Aging is associated with increased carotid artery stiffness, a predictor of incident stroke, and reduced cognitive performance and brain white matter integrity (WMI) in humans. Therefore, we hypothesized that higher carotid stiffness/lower compliance would be independently associated with slower processing speed, higher working memory cost, and lower WMI in healthy middle-aged/older (MA/O) adults. Carotid β-stiffness ( < 0.001) was greater and compliance ( < 0.001) was lower in MA/O ( = 32; 64.4 ± 4.3 yr) vs. young ( = 19; 23.8 ± 2.9 yr) adults. MA/O adults demonstrated slower processing speed (27.4 ± 4.6 vs. 35.4 ± 5.0 U/60 s, < 0.001) and higher working memory cost (-15.4 ± 0.14 vs. -2.2 ± 0.05%, < 0.001) vs. young adults. Global WMI was lower in MA/O adults ( < 0.001) and regionally in the frontal lobe ( = 0.020) and genu ( = 0.009). In the entire cohort, multiple regression analysis that included education, sex, and body mass index, carotid β-stiffness index (B = -0.53 ± 0.15 U, = 0.001) and age group (B = -4.61 ± 1.7, = 0.012, adjusted = 0.4) predicted processing speed but not working memory cost or WMI. Among MA/O adults, higher β-stiffness (B = -0.60 ± 0.18, = 0.002) and lower compliance (B = 0.93 ± 0.26, = 0.002) were associated with slower processing speed but not working memory cost or WMI. These data suggest that greater carotid artery stiffness is independently and selectively associated with slower processing speed but not working memory among MA/O adults. Carotid artery stiffening may modulate reductions in processing speed earlier than working memory with healthy aging in humans. Previously, studies investigating the relation between large elastic artery stiffness, cognition, and brain structure have focused mainly on aortic stiffness in aged individuals with cardiovascular disease risk factors and other comorbidities. This study adds to the field by demonstrating that the age-related increases in carotid artery stiffness, but not aortic stiffness, is independently and selectively associated with slower processing speed but not working memory among middle-aged/older adults with low cardiovascular disease risk factor burden.
A diet high in trans-fatty acids (TFAs) is associated with higher risk of
cardiovascular disease (CVD) than a diet high in saturated fatty acids (SFAs)
but the mechanisms remain unclear. We hypothesized that a beverage high in TFAs
would cause a larger reduction in postprandial endothelial function and increase
in arterial stiffness in part from greater reductions in insulin sensitivity
compared with a beverage high in SFAs. Eleven healthy adults (age=47±5
yrs) ingested a warm test beverage (520kcal, 56g total fat, 5g carbohydrate, 1g
protein) high in either TFAs or SFAs in a randomized cross-over study. Ingestion
of the high TFAs (P<0.01), but not SFAs (P=0.49) beverage decreased
endothelial function (brachial artery flow-mediated dilation, mmΔ) at 3
hours (P<0.01 for time; p=0.034 for interaction), but did not alter
aortic stiffness or carotid β-stiffness. Homeostasis model of insulin
resistance (interaction P=0.062) tended to decrease after SFAs but not TFAs. A
beverage high in TFAs but not SFAs results in a postprandial reduction in
endothelial function and a trend for insulin sensitivity potentially explaining
the higher risk of CVD with a diet high in TFAs.
Cerebrovascular reactivity (CVR) to a physiological stimulus is a commonly used surrogate of cerebrovascular health. Cross-sectional studies using Blood Oxygen Level Dependent (BOLD) neuroimaging demonstrated lower BOLD-CVR to hypercapnia among adults with high compared with lower cardiorespiratory fitness (CRF) in contrast to transcranial Doppler studies. However, whether BOLD-CVR changes following chronic aerobic exercise in older, cognitively intact adults are unclear. This study evaluated relations between BOLD-CVR with CRF (VO2peak) using a cross-sectional and interventional study design. We hypothesized that 1) greater CRF would be associated with lower BOLD-CVR in older adults (n=114; 65±6.5 years) with a wide range of CRF; 2) BOLD-CVR would be attenuated after exercise training in a subset (n=33) randomized to 3-months of moderate or light intensity cycling. CVR was quantified as the change in the BOLD signal in response to acute hypercapnia using a blocked breath-hold design from a region-of-interest analysis for cortical networks. In the cross-sectional analysis, there was a quadratic relation between VO2peak (p=0.03), but not linear (p=0.87), and cortical BOLD-CVR. BOLD-CVR increased until a VO2peak ~28 ml/kg/min after which BOLD-CVR declined. The nonlinear trend was consistent across all networks (p-value=0.04-0.07). In the intervention, both the active and light intensity exercise groups improved CRF similarly (6% vs. 10.8%, p=0.28). The percent change in CRF was positively associated with change in BOLD-CVR in the default mode network only. These data suggest that BOLD-CVR is non-linearly associated with CRF and that in lower-fit adults default mode network may be most sensitive to CRF-related increases in BOLD-CVR.
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