Sex-specific microvascular and hemodynamic responses to passive limb heating in young adults.

OBJECTIVE: We examined sex-specific microvascular reactivity and hemodynamic responses under conditions of augmented resting blood flow induced by passive heating compared to normal blood flow. METHODS: Thirty-eight adults (19 females) completed a vascular occlusion test (VOT) on two occasions preceded by rest with or without passive heating in a randomized, counterbalanced order. Skeletal muscle tissue oxygenation (StO2, %) was assessed with near-infrared spectroscopy (NIRS), and the rate of desaturation and resaturation as well as maximal StO2 (StO2max) and prolonged hypersaturation (area under the curve, StO2AUC) were quantified. Before the VOT, brachial artery blood flow (BABF), vascular conductance, and relative BABF (BABF normalized to forearm lean mass) were determined. Sex × condition ANOVAs were used. A p-value ≤.05 was considered statistically significant. RESULTS: Twenty minutes of heating increased BABF compared to the control (102.9 ± 28.3 vs. 36.0 ± 20.9 mL min-1; p < .01). Males demonstrated greater BABF than females (91.9 ± 34.0 vs. 47.0 ± 19.1 mL min-1; p < .01). There was no sex difference in normalized BABF. There were no significant interactions for NIRS-VOT outcomes, but heat did increase the rate of desaturation (-0.140 ± 0.02 vs. -0.119 ± 0.03% s-1; p < .01), whereas regardless of condition, males exhibited greater rates of resaturation and StO2max than females. CONCLUSIONS: These results suggest that blood flow is not the primary factor causing sex differences in NIRS-VOT outcomes.

Arterial stiffness mediates the association between age and processing speed at low levels of microvascular function in humans across the adult lifespan.

The function of micro- and macrovessels within the peripheral vasculature has been identified as a target for the investigation of potential cardiovascular-based promoters of cognitive decline. However, little remains known regarding the interaction of the micro- and macrovasculature as it relates to cognitive function, especially in cognitively healthy individuals. Therefore, our purpose was to unravel peripheral factors that contribute to the association between age and processing speed. Ninety-nine individuals (51 men, 48 women) across the adult life span (19-81 yr) were used for analysis. Arterial stiffness was quantified as carotid-femoral pulse-wave velocity (cfPWV) and near-infrared spectroscopy assessed maximal tissue oxygenation (Sto2max) following a period of ischemia. Processing speed was evaluated with Trail Making Test (TMT) Parts A and B. Measures of central (cPP) and peripheral pulse pressure (pPP) were also collected. Moderated mediation analyses were conducted to determine contributions to the age and processing speed relation, and first-order partial correlations were used to assess associations while controlling for the linear effects of age. A P ≤ 0.05 was considered statistically significant. At low levels of Sto2max, there was a significant positive (b = 1.92; P = 0.005) effect of cfPWV on time to completion on TMT part A. In addition, cPP (P = 0.028) and pPP (P = 0.027) remained significantly related to part A when controlling for age. These results suggested that the peripheral microvasculature may be a valuable target for delaying cognitive decline, especially in currently cognitively healthy individuals. Furthermore, we reinforced current evidence that pulse pressure is a key endpoint for trials aimed at preventing or delaying the onset of cognitive decline.NEW & NOTEWORTHY Arterial stiffness partially mediates the association between age and processing speed in the presence of low microvascular function, as demarcated by maximum tissue oxygenation following ischemia. Central and peripheral pulse pressure remained associated with processing speed even after controlling for age. Our findings were derived from a sample that was determined to be cognitively healthy, which highlights the potential for these outcomes to be considered during trials aimed at the prevention of cognitive decline.