The influence of acute hyperglycaemia on brachial artery flow-mediated dilatation in the early and late follicular phases of the menstrual cycle

New Findings: What is the central question of the study? This is the first study to examine the impact of acute hyperglycaemia on endothelial function [flow-mediated dilatation (FMD)] in premenopausal women across the early and late follicular (EF and LF) phases of the menstrual cycle. What is the main finding and its importance? Flow-mediated dilatation was impaired 90 min after glucose ingestion, with no significant difference between phases. This indicates that women are susceptible to acute hyperglycaemia-induced endothelial dysfunction in both the EF and LF phases of the menstrual cycle, despite potentially vasoprotective elevations in estradiol levels during the LF phase. Abstract: Acute hyperglycaemia transiently impairs endothelial function in healthy men when assessed via flow-mediated dilatation (FMD). However, research in female participants is lacking, and the impact of menstrual phase [early follicular (EF) and late follicular (LF)] on vulnerability to acute hyperglycaemia-induced endothelial dysfunction is unknown. Seventeen healthy, naturally menstruating women [21 ± 1 years old (mean ± SD)] participated in three visits. During two visits (EF_Glucose and LF_Glucose), brachial artery FMD was assessed before and 60, 90 and 120 min after an oral glucose challenge (75 g glucose). During an additional EF visit, participants ingested 300 ml of water (EF_TimeControl). Blood glucose and insulin increased 30 min after glucose ingestion (P < 0.001), with no difference between phases. Flow-mediated dilatation did not change in EF_TimeControl (P = 0.748) but was reduced 90 min after glucose ingestion (Pre, 8.5 ± 2.5%; Post90, 6.6 ± 2.4%, P = 0.001; Cohen's d = 0.82), with no difference between phases (main effect of phase, P = 0.506; phase by time interaction, P = 0.391). To account for individual variability in the time course of the impact of hyperglycaemia, the maximal hyperglycaemia-induced impairment in FMD was determined in each participant and compared between phases, revealing no significant phase differences (EF_Glucose, −3.1 ± 2.8%; LF_Glucose, −2.4 ± 2.1%, P = 0.181; d = 0.34). These results indicate that, similar to findings in men, acute hyperglycaemia results in FMD impairment in young women. We did not detect significant protection from acute hyperglycaemia-induced endothelial dysfunction in the LF ‘high-oestrogen’ phase in this sample, and further research is needed to examine the potential for a protective effect of oestrogen exposure, including oral contraceptive pills and hormone replacement therapy.