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Updated: May 5, 2026
Visualization of Intensity Levels to Reduce the Gap Between Self-Reported and Directly Measured Physical Activity
Published on: March 7, 2019
Accelerometer-measured intensity-specific physical activity, genetic susceptibility, and back pain risk: a UK Biobank
Yuanpeng Zhu1, Di Liu1, Xiangjie Yin1
1Department of Orthopedic Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, No.1 Shuaifuyuan, Beijing, 100730, China; Beijing Key of Big Data Innovation and Application for Skeletal Health Medical Care, No.1 Shuaifuyuan, Beijing, 100730, China; Key Laboratory of Big Data for Spinal Deformities, Chinese Academy of Medical Sciences, No.1 Shuaifuyuan, Beijing, 100730, China.
Background Context:
Current clinical guidelines lack clear, quantitative recommendations on intensity-specific physical activity (PA) levels for preventing back pain. Moreover, accelerometer-based evidence regarding dose-response relationships and interactions between PA and genetic susceptibility remains limited.
Purpose:
To determine the relationships between accelerometer-measured total and intensity-specific PA and incident back pain, and to assess potential effect modification by polygenic risk scores (PRS).
Study Design:
Prospective, large-scale, population-based study using UK Biobank data.
Patient Sample:
UK Biobank participants who wore wrist accelerometers for 7 days (N=71,601).
Outcome Measures:
Incident back pain, defined as the first recorded ICD-10 dorsalgia code (M54).
Methods:
Total PA, light PA (LPA), and moderate-to-vigorous PA (MVPA) were derived using validated machine-learning algorithms from raw accelerometer data. Dose-response relationships were modeled using restricted cubic splines within Cox proportional hazards models, with adjustment for and stratification by a polygenic risk score (PRS). Point estimates for the population attributable fraction (PAF) were then calculated. Body mass index (BMI) mediation was assessed.
Results:
Over a median follow-up of 7.0 years, total PA and MVPA exhibited nonlinear inverse associations with incident back pain, independent of genetic risk, with thresholds at approximately 35 milli-g (total PA) and 60 min/day (MVPA). The adjusted PAF was 15.9% for low MVPA and 9.9% for low total PA. Associations were strongest for MVPA, followed by total PA; no significant association was observed for LPA. Within both PRS strata, risk declined monotonically across PA quartiles, with similar effect sizes and no PA × PRS interaction. Notably, participants with high PRS and high PA had lower risk than those with low PRS and low PA. BMI mediated 26.2% of the total PA association and 15.5% of the MVPA association.
Conclusions:
Accelerometer-measured MVPA robustly reduces back-pain risk, independent of genetic predisposition. Future guidelines should provide clear, intensity-specific recommendations and account for the observed nonlinear dose-response to optimize prevention.
