Cutaneous and cerebral microvascular response to the ingestion of flavanols in young and older humans : role of nitric oxide
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These studies explored interactions between flavanols and nitric oxide in order to investigate implications for vascular health. Study 1 investigated acute effects of flavanol consumption on cutaneous microvascular endothelial function in young and older individuals along with chronic exposure in older individuals. This was accomplished by assessing skin blood flow response to local heating (thermal reactivity, TR); skin was clamped at 34°C and 40°C and values were normalized to those attained at 43°C. Older individuals demonstrated an attenuated TR at baseline during the entire local heating phase (58.4 ± 2.5% versus 49.3 ± 2.6%, p<0.05). Acutely following flavanol ingestion there was a significant increase in TR (52.4 ± 2.1% versus 56.1 ± 2.0%, p=0.05) that was not different with age. There was no effect of chronic flavanol exposure on TR in older individuals; however, there was a significant decrease in mean arterial pressure (95 ± 3 mmHg versus 91 ± 3 mmHg, p<0.001). These results contribute to research regarding flavanols increasing NO bioavailability; acutely via an improvement in cutaneous microvascular endothelial function and chronically via a reduction in blood pressure. Study 2 investigated the acute effects of flavanol consumption on cerebrovascular endothelial function in young and older individuals along with chronic flavanol exposure in older individuals. This was accomplished by assessing basal cerebral blood flow indices (cerebral vascular conductance index, CVCi) and CBF response to hypercapnia (cerebral vasomotor reactivity; CVMR). At baseline older individuals demonstrated a reduced CVCi (0.85 ± 0.04 cm/s*mmHg versus 0.55 ± 0.04 cm/s*mmHg p=0.001) and CVMR (8.6 ± 0.6 versus 6.9 ± 0.4, p=0.05). An unexpected finding was that flavanol ingestion led to an acute decrease in CVCi (0.71 ± 0.04 cm/s*mmHg versus 0.62 ± 0.04 cm/s*mmHg p<0.05) and CVMR (8.6 ± 0.6 versus 6.1 ± 0.5, p=0.001) that was not different with age. In older individuals, chronic exposure led to a significant increase in CVCi (0.60 ± 0.05 cm/s*mmHg versus 0.72 ± 0.06 cm/s*mmHg, p<0.05) but had no effect on CVMR. These data provide evidence for an improvement in cerebral hemodynamics following chronic exposure in older individuals.