Arterial stiffness, biological age and frailty in incident probable sarcopenia and sarcopenia (UK Biobank cohort)
In 32,451 UK Biobank participants free of probable sarcopenia and sarcopenia at baseline, higher arterial stiffness index was associated with higher risks of both outcomes; biological age acceleration mediated part of these associations and frailty modified their magnitude. [1]
Automatic summary · not editorially reviewed
The key findings
The prospective cohort included 32,451 UK Biobank participants free of probable sarcopenia and sarcopenia at baseline. [1]
Compared with the lowest ASI tertile, the highest tertile had higher risks of probable sarcopenia (HR 1.38, 95% CI 1.22-1.55) and sarcopenia (HR 1.56, 95% CI 1.11-2.18). [1]
Biological age acceleration mediated 8.66% and 18.85% of the associations, and frailty modified their magnitude, with associations largely confined to non-frail participants. [1]
The source at a glance
- Study type / format
- Prospective cohort study (abstract)
- Population / context
- 32,451 UK Biobank participants free of probable sarcopenia and sarcopenia at baseline
- Summary based on
- Study abstract
- Original publication
- September 14, 2026
UK Biobank cohort without sarcopenia at baseline
This prospective cohort study followed 32,451 UK Biobank participants who were free of probable sarcopenia and sarcopenia at baseline. Arterial stiffness was measured as an arterial stiffness index (ASI). Cause-specific Cox proportional hazards models examined associations between ASI and incident probable sarcopenia and sarcopenia, and restricted cubic spline analyses described dose-response relationships.
Supporting source [1]
Higher ASI tertile and incident outcomes
During follow-up, 1,901 participants developed probable sarcopenia and 277 developed sarcopenia. Compared with the lowest ASI tertile, participants in the highest tertile had higher risks of probable sarcopenia (HR 1.38, 95% CI 1.22-1.55) and sarcopenia (HR 1.56, 95% CI 1.11-2.18). ASI showed a nonlinear association with probable sarcopenia but a linear association with sarcopenia.
Supporting source [1]
Biological age mediation and frailty modification
Klemera-Doubal biological age acceleration (KDM-BAacc) significantly mediated 8.66% of the association with probable sarcopenia and 18.85% of the association with sarcopenia. Frailty significantly modified these associations, with the associations largely confined to non-frail participants. The authors describe arterial stiffness as a potential upstream determinant, biological aging as a mediating pathway and frailty as a modifier of susceptibility; these are associations, not established causes.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Follow-up duration, ASI measurement details, frailty definition and adjustment variables are not reported here. The findings are observational associations from one cohort and do not establish that arterial stiffness causes sarcopenia.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Sun A, Du Y, Yang X, Liu H, Zeng R, Wu Y, Liu Z. · europepmc.org · September 14, 2026