Corresponding author: Junya Sakamoto, Department of Physical Therapy Science, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8520, Japan, Tel: +81-95-819-7967, Fax: +81-95-819-7967, E-mail: jun-saka@nagasaki-u.ac.jp

Received 2025 March 10; Revised 2025 April 28; Accepted 2025 May 12.

Abstract

Study Design

Longitudinal cohort study.

Purpose

To investigate factors associated with chronic pain (CP) development following vertebral fracture (VF).

Overview of Literature

Factors contributing to CP development after VFs are not well characterized.

Methods

Hospitalized patients with acute VFs underwent assessment of vertebral morphology and paraspinal muscles. Two weeks post-admission, patients were evaluated for pain intensity (using the Verbal Rating Scale [VRS]), pain sensitivity (Pressure Pain Threshold [PPT] and Conditioned Pain Modulation), psychological factors, physical function, and activity levels. At 12 weeks, patients were categorized into CP and non-CP (NCP) groups based on VRS scores. Between-group comparisons and logistic regression analysis were performed to identify predictors of CP development.

Results

The CP group exhibited significantly lower remote PPT and reduced low-intensity physical activity time, but higher Pain Catastrophizing Scale rumination scores and prolonged 5-Times Sit-to-Stand Test (5SST) compared to the NCP group. Logistic regression identified prolonged 5SST and reduced low-intensity physical activity as independent predictors of CP development.

Conclusions

Prolonged 5SST and reduced low-intensity physical activity may predict CP development after VFs. Early assessment of these factors may facilitate CP risk screening in hospitalized patients with VFs.

Keywords: Spinal fractures; Chronic pain; Low back pain; Physical activity; Physical functional performance

Introduction

The incidence of fragility fractures attributable to osteoporosis is rising annually in orthopedic practice. Vertebral fractures (VFs) due to osteoporosis frequently result from minimal trauma during daily activities. Among individuals aged ≥65 years, the incidence rate of acute VFs diagnosed based on clinically apparent symptoms like back pain is 15.6 per 1,000 [1]. Acute low back pain is the primary symptom following VF, significantly impairing activities of daily living (ADL) and physical function. Conservative treatment is commonly applied after VF injury, typically involving a combination of orthotic therapy, pharmacotherapy, and rehabilitation. Studies have shown that patients with VFs who wear rigid or soft orthoses experience greater pain relief than those without orthotic support [2]. Furthermore, pharmacotherapy using nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and weak opioids effectively manages pain associated with VFs [3]. Early initiation of therapeutic exercise during rehabilitation improves ADL [4]. Although conservative treatment often leads to pain subsidence and bone healing, some patients develop chronic pain (CP) persisting beyond 12 weeks. Approximately 40% of patients with conservatively treated VFs experience CP (Visual Analog Scale [VAS] ≥35 mm) 1 year post-injury [5,6]. This CP reduces physical function and ADL, increasing the risk of long-term care dependency and impaired quality of life (QOL) [7,8].

To prevent CP after VFs, early identification of contributing factors is crucial. Most studies have investigated vertebral body and paraspinal muscle changes using radiographs and magnetic resonance imaging (MRI). Severe anterior vertebral collapse, fluid sign on T2-weighted MRI, and intense acute-phase pain are associated with CP development [5]. Furthermore, high fatty infiltration in the multifidus and erector spinae muscles has been linked to CP [9], potentially due to its role in spinal instability [10]. These findings suggest that patients with compromised spinal stability after VFs are at higher risk for CP.

Previous studies have linked depression and catastrophizing to persistent low back pain in patients with nonspecific low back pain [11,12]. Reduced physical activity has also been associated with CP in this population [13]. Furthermore, alterations in pain modulation, including peripheral and central sensitization and impaired descending pain inhibition, contribute to CP development in patients with nonspecific low back pain [14,15].

Thus, CP after VFs likely involves a complex interplay of organic, psychological, and neuromuscular factors. Despite this, no studies have comprehensively evaluated these aspects. Identifying key contributors through a multifaceted approach may enable early screening and targeted interventions to prevent CP. The objective of this study was to investigate factors associated with CP development following VF injury.

Materials and Methods

Ethics statement

This study was conducted in compliance with the principles of the Declaration of Helsinki and approved by the Research Ethics Committee of the Graduate School of Biomedical Sciences at Nagasaki University (approval number: 21101406-2). All participants received written and oral information about the study’s purpose and procedures, had the opportunity to ask questions, were given sufficient time to decide on participation, and provided written consent.

Study design

This longitudinal cohort study involved a multidimensional assessment within 2 weeks of admission, followed by a pain survey via telephone at 12 weeks post-admission. Participants were patients diagnosed with acute VFs based on MRI or lateral radiographs, and who received conservative treatment at the Department of Orthopaedic Surgery, Nagasaki Memorial Hospital, Japan, between December 2021 and December 2023. Patients with VF classified as A1 to A4 according to the AOSpine Thoracolumbar Injury Classification System [16], and without neurological symptoms such as paralysis, were treated conservatively. Japanese-speaking patients aged ≥65 years who consented to participate were included. Exclusion criteria were injury from high-impact trauma, cognitive impairment (Mini-Mental State Examination [MMSE] score <23 after 2 weeks), comorbidities hindering rehabilitation, acute illness, or new VFs within 12 weeks of admission.

Conservative treatment, including orthotic support and medical therapy

Previous studies have reported that patients with VF who wear rigid or soft orthoses experience greater pain relief than those without orthoses [2]. Therefore, based on the attending physician’s judgment, each patient was prescribed either a rigid or soft orthosis. A previous study reported the achievement of pain relief with up to 6 months of orthosis use [2]. Another study has demonstrated similar analgesic effects with orthosis use for 6 to 12 weeks [17]. Additionally, a prior study showed suppressed vertebral body collapse following 12 weeks of orthosis application [18]. Based on these findings, the duration of orthosis use in this study was set at 12 weeks from hospital admission. Additional medical treatment was prescribed at the discretion of the attending physician. NSAIDs, acetaminophen, and weak opioids, which are effective in managing pain associated with VF [3], were used as part of the pain management strategy.

Rehabilitation interventions as part of conservative treatment

The rehabilitation program started immediately after admission, following conservative treatment protocols described in previous studies [19]. Initially, patients rested until orthosis completion, with bed rest or assisted toilet use. The orthosis was adjusted according to injury status. Once the orthosis was fitted, patients could mobilize while wearing it. Rehabilitation began upon admission or the next day, starting with limb movements in bed to prevent inactivity. After orthosis completion, patients progressed to standing and walking exercises. The program included individualized muscle strengthening, ADL, and instrumental ADL (IADL) exercises to prepare patients for discharge home.

Epidemiological characteristics of the study population

Data collected included age, sex, height, weight, VF site, number of existing VFs, comorbidities before admission, ADL and IADL before admission, medication use (pain and osteoporosis medications) after admission, and cognitive function at 2 weeks post-admission. Body mass index (BMI) was calculated using height and weight. The Charlson comorbidity index (CCI) was calculated based on pre-admission comorbidities. ADLs before admission were assessed using the Barthel index (BI), IADL using the Tokyo Metropolitan Institute of Gerontology Index of Competence (TMIG-IC), and cognitive function using the MMSE.

Pain assessment

The primary outcome was back pain intensity during movement, assessed at admission and 2 and 12 weeks post-admission using a 5-point Verbal Rating Scale (VRS) (0=no pain, 1=mild, 2=moderate, 3=severe, 4=intolerable). Patients reported their most intense pain. Assessments were conducted in person at admission and 2 weeks, and via telephone interview at 12 weeks. Pain sensitivity was assessed using Pressure Pain Threshold (PPT) and Conditioned Pain Modulation (CPM). PPT was measured at the affected site (affected) and remote sites (remote) using a digital force gauge (RZE-100; Aikoh Engineering Co., Osaka, Japan), referring to previous studies [20,21]. The affected PPT was measured bilaterally at the erector spinae muscles 2.5 cm lateral to the spinous process of the injured vertebra, while the remote PPT was measured at the central part of the biceps brachii muscle belly on the non-dominant hand side (Fig. 1). Pressure stimuli were progressively increased at an acceleration rate of 3 N per second, and participants were instructed to say “stop” when the pressure caused sharp pain. Three measurements were taken at 60-second intervals at each site, and the mean value was used. For CPM, ischemic compression of the arm served as the conditioned stimulus, and the affected PPT was used as the test stimulus [22]. PPT was first measured at the affected site before applying the conditioned stimulus. Next, ischemic compression of the arm was applied to elicit diffuse noxious inhibitory control. Finally, the affected PPT was measured after the conditioned stimulus reached a VRS score of 3 (Fig. 2).

Fig. 1

Pressure Pain Threshold measurement. (A) Digital force gauge (RZE-100; Aikoh Engineering Company, Japan). (B) The erector spinae muscle is 2.5 cm lateral to the spinous process of the injured vertebral body. (C) Biceps brachii.

Fig. 2

Conditioned Pain Modulation measurement. (A) Pressure Pain Threshold (PPT) on the affected side was measured before the conditioning stimulus. (B) Ischemic compression of the arm was applied as the conditioning stimulus to evoke diffuse noxious inhibitory control (DNIC). (C) PPT on the affected side was measured again after the conditioning stimulus reached a Verbal Rating Scale score of 3.

Imaging evaluation

Imaging evaluation included MRI at admission and lateral radiography at 2 weeks post-admission. Vertebral compression was assessed on lateral radiographs based on a previous study [19]. The heights of the anterior, middle, and posterior vertebral walls were expressed as percentages relative to the posterior wall height of the superior vertebra, with lower values indicating more severe compression.

Signal changes in the injured vertebrae were classified using MRI T2-weighted images (T2WI) under radiologist (N.A.) supervision, based on previous studies [23]. Sagittal T2WI were analyzed in three slices (midline, bilateral vertebral arch root medial margins) and classified as confined low-signal change, diffuse low-signal change, diffuse high-signal change, or fluid sign (Fig. 3A–D). The diffuse type was defined as signal changes affecting ≥50% of the vertebral body in at least two slices. Paraspinal muscle cross-sectional area (CSA) was evaluated using MRI at admission. The multifidus and erector spinae muscles between Th12–L1 and L4–L5 were collectively analyzed as paraspinal muscles. Measurements included CSA, functional CSA (fCSA, excluding fatty infiltration), and fat infiltration percentage (FI%), as described elsewhere [24]. The mean CSA of the left and right paraspinal muscles at the vertebral body level was used (Fig. 3E). MRI images were converted to 8-bit grayscale (0–255), with areas >120 classified as muscle and areas ≤120 as fat (Fig. 3F). fCSA was calculated by subtracting the fat-infiltrated area from the CSA, and FI% was calculated as the percentage of fat within the CSA. Image processing was conducted using ImageJ ver. 1.47 (National Institutes of Health, Bethesda, MD, USA).

Fig. 3

Classification of vertebral fractures (VFs) and measurement of paraspinal muscles on T2-weighted images: VFs were classified as (A) confined low-signal change, (B) diffuse low-signal change, (C) diffuse high-signal change, and (D) fluid sign. Paraspinal muscle assessment included (E) measurement of the region of interest to calculate the cross-sectional area and (F) conversion of the fat infiltration area to white, with the red area representing the functional cross-sectional area.

Psychological status

The Pain Catastrophizing Scale-6 (PCS-6) was used to assess catastrophic thinking, the Geriatric Depression Scale-5 (GDS-5) to evaluate depression, and the Tampa Scale for Kinesiophobia-11 (TSK-11) to measure fear of movement. Higher scores on each scale indicated greater symptom severity.

Physical performance and ADL

Physical function was assessed using hand grip strength, isometric knee extension strength, the Timed Up and Go test, the 5-Times Sit-to-Stand Test (5SST), and the 6-Minute Walking Distance (6MWD). ADL ability was assessed using the motor-Functional Independence Measure (motor-FIM).

Physical activity

Physical activity was assessed using the Active-style Pro (HJA-750C; Omron, Kyoto, Japan). The device recorded sedentary time (1.0–1.5 metabolic equivalents of task [METs]), low-intensity activity time (1.6–2.9 METs), and moderate-to-vigorous intensity activity time (≥3.0 METs). The analysis used mean values of each activity time during the first week following 2 weeks of hospitalization.

Data analysis

Patients were categorized into two groups based on motion pain severity at 12 weeks post-admission: non-chronic pain (NCP) (VRS 0–1) and CP (VRS 2–4) groups, following our previous study [19]. Group comparisons were conducted using t-tests, Mann-Whitney U test, and chi-square test. Binomial logistic regression with likelihood ratio-based variable reduction was used to assess the predictors of CP at 12 weeks, adjusting for age and BMI. Variables with significant group differences were included as independent variables. Model fit was evaluated using the Hosmer-Lemeshow test, with p>0.05 indicating adequacy. Statistical significance was set at p<0.05. Analyses were performed using IBM SPSS Statistics ver. 27.0 (IBM Corp., Armonk, NY, USA).

Results

Study population

During the study period, 172 patients were admitted to the hospital. Of these, 71 patients met the inclusion criteria after excluding patients with cognitive impairment (MMSE ≤23) (n=50), those transferred to another hospital within 2 weeks of admission (n=13), those injured by high-energy trauma (n=10), those whose rehabilitation was hindered by comorbidities or complications (n=23), and those who did not provide consent (n=5). Of the 71 eligible patients, 66 were included in the final analysis after further excluding those who developed acute illnesses (n=2) and those who were re-injured (n=3) within 12 weeks post-admission. Of the analyzed participants, 39 (59.1%) were in the NCP group (VRS <2 at 12 weeks), while 27 (40.9%) were in the CP group (VRS ≥2) (Fig. 4).

Fig. 4

Patient selection and classification flow chart. NCP, non-chronic pain; CP, chronic pain.

Baseline characteristics

There were no significant between-group differences with respect to age at admission, sex, BMI, CCI, BI, and TMIG before injury, number and site of acute or previous VFs, pain medications, osteoporosis medications, MMSE scores, VRS at admission, or the type of orthosis used (Table 1).

Table 1

Patient characteristics

Image assessment

The imaging assessment results are summarized in Table 2. There were no significant between-group differences regarding vertebral height loss at 2 weeks post-admission or MRI findings at hospitalization.

Table 2

Image assessment

Differences in multifaceted outcome measures

Table 3 summarizes the comparison of outcome measures between the two groups at 2 weeks after admission. The CP group had significantly lower remote PPT and low-intensity activity time than the NCP group (p=0.010 and p<0.001, respectively). The CP group also had significantly higher PCS-6 rumination scores and 5SST times than the NCP group (p=0.012 and p=0.020, respectively). There were no significant between-group differences regarding the other outcomes.

Table 3

Comparison of outcomes at 2 weeks after admission

Multiple logistic regression analysis

Table 4 shows the binomial logistic regression analysis results, identifying two significant early risk factors for transitioning to CP 12 weeks post-hospitalization. The 5SST score was associated with an increased likelihood of developing CP (odds ratio [OR], 1.11; 95% confidence interval [CI], 1.01–1.21; p=0.041), while low-intensity activity time was associated with a decreased likelihood (OR, 0.98; 95% CI, 0.96–0.99; p=0.007). The logistic regression model demonstrated an adequate fit according to the Hosmer-Lemeshow test (χ²=3.05, degrees of freedom=7, p=0.880).

Table 4

Multiple logistic regression analysis

Discussion

This study investigated early factors contributing to chronic pain in patients with VFs using a multimodal evaluation. The results indicated that lower remote PPT, increased pain catastrophizing (PCS-6 rumination), prolonged 5SST times, and reduced low-intensity physical activity were associated with CP. Furthermore, logistic regression analysis identified 5SST and low-intensity physical activity as independent predictors of CP.

Our study found a 40.9% incidence of CP after VFs. This rate is consistent with existing literature, where Venmans et al. [6] reported 50% of patients experiencing chronic low back pain (VAS >40 mm) 3 months post-VF, and Inose et al. [5] found 40% had chronic low back pain (VAS >35 mm) 1 year post-fracture. Despite variations in definitions, the incidence of CP post-VF generally ranges from 40% to 50%.

While severe anterior vertebral collapse [5] or the presence of a fluid sign can lead to bony fusion failure, potentially causing spinal instability and CP [25,26], and paraspinal muscle atrophy and fatty infiltration have been linked to CP due to reduced spinal stability [27], our study did not observe such associations. Variations in follow-up periods might contribute to these discrepancies. Some studies align with our findings, reporting no significant association with vertebral collapse [19]. These results highlight the need for a multidimensional assessment beyond imaging.

Subjective pain intensity at 2 weeks post-injury did not significantly differ between groups, indicating that early pain intensity may not be a reliable predictor of CP. However, remote PPT was significantly lower in the CP group, indicating central sensitization, a key mechanism in CP development [22]. This is consistent with a previous study showing reduced remote PPT reflects heightened central nervous system excitability, contributing to the transition from acute to CP [28]. Our results suggest early signs of central sensitization may contribute to CP development following VFs.

The CP group had significantly higher rumination scores, as measured by the PCS-6. Rumination, characterized by excessive focus on pain, has been linked to persistent pain states [29]. High levels of rumination can lead to negative perceptions of pain and reduced treatment responsiveness [30], contributing to CP.

The CP group also had significantly prolonged 5SST times. Although this test reflects lower limb strength [31], no significant difference in isometric knee extension strength was observed between groups, suggesting other factors. Instead, prolonged 5SST times may be attributed to protective inhibition of trunk movement, a common phenomenon in patients with low back pain [32,33]. This excessive inhibition may contribute to prolonged 5SST. Additionally, previous studies have linked prolonged standing movement time in early-stage low back pain to CP development [34]. Our findings support this association, suggesting that excessive trunk movement inhibition may contribute to CP after VFs.

The CP group engaged in significantly less low-intensity physical activity. This finding is consistent with previous research reporting an association between reduced activity duration and prolonged nonspecific acute low back pain [34]. Additionally, decreased physical activity in older adults has been linked to impaired pain inhibitory mechanisms and increased pain sensitization [35], which may contribute to CP following VFs.

The study’s findings revealed several key characteristics among patients with VF, including central sensitization, pain catastrophizing, delayed sit-to-stand movements indicating reduced physical function, and decreased physical activity. These factors have also been reported as risk factors for chronicity in other conditions [28,29,34,35]. VF patients with such characteristics may enter a negative feedback cycle, such as fear-avoidant behavior, which can lower their pain threshold and increase the likelihood of developing CP [36]. Based on the multiple regression analysis, assessing physical activity levels and motor performance early in treatment may help identify patients at high risk of developing CP.

Our findings suggest that preventing the transition to CP in VF patients may require tailored, multifaceted rehabilitation strategies beyond standard care. Patients exhibiting central sensitization or pain catastrophizing may benefit from interventions such as pain education and cognitive restructuring [37]. Those with impaired physical function due to unconscious motor control deficits may benefit from motor control exercises [38]. For patients with reduced physical activity, strategies to encourage movement and behavioral medicine interventions should be incorporated [39]. These individualized approaches, guided by specific assessment, warrant further investigation in future interventional studies.

Some limitations of this study should be considered while interpreting the findings. First, the relatively small sample size may have limited statistical power, and larger studies with longitudinal designs are required to confirm these associations. Second, the small number of male participants (only two male patients were included) may limit the generalizability of the findings to all male patients with VFs. Third, pain progression was assessed only up to 12 weeks, potentially explaining differences from previous studies. However, prior research suggests that pain relief beyond 3 months post-VF is minimal, which may mitigate the impact of this limitation [6]. Finally, 50 patients were excluded due to cognitive decline. Future studies should examine the characteristics of patients with VFs and cognitive decline.

Conclusions

This study identified prolonged 5SST times and reduced low-intensity physical activity as key factors influencing CP development after VFs. Early assessment of these factors may help screen for CP risk in hospitalized patients with VFs.

Key Points

This study employed a multimodal evaluation to identify early risk factors for chronic pain development following vertebral fractures.
Lower remote pressure pain threshold, higher pain catastrophizing, prolonged 5-times Sit-to-Stand Test (5SST), and reduced low-intensity physical activity were associated with chronic pain.
Logistic regression identified prolonged 5SST and reduced low-intensity physical activity as independent predictors of chronic pain.
Early assessment of functional and psychological factors may help identify patients at risk of chronic pain following vertebral fractures.

Notes

Conflict of Interest

No potential conflict of interest relevant to this article was reported.

Acknowledgments

We are grateful to all patients who provided data, and we also acknowledge the support of the staff of Nagasaki Memorial Hospital and our laboratory members.

Funding

This work was supported by the Japan Society for the Promotion of Science (JSPS) KAKENHI (grant number: JP 21K11169).

Author Contributions

Conceptualization: Yutaro Kondo, Hideki Kataoka. Investigation: Yutaro Kondo, Yutaro Nomoto, Koichi Nakagawa. Formal analysis: Yutaro Kondo, Hideki Kataoka, Yuki Nishi, Junya Sakamoto. Writing–original draft: Yutaro Kondo, Hideki Kataoka, Junya Sakamoto. Methodology: Hideki Kataoka, Kaoru Morita. Data curation: Kyo Goto. Project administration: Junichiro Yamashita, Junya Sakamoto. Diagnosis: Kaoru Morita. Image assessment: Nobuya Aso. Resources: Junya Sakamoto. Supervision: Minoru Okita. Final approval of the manuscript: all authors.

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Characteristic	NCP group (n=39)	CP group (n=27)	p-value
Age (yr)	80 (71–87)	86 (78–87)	0.287
Sex			0.084
Male	0	2
Female	39	25
Body mass index (kg/m²)	21.5 (19.6–24.3)	21.6 (20.1–24.8)	0.907
Fresh VFs location			0.654
Th6–Th10	2	3
Th11–L2	30	19
L3–L5	7	5
No. of previous VFs			0.353
0	22	10
1	7	5
2	7	7
>2	3	5
Charlson comorbidity index	1 (0–1.5)	1 (0–2)	0.493
Pre-admission BI	100 (95–100)	100 (90–100)	0.307
Pre-admission TMIG	9 (5–12)	9 (5–10)	0.130
Pain medications			0.751
NSAIDs	15	11
Acetaminophen	26	19
Weak opioid	3	2
Osteoporosis medications			0.785
Calcitonin analogs	2	1
Bisphosphonates	4	3
Active vitamin D3 analogs	3	1
MMSE	26.5 (24–29)	26 (24–29)	0.633
VRS at admission	4 (3–4)	3 (2–4)	0.09
Type of orthosis			0.184
Rigid	13	5
Soft	26	22

Variable	NCP group (n=39)	CP group (n=27)	p-value
Vertebral body compression (%)
Anterior	64.7±16.0	65.9±23.7	0.814
Center	52.0±13.9	52.1±16.5	0.986
Posterior	93.9±12.8	91.2±11.3	0.388
Classification of VFs on T2WI
Confined low-signal change	9	9	0.546
Diffuse low-signal change	10	6	0.726
Diffuse high-signal change	7	4	0.737
Fluid sign	1	1	1.000
Th12/L1 paraspinal muscles
CSA (cm²)	13.9±2.8	13.7±1.8	0.829
fCSA (cm²)	11.7±3.5	11.2±2.3	0.651
FI (%)	17.1±15.5	18.4±10.5	0.761
L4/L5 paraspinal muscles
CSA (cm²)	18.5±2.5	18.4±2.6	0.903
fCSA (cm²)	13.7±3.2	12.5±2.7	0.184
FI (%)	25.4±15.5	31.2±15.0	0.219

Variable	NCP group (n=39)	CP group (n=27)	p-value
Verbal Rating Scale	2.0±0.8	2.2±0.7	0.341
Pressure Pain Threshold (N)			0.427
Affected	34.9±11.2	32.0±17.7
Remote	13.9±4.7	10.5±4.4	0.004^*
Conditioned Pain Modulation (%)	109.5±21.1	114.4±21.7	0.364
Pain Catastrophizing Scale-6
Rumination	3.5±2.1	5.0±2.2	0.007^*
Helplessness	3.1±2.3	3.4±2.5	0.636
Magnification	2.6±2.2	3.9±2.5	0.066
Geriatric Depression Scale-5	2.1±1.5	1.9±1.4	0.492
Tampa Scale for Kinesiophobia-11	25.4±4.9	27.9±5.5	0.075
Hand grip strength (kg)	18.2±4.9	16.3±3.7	0.096
Isometric knee extension strength (%)	32.1±12.3	28.7±14.1	0.307
Timed up-and-go test (sec)	18.5±9.1	18.7±8.5	0.918
6-Minute Walking Distance (m)	262.2±108.6	213.0±97.4	0.062
5-Times Sit-to-Stand Test (sec)	15.2±7.0	20.3±8.9	0.014^*
Activity time (min)
Sedentary	547.5±178.0	518.9±292.9	0.653
Low intensity	171.1±60.8	102.3±66.7	<0.001^*
Moderate-to-vigorous	15.4±18.1	10.4±9.4	0.257
motor-Functional Independence Measure	59.2±14.9	52.2±14.0	0.110

	Odds ratio (95% CI)	p-value
5-Times Sit-to-Stand Test	1.11 (1.01–1.21)	0.041^*
Low-intensity activity time	0.98 (0.96–0.99)	0.007^*