Key result
Acute flavanol intake improves hypercapnic cerebral vasodilatory capacity in African Americans to match Caucasian levels.
Why the study?
African Americans have attenuated cerebral vasodilator capacity during hypercapnia relative to Caucasian Americans, contributing to increased cerebrovascular disease risk.
Does acute flavanol consumption improve cerebral vasodilatory capacity during hypercapnia in African Americans?
RCT (n=28)
Does acute flavanol consumption improve cerebral vasodilatory capacity during hypercapnia in African Americans?
Acute flavanol consumption normalizes the attenuated cerebral vasodilatory response to hypercapnia in healthy young African Americans, suggesting a potential dietary intervention to offset cerebrovascular risk.
Answers are grounded in this paper and cite their sources.
Acute flavanol intake may enhance cerebral vasodilation in African Americans; hypothesis-generating and requires larger trials before clinical consideration.
NEW FINDINGS: What is the central question of this study? The purpose was to determine whether acute flavanol consumption improves cerebral vasodilatory capacity during rebreathing-induced hypercapnia in African Americans. What is the main finding and its importance? The reduced cerebral vasodilatory response to hypercapnia in young healthy African Americans was improved acutely following consumption of a flavanol-rich beverage. This may have important clinical implications regarding racial differences in cerebrovascular disease risk and possible interventional approaches to offset this risk. African Americans (AAs) have increased risk for cardiovascular and cerebrovascular disease. African Americans have attenuated cerebral vasodilator capacity during hypercapnia relative to Caucasian Americans (CAs). This study tested the hypothesis, using a placebo-controlled crossover design, that acute flavanol consumption improves the range of change in cerebral vascular conductance [CVCI, (a)] and the maximal CVCI (y0) achieved during rebreathing-induced increases in end-tidal carbon dioxide tension. Fourteen college-aged AAs and 14 CAs participated. Both a and y0 were lower in AAs prior to flavanols (for a, AAs, 46 ± 16 versus CAs, 74 ± 18% CVCI, P < 0.001; and for y0, AAs, 151 ± 18 versus CAs, 176 ± 20% CVCI, P = 0.002); however, these variables were increased after flavanols such that there were no differences between groups (for a, AAs, 64 ± 19 versus CAs, 72 ± 22% CVCI, P = 0.35; and for y0, AAs, 166 ± 22 versus CAs, 176 ± 22% CVCI, P = 0.26). Both a and y0 were also lower in AAs prior to placebo (for a, AAs, 52 ± 19 versus CAs, 76 ± 15% CVCI, P = 0.002; and for y0, AAs, 156 ± 20 versus CAs, 177 ± 21% CVCI, P = 0.015), and these differences remained following placebo (for a, AAs, 52 ± 17 versus CAs, 80 ± 20% CVCI, P < 0.001; and for y0, AAs, 152 ± 18 versus CAs, 181 ± 25% CVCI, P = 0.003). These data suggest that acute flavanol consumption improves cerebral vasodilatory capacity during hypercapnia in AAs.
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Hurr et al. (2015) conducted an RCT in Healthy (n=28). Acute flavanol consumption vs. Placebo was evaluated on Range of change in cerebral vascular conductance (a) and maximal CVCI (y0) during rebreathing-induced hypercapnia. Acute flavanol consumption improved cerebral vasodilatory capacity during hypercapnia in African Americans, increasing the range of change in vascular conductance to match Caucasian Americans.
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