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- Fortuin-de Smidt, Melony, et al.
(författare)
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Early adulthood exercise capacity, but not muscle strength, associates with subclinical atherosclerosis 40 years later in Swedish men
- 2023
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Ingår i: European Journal of Preventive Cardiology. - : Oxford University Press. - 2047-4873 .- 2047-4881. ; 30:5, s. 407-415
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: Poor exercise capacity and muscle strength in early adulthood are risk factors for cardiovascular disease (CVD). However, it is unclear how these factors relate to subclinical atherosclerosis due to a lack of longitudinal studies. This study investigated whether early adulthood exercise capacity and muscle strength associated with later adulthood subclinical atherosclerosis.METHODS AND RESULTS: This study included Swedish men (n = 797) who were eligible for military conscription (at ∼18-years of age) and who participated in the baseline assessment of the visualization of asymptomatic atherosclerotic disease for optimum cardiovascular prevention trial between 2013 and 2016 (at 60 years of age). At conscription, isometric muscle strength (dynamometer) and maximum exercise capacity (maximal load cycle ergometer test) were measured. During later adulthood (at 60 years old), the presence of carotid plaques and intima media thickness were measured by using high-resolution ultrasound. At follow-up, plaques were present in 62% (n = 493) of men. Exercise capacity in early adulthood associated with 19% lower odds of plaques [odds ratio (OR) 0.81, 95% confidence interval (CI) 0.68-0.96], independent of muscle strength. This association was not mediated by any single CVD risk factor. However, the total indirect effect of later, but not early, adulthood CVD risk factors was significant, while the direct effect was non-significant (OR 0.85, 95% CI 0.71-1.02). Associations between muscle strength and subclinical atherosclerosis were non-significant.CONCLUSION: Higher exercise capacity during early adulthood, but not muscle strength, may protect against carotid plaque development during adulthood mediated by the combination rather than a single later adulthood CVD risk factors.
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