Nicholas Joy, Thomas J. Donnelly, Jonathan Soslow, William Bryan Burnette, Christopher Spurney, Nazia Husain, Katheryn Gambetta, Brian D. Soriano, Frank J. Raucci Jr, Kan Hor, Larry W. Markham, Kimberly Crum, Catherine E. Lang.
Abstract
Duchenne muscular dystrophy (DMD) is characterized by progressive decline in skeletal muscle function leading to loss of ambulation and premature cardiopulmonary failure. The ability to monitor declines in skeletal muscle function in a free-living setting would be advantageous. Prior studies have utilized accelerometer measures of movement quantity (e.g., counts per minute, fraction of activity time), but accelerometry research on measures of movement quality in DMD is limited.
Introduction
Duchenne muscular dystrophy (DMD) is an X-linked recessive disorder affecting the dystrophin protein caused by a loss-of-function mutation in the DMD gene [1]. The condition has an estimated global incidence of 1 in every 3000–5000 live male births [2]. The progressive disorder is characterized by decline in skeletal and cardiac muscle function leading to loss of ambulation, decreased pulmonary capacity, cardiomyopathy, and premature death—at a median age of 27 (though some variation in life expectancy from the late teens to early 40’s) [3].
Methods
Ethics statement
All procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional committees and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. The study was approved by the Vanderbilt University Medical Center Institutional Review Board (Nashville, TN) and WashU Medicine Institutional Review Board (St Louis, MO).
Results
Participant demographics
Accelerometer data from 100 male participants with DMD and 92 healthy male control participants were analyzed. Their demographic and anthropometric information is summarized in Table 2. The cohorts did not differ significantly in terms of participant age, weight, race and ethnicity distributions (Table 2). Participant height and subsequent BMI did differ significantly (Table 2) with individuals with DMD being shorter and having higher BMI Z-scores on average.
Discussion
Due to progressive skeletal myopathy associated with DMD, we expected that individuals with DMD would produce movements of higher entropy, jerk, and mean frequency. In comparison with healthy individuals, however, individuals with DMD produced on average lower entropy and jerk, and higher mean frequency (Table 3). In addition, accelerometer-derived measurements of movement quantity and quality were associated with moderate strength among both participants with DMD and healthy controls.
Conclusion
Acknowledgments
We thank the children and families who participated in this study. We would also like to thank Keith Lohse, PhD for his efforts developing the code for the accelerometer measures. Membership of DMDCCC Investigators is as follows: Jonathan Dayan, Division of Pediatric Cardiology, Department of Pediatrics, University of California Davis; M. Jay Campbell and Jennifer Li, Division of Pediatric Cardiology, Department of Pediatrics, Duke University Medical Center; Beth Kaufman, Division of Pediatric Cardiology, Department of Pediatrics, Lucile Packard Children’s Hospital at Stanford; Carol Wittlieb-Weber, Division of Pediatric Cardiology, Department of Pediatrics, Children’s Hospital of Philadelphia; Teresa Wang, Division of Cardiovascular Medicine, Department of Medicine, University of Pennsylvania
Citation: Joy N, Donnelly TJ, Soslow J, Burnette WB, Spurney C, Husain N, et al. (2026) Assessing movement quality in individuals with Duchenne muscular dystrophy utilizing accelerometry: Comparisons with healthy controls. PLOS Digit Health 5(6): e0001315. https://doi.org/10.1371/journal.pdig.0001315
Editor: Lawrence D. Hayes, Lancaster University, UNITED KINGDOM OF GREAT BRITAIN AND NORTHERN IRELAND
Received: March 5, 2026; Accepted: May 12, 2026; Published: June 2, 2026
Copyright: © 2026 Joy et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: The data for the typically developing children cohort is available on the NICHD DASH repository (DOI: 10.57982/fayx-p832; 10.57982/72z7-m179). The data for the Duchenne muscular dystrophy cohort is available through the Rare Disease Cures Accelerator - Data and Analytics Platform (RDCA-DAP) repository funded by FDA Grant U18FD005320 and administered by Critical Path Institute (C-Path). Both repositories provide free and easy access to anyone of interest.
Funding: Data from typically developing children were harmonized and shared using funding by National Institutes of Health grants (R37HD068290 and T32HD007434 to CL). Dr. Raucci is funded by the National Heart, Lung, and Blood Institute (K08HL155852 to FR). Dr. Soslow is supported by the National Heart, Lung, and Blood Institute (K23HL123938, R56HL141248, and R01HL167969 to JS), the Food and Drug Administration (FDA) (1R01FD006649 to JS), and National Center for Advancing Translational Science (UL1-TR002243 to JS). Dr. Soslow has received a grant from Ametris, LLC. to conduct an observational study, however no associated data was used in development of this manuscript. Dr. Tamaroff is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (3R01DK118407-03S1 to JT) and the American Heart Association (23SCEFIA1156470 to JT). This project was supported by Fight DMD. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: I have read the journal’s policy and the authors of this manuscript have the following competing interests: JS has received a grant from Ametris, LLC. to conduct an observational study, however no associated data was used in development of this manuscript.
