Diabetes, obesity & metabolism · 2026
Leisure-Time Physical Activity on Age-Modelled Trajectories of Body Mass Index and Obesity Risk Throughout Life: Multivariable Regression and Mendelian Randomization Analyses Using Electronic Health Record Data From the CORDELIA-Catalunya Study.
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Hernando-Redondo Javier, Camps-Vilaró Anna, Elosua Roberto, Fornara Eleonora, Bermúdez-López Marcelino, Torán-Monserrat Pere, Jiménez-Navarro Ainara, Valdivielso José M, López-Lifante Víctor M, Salas-Fernández Tomàs, Cambray Serafí, Cruz Raquel, Marrugat Jaume, Hernáez Álvaro
Аннотация
AIMS: To assess whether self-reported leisure-time physical activity, moderate-to-vigorous leisure-time physical activity, and genetically determined cardiorespiratory fitness are associated with age-related BMI trajectories and incident obesity.
METHODS: We pooled 14 993 adults (30-90 years; 52.7% women; cohorts: REGICOR-ACRISC, ILERVAS, ARTPER) with estimated LTPA (moderate-to-vigorous LTPA [MVLTPA] in REGICOR-ACRISC), genotype, and 120 352 repeated BMI measurements from electronic health records (1990-2024). LTPA was categorised into cohort-specific quartiles; MVLTPA in 0, < 100, < 200, and ≥ 200 METs-min/day. In one-sample Mendelian randomisation analyses, we categorised participants in quartiles of a cardiorespiratory fitness polygenic risk score derived from a large GWAS in UK Biobank. Group-dependent BMI trajectories were modelled using spline mixed-effects models. Obesity onset (first BMI ≥ 30 kg/m2) was analysed with IPW-weighted Kaplan-Meier curves and Cox models.
RESULTS: Higher LTPA was associated with slower BMI increases in ages 30-60 (Q1: +0.120 vs. Q4: +0.075 kg/m2·year), slower declines in ages 70-90 (Q1: -0.143 vs. Q4: -0.123 kg/m2·year), and lower obesity risk (Q4 vs. Q1: HR 0.83, 95% CI 0.72-0.96). Similar trends were observed for MVLTPA. Higher genetically determined cardiorespiratory fitness showed parallel gradients (ages 30-60, Q1: +0.109 vs. Q4: +0.101 kg/m2·year; ages 70-90, Q1: -0.130 vs. Q4: -0.102 kg/m2·year) and lower obesity risk (Q4 vs. Q1: HR 0.66, 0.56-0.78). Associations were present for women and men separately, but were stronger in men.
CONCLUSIONS: Higher LTPA and MVLTPA were associated with more favourable lifelong BMI trajectories, delayed obesity risk, and convergent support from Mendelian randomisation analyses, supporting a causal protective role of physical activity (in both sexes but stronger in men).
METHODS: We pooled 14 993 adults (30-90 years; 52.7% women; cohorts: REGICOR-ACRISC, ILERVAS, ARTPER) with estimated LTPA (moderate-to-vigorous LTPA [MVLTPA] in REGICOR-ACRISC), genotype, and 120 352 repeated BMI measurements from electronic health records (1990-2024). LTPA was categorised into cohort-specific quartiles; MVLTPA in 0, < 100, < 200, and ≥ 200 METs-min/day. In one-sample Mendelian randomisation analyses, we categorised participants in quartiles of a cardiorespiratory fitness polygenic risk score derived from a large GWAS in UK Biobank. Group-dependent BMI trajectories were modelled using spline mixed-effects models. Obesity onset (first BMI ≥ 30 kg/m2) was analysed with IPW-weighted Kaplan-Meier curves and Cox models.
RESULTS: Higher LTPA was associated with slower BMI increases in ages 30-60 (Q1: +0.120 vs. Q4: +0.075 kg/m2·year), slower declines in ages 70-90 (Q1: -0.143 vs. Q4: -0.123 kg/m2·year), and lower obesity risk (Q4 vs. Q1: HR 0.83, 95% CI 0.72-0.96). Similar trends were observed for MVLTPA. Higher genetically determined cardiorespiratory fitness showed parallel gradients (ages 30-60, Q1: +0.109 vs. Q4: +0.101 kg/m2·year; ages 70-90, Q1: -0.130 vs. Q4: -0.102 kg/m2·year) and lower obesity risk (Q4 vs. Q1: HR 0.66, 0.56-0.78). Associations were present for women and men separately, but were stronger in men.
CONCLUSIONS: Higher LTPA and MVLTPA were associated with more favourable lifelong BMI trajectories, delayed obesity risk, and convergent support from Mendelian randomisation analyses, supporting a causal protective role of physical activity (in both sexes but stronger in men).