Athletic amenorrhea and endothelial dysfunction.

OBJECTIVES: To determine if menstrual status changed in amenorrheic college runners over a 2-year period and what effect this had on brachial artery flow-mediated dilation. PARTICIPANTS: Eighteen athletes first studied in our laboratory 2 years prior were available for follow-up. Nine of the 10 original women with athletic amenorrhea (mean +/- SE, age 21.3 +/- 1.2 yrs), and 9 of the 11 eumenorrheics/controls (age 20.1 +/- 0.5 yrs) were studied 2 years after baseline measurements. METHODS: Questionnaires/personal interviews and blood draws were performed to determine menstrual status. A non-invasive ultrasound technique was used to determine brachial artery flow-mediated dilation (endothelium-dependent). RESULTS: Menstrual status changed in 7 of 9 original amenorrheic subjects (2 were taking hormone replacement, 2 were taking oral contraceptives, 3 had a natural menstrual period prior to testing, and 2 remained amenorrheic). Endothelium-dependent brachial artery dilation, measured as the percent change in maximal brachial artery diameter from baseline during reactive hyperemia, was improved in the original amenorrheic subjects (a 1.1% +/- 1.0 increase in the original study versus 5.6% + 1.1 increase in the current study, P=0.01) while in the eumenorrheic/control group there was no change (6.3% +/- 1.7 versus 8.0% +/- 1.3, P=0.42). CONCLUSIONS: Menstrual status changed in 7 of the 9 original amenorrheic athletes, and this change was associated with an improvement in brachial artery flow-mediated dilation.

Quantitative trait locus mapping of genes that regulate HDL cholesterol in SM/J and NZB/B1NJ inbred mice.

To investigate the quantitative trait loci (QTL) regulating plasma cholesterol, the female progeny of an (SMxNZB/ B1NJ)xNZB/B1NJ backcross were fed an atherogenic diet. After 18 wk, plasma total cholesterol and high-density lipoprotein cholesterol (HDL-C) was measured. HDL-C concentrations were greater in NZB than in SM mice. For standard chow-fed mice, QTL were found near D5Mit370 and D18Mit34. For mice fed an atherogenic diet, a QTL was found near D5Mit239. The QTL for chow-fed and atherogenic-fed mice on chromosome 5 seem to be two different loci. We used a multitrait analysis to rule out pleiotropy in favor of a two-QTL hypothesis. Furthermore, the HDL-C in these strains was induced by the high-fat diet. For inducible HDL-C, one significant locus was found near D15Mit39. The gene for an HDL receptor, Srb1, maps close to the HDL-C QTL at D5Mit370, but the concentrations of Srb1 mRNA and SR-B1 protein and the gene sequence of NZB/B1NJ and SM/J did not support Srb1 as a candidate gene. With these QTL, we have identified chromosomal regions that affect lipoprotein profiles in these strains.