in the development of low back pain during prolonged standing. Hum Mov Sci. 2011; 30(1): 63-73. doi: 10.1016/j.humov.2010.08.017.

Gregory

Callaghan

. Prolonged standing as a precursor for the development of low back discomfort: An investigation of possible mechanisms. Gait Posture. 2008; 28(1): 86-92. doi: 10.1016/j.gaitpost.2007.10.005.

Nelson-Wong

Callaghan

. 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(2): 256-63. doi: 10.1016/j.jelekin.2009.04.009.

Spencer

Briffa

. Breast size, thoracic kyphosis & thoracic spine pain – association & relevance of bra fitting in post-menopausal women: A correlational study. Chiropr Man Ther. 2013; 21(1): 1-8. doi: 10.1186/2045-709X-21-20.

10.

Findikcioglu

Ozmen

Guclu

. The impact of breast size on the vertebral column: A radiologic study. Aesthetic Plast Surg. 2007; 31(1): 23-7. doi: 10.1007/s00266-006-0178-5.

11.

Hall-Findlay

. A simplified vertical reduction mammaplasty: shortening the learning curve. Plast Reconstr Surg. 1999; 104(3): 748-59. doi: 10.1097/00006534-199909010-00020.

12.

Chadbourne

Zhang

Gordon

Ross

Schnur

, et al. Clinical outcomes in reduction mammaplasty: A systematic review and meta-analysis of published studies. Mayo Clin Proc. 2001; 76(5): 503-10. doi: 10.4065/76.5.503.

13.

McGhee

Steele

. Biomechanics of Breast Support for Active Women. Exerc Sport Sci Rev. 2020; 48(3): 99-109. doi: 10.1249/JES.0000000000000221.

14.

Schinkel-Ivy

Drake

JDM

. Breast size impacts spine motion and postural muscle activation. J Back Musculoskelet Rehabil. 2016; 29(4): 741-8. doi: 10.3233/BMR-160680.

15.

McGhee

Coltman

Riddiford-Harland

Steele

. Upper torso pain and musculoskeletal structure and function in women with and without large breasts: A cross sectional study. Clin Biomech. 2018; 51: 99-104. doi: 10.1016/j.clinbiomech.2017.12.009.

16.

Steele

Coltman

McGhee

. Effects of obesity on breast size, thoracic spine structure and function, upper torso musculoskeletal pain and physical activity in women. J Sport Heal Sci. 2020; 9(2): 140-8. doi: 10.1016/j.jshs.2019.05.003.

17.

McGhee

Steele

. Breast volume and bra size. Int J Cloth Sci Technol. 2011; 23(5): 351-60. doi: 10.1108/09556221111166284.

18.

Stegeman

Hermens

. Standards for surface electromyography: The European project Surface EMG for non-invasive assessment of muscles (SENIAM). 2007; 108-12.

19.

Kelly

. The minimum clinically significant difference in visual analogue scale pain score does not differ with severity of pain. Emerg Med J. 2001; 18(3): 205-7. doi: 10.1136/emj.18.3.205.

20.

Bombardier

Hayden

Beaton

. Minimal clinically important difference. Low back pain: Outcome measures. J Rheumatol. 2001; 28(2): 431-8.

21.

Dankaerts

O’sullivan

Burnett

Straker

Danneels

. 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(3): 333-42. doi: 10.1016/j.jelekin.2003.07.001.

22.

Park

Yoo

. Comparison of exercises inducing maximum voluntary isometric contraction for the latissimus dorsi using surface electromyography. J Electromyogr Kinesiol. 2013; 23(5): 1106-10. doi: 10.1016/j.jelekin.2013.05.003.

23.

Winter

. Biomechanics and motor control of human movement. John Wiley & Sons; 2009; doi: 10.1002/9780470549148.

24.

Drake

JDM

Callaghan

. Elimination of electrocardiogram contamination from electromyogram signals: An evaluation of currently used removal techniques. J Electromyogr Kinesiol. 2006; 16(2): 175-87. doi: 10.1016/j.jelekin.2005.07.003.

25.

Schinkel-Ivy

Nairn

Drake

JDM

. Investigation of trunk muscle co-contraction and its association with low back pain development during prolonged sitting. J Electromyogr Kinesiol. 2013; 23(4): 778-86. doi: 10.1016/j.jelekin.2013.02.001.

26.

Lewek

Rudolph

Snyder-Mackler

. Control of frontal plane knee laxity during gait in patients with medial compartment knee osteoarthritis. Osteoarthr Cartil. 2004; 12(9): 745-51. doi: 10.1016/j.joca.2004.05.005.

27.

Erdfelder

Faul

Buchner

. GPOWER: A general power analysis program. Behav Res Methods, Instruments, Comput. 1996; 28(1): 1-11. doi: 10.3758/BF03203630.

28.

Muller

LaVange

Ramey

. Power Calculations for General Linear Multivariate Models Including Repeated Measures Applications. J Am Stat Assoc. 1992; 87(420): 1209. doi: 10.1080/01621459.1992.10476281.

29.

Schinkel-Ivy

Drake

JDM

. Sequencing of superficial trunk muscle activation during range-of-motion tasks. Hum Mov Sci. 2015; 43: 67-77. doi: 10.1016/j.humov.2015.07.003.

30.

Van Dieën

Selen

LPJ

Cholewicki

. Trunk muscle activation in low-back pain patients, an analysis of the literature. J Electromyogr Kinesiol. 2003; 13(4): 333-51. doi: 10.1016/S1050-6411(03)00041-5.

31.

Sigurdson

Mykhalovskiy

Kirkland

Pallen

. Symptoms and related severity experienced by women with breast hypertrophy. Plast Reconstr Surg. 2007; 119(2): 481-6. doi: 10.1097/01.prs.0000246407.87267.46.

32.

Hemming

Sheeran

Van Deursen

Sparkes

. Investigating differences in trunk muscle activity in non-specific chronic low back pain subgroups and no-low back pain controls during functional tasks: A case-control study. BMC Musculoskelet Disord. 2019; 20(1): 1-10. doi: 10.1186/s12891-019-2843-2.

33.

Lee

Rogers

Granata

. Active Trunk Stiffness Increases with Co-contraction. J Electromyogr Kinesiol. 2006; 16(1): 51-7. doi: 10.1016/j.jelekin.2005.06.006.

34.

Briggs

Van Dieën

Wrigley

Greig

Phillips

, et al. Thoracic Kyphosis Affects Spinal Loads and Trunk Muscle Force. Phys Ther. 2007; 87(5): 595-607. doi: 10.2522/ptj.20060119.

35.

Granata

Marras

. Cost-benefit of muscle cocontraction in protecting against spinal instability. Spine. 2000; 25(11): 1398-404. doi: 10.1097/00007632-200006010-00012.

36.

Mirka

Marras

. A stochastic model of trunk muscle coactivation during trunk bending. Spine. 1993; 18(11): 1396-409. doi: 10.1097/00007632-199318110-00003.

Investigating women’s chest size,trunk muscle co-contraction and back pain during prolonged standing

Abstract

BACKGROUND:

OBJECTIVE:

METHODS:

RESULTS:

CONCLUSIONS:

Keywords

1. Background

2. Methods

Table 1 Participant characteristics and average 2-hr thoracic and lumbar angle represented as mean (SD). *Significant difference between groups

2.2 Instrumentation

2.3 Maximum voluntary contractions (MVC)

Table 2 Normalized average muscle activation over 2-hour prolonged standing for small (NPD: non pain developers, PD: pain developers) and large chest groups, no significant differences for time ( p = 0.08), therefore reported are mean (SD) for the entire prolonged stand

2.5 Data processing and analysis

3.1 Participant characteristics and pain development

5. Conclusion

Availability of data and materials

Consent for publication

Ethics approval and consent to participate

Funding

Supplementary data

Footnotes

Conflict of interest

References

Table 1
Participant characteristics and average 2-hr thoracic and lumbar angle represented as mean (SD). *Significant difference between groups

Table 2
Normalized average muscle activation over 2-hour prolonged standing for small (NPD: non pain developers, PD: pain developers) and large chest groups, no significant differences for time ( $p=$ 0.08), therefore reported are mean (SD) for the entire prolonged stand