Effect of the Menstrual Cycle on Maximum Oxygen Consumption and Endothelium-Dependent Vasodilation.
Abstract
Endogenous estradiol and progesterone may have important effects on endothelial flinction in pre-menopausal women and may thereby influence the time course of atherogenesis. This effect may also correlate with changes in exercise and could influence how women perform during times 6f stress. We studied endothelium-dependent vasodilation of the brachial artery during three phases of the menstrual cycle in 20 eumenorrheic subjects to determine the effect of endogenous estradiol and progesterone. The degree of endothelium-dependent, flow-mediated vasodilation was assessed using high resolution brachial artery ultrasound comparing baseline diameter to that obtained during reactive hyperemia. Endothelium-independent vasodilation was similarly assessed by measuring brachial artery diameter after administration of sublingual nitroglycerin. Exercise performance was measured by determining the maximum oxygen consumption and the endurance time on an anaerobic speed test (AST). Serum lipids were measured along with the estradiol and progesterone levels was also determined. Each subject was studied at three phases of the menstrual cycle: early follicular phase when estradiol and progesterone levels are low, at mid-cycle when estradiol levels are elevated and progesterone levels remain low, and during the luteal phase when levels of both hormones are elevated. Compared to the early follicular and luteal phases, flow-mediated vasodilation was greatest at mid-cycle (follicular 8.0+1- 1.1%; mid-cycle 10.9+1- 1.4%, luteal 7.6+1- 1.1%. p 0.059). The serum progesterone level was a significant negative correlated of flow-mediated vasodilation (R-- -0.261, p=0.027). Lipid levels, maximum oxygen consumption and AST times did not change significantly during the three phases of the menstrual cycle.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 01, 1997
- Accession Number
- ADA338769
Entities
People
- Thomas C. Andrews