Synergistic impact of rest-activity circadian rhythms and physical activity on all-cause and cardiovascular mortality.

Baichuan Gu, Haoyu Zhang, Ming Yi, Jin Si, Keling Xiao, Lijie Sun, Jinghao Sun, Huan Zhao, Ou Zhao, Yixin Ma, Hongyu Luo, Jing Li
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Abstract

Background: This study investigated the independent and joint associations of rest-activity circadian rhythms (RACRs) and physical activity (PA) with all-cause and cardiovascular mortality, and explored the potential role of accelerated biological aging.

Methods: We included 6621 adults from NHANES 2011-2014. RACR parameters were derived from wrist-worn ActiGraph GT3X+ data. Accelerated biological aging was assessed using Phenotypic Age Acceleration (PhenoAgeAccel) and Biological Age Acceleration (BioAgeAccel). Cox proportional hazards models were applied to investigate the associations of RACRs and PA with all-cause and cardiovascular mortality. Exploratory mediation analyses were used to explore the associations between accelerated biological aging, RACRs, and mortality risks.

Results: Over a median follow-up of 6.75 years, 518 all-cause deaths and 165 cardiovascular deaths were recorded. Compared with weak RACRs and inadequate PA, participants with strong RACRs and adequate PA had significantly lower risks of all-cause mortality (HR: 0.35, 95% CI: 0.24 to 0.51; p < .001) and cardiovascular mortality (HR: 0.25, 95% CI: 0.14 to 0.45; p < .001). In exploratory analyses, PhenoAgeAccel accounted for an estimated 13.55% (p < .001) and 21.67% (p = .002) of the associations between RACRs and all-cause and cardiovascular mortality, respectively, while BioAgeAccel accounted for an estimated 5.06% (p < .001) and 8.06% (p = .004).

Conclusions: Disrupted RACRs are associated with higher mortality risks that could be attenuated by adequate physical activity. Exploratory analyses suggest that the associations between RACRs and mortality may be mediated in part by accelerated biological aging, but additional studies are needed to test this hypothesis.

休息-活动昼夜节律和身体活动对全因死亡率和心血管死亡率的协同影响。
背景:本研究探讨了休息-活动昼夜节律(RACRs)和身体活动(PA)与全因死亡率和心血管死亡率的独立和联合关系,并探讨了加速生物衰老的潜在作用。方法:我们纳入了6621名来自NHANES 2011-2014的成年人。RACR参数来源于腕带ActiGraph GT3X+数据。使用表型年龄加速(PhenoAgeAccel)和生物年龄加速(BioAgeAccel)来评估加速的生物衰老。应用Cox比例风险模型研究racr和PA与全因死亡率和心血管死亡率的关系。探索性中介分析用于探索加速生物老化、RACRs和死亡风险之间的关系。结果:在中位随访6.75年期间,记录了518例全因死亡和165例心血管死亡。与弱racr和不充分的PA相比,强racr和适当PA的参与者的全因死亡风险显著降低(HR: 0.35, 95% CI: 0.24 ~ 0.51; P)结论:racr中断与较高的死亡风险相关,可通过适当的体育活动减弱。探索性分析表明,racr与死亡率之间的关联可能部分是由加速的生物衰老介导的,但需要进一步的研究来验证这一假设。
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