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Effectiveness of HIIT compared to moderate continuous training in improving vascular parameters in inactive adults.
Ramírez-Vélez, R, Hernández-Quiñones, PA, Tordecilla-Sanders, A, Álvarez, C, Ramírez-Campillo, R, Izquierdo, M, Correa-Bautista, JE, Garcia-Hermoso, A, Garcia, RG
Lipids in health and disease. 2019;(1):42
Abstract
BACKGROUND Strong evidence shows that physical inactivity increases the risk of many adverse health conditions, including major non-communicable diseases, such as cardiovascular disease (CVD), metabolic syndrome, and breast and colon cancers, and shortens life expectancy. We aimed to determine the effects of moderate (MCT)- versus high-intensity interval training (HIT) on vascular function parameters in physically inactive adults. We hypothesized that individualized HIT prescription would improve the vascular function parameters more than the MCT in a greater proportion of individuals. METHODS Twenty-one inactive adults were randomly allocated to receive either MCT group (60-75% of their heart rate reserve, [HRR] or HIT group (4 min at 85-95% of peak HRR), 3 days a week for 12 weeks. Vascular function (brachial artery flow-mediated dilation, FMD [%], normalized brachial artery flow-mediated dilation, FMDn [%], aortic pulse wave velocity, PWV [m·s- 1], AIx, augmentation index: aortic and brachial [%]), were measured at baseline and over 12 weeks of training. In order for a participant to be considered a responder to improvements in vascular function parameters (FMDn and PWV), the typical error was calculated in a favorable direction. RESULTS FMD changed by - 1.0% (SE 2.1, d = 0.388) in the MCT group, and + 1.8% (SE 1.8, d = 0.699) in the HIT group (no significant difference between groups: 2.9% [95% CI, - 3.0 to 8.8]. PWV changed by + 0.1 m·s- 1 (SE 0.2, d = 0.087) in the MCT group but decreased by - 0.4 m·s- 1 in the HIT group (SE 0.2, d = 0.497), with significant difference between groups: - 0.4 [95% CI, - 0.2 to - 0.7]. There was not a significant difference in the prevalence of no-responder for FMD (%) between the MCT and HIT groups (66% versus 36%, P = 0.157). Regarding PWV (m·s- 1), an analysis showed that the prevalence of no-responder was 77% (7 cases) in the MCT group and 45% (5 cases) in the HIT group (P = 0.114). CONCLUSIONS Under the conditions of the present study, both groups experienced changed in vascular function parameters. Compared to MCT group, HIT is more efficacious for improving FMD and decreasing PWV, in physically inactive adults. TRIAL REGISTRATION ClinicalTrials.gov NCT02738385 registered on 23 March 2016.
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Patterns and severity of vascular amyloid in Alzheimer's disease associated with duplications and missense mutations in APP gene, Down syndrome and sporadic Alzheimer's disease.
Mann, DMA, Davidson, YS, Robinson, AC, Allen, N, Hashimoto, T, Richardson, A, Jones, M, Snowden, JS, Pendleton, N, Potier, MC, et al
Acta neuropathologica. 2018;(4):569-587
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Abstract
In this study, we have compared the severity of amyloid plaque formation and cerebral amyloid angiopathy (CAA), and the subtype pattern of CAA pathology itself, between APP genetic causes of AD (APPdup, APP mutations), older individuals with Down syndrome (DS) showing the pathology of Alzheimer's disease (AD) and individuals with sporadic (early and late onset) AD (sEOAD and sLOAD, respectively). The aim of this was to elucidate important group differences and to provide mechanistic insights related to clinical and neuropathological phenotypes. Since lipid and cholesterol metabolism is implicated in AD as well as vascular disease, we additionally aimed to explore the role of APOE genotype in CAA severity and subtypes. Plaque formation was greater in DS and missense APP mutations than in APPdup, sEOAD and sLOAD cases. Conversely, CAA was more severe in APPdup and missense APP mutations, and in DS, compared to sEOAD and sLOAD. When stratified by CAA subtype from 1 to 4, there were no differences in plaque scores between the groups, though in patients with APPdup, APP mutations and sEOAD, types 2 and 3 CAA were more common than type 1. Conversely, in DS, sLOAD and controls, type 1 CAA was more common than types 2 and 3. APOE ε4 allele frequency was greater in sEOAD and sLOAD compared to APPdup, missense APP mutations, DS and controls, and varied between each of the CAA phenotypes with APOE ε4 homozygosity being more commonly associated with type 3 CAA than types 1 and 2 CAA in sLOAD and sEOAD. The differing patterns in CAA within individuals of each group could be a reflection of variations in the efficiency of perivascular drainage, this being less effective in types 2 and 3 CAA leading to a greater burden of CAA in parenchymal arteries and capillaries. Alternatively, as suggested by immunostaining using carboxy-terminal specific antibodies, it may relate to the relative tissue burdens of the two major forms of Aβ, with higher levels of Aβ40 promoting a more 'aggressive' form of CAA, and higher levels of Aβ42(3) favouring a greater plaque burden. Possession of APOE ε4 allele, especially ε4 homozygosity, favours development of CAA generally, and as type 3 particularly, in sEOAD and sLOAD.