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Endogenous estrogen enhances brachial blood conductance during dynamic handgrip in young healthy and metabolic syndrome women
Author(s) -
Restaino Robert,
Schwermann Trace,
Blankenship Aaron,
Barlow Matthew A
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1136.9
Subject(s) - estrogen , brachial artery , medicine , endocrinology , blood pressure , heart rate , vascular resistance , vasoconstriction , hemodynamics , cardiology
Fadel et al. (2004) reported that in women, estrogen can attenuate sympathetic vasoconstriction as seen in postmenopausal women given estrogen treatment and increased vascular conductance. We hypothesize that women during the low estrogen phase of menses with metabolic syndrome (MetS) have an attenuated brachial conductance compared to normal controls. Participants were tested during the early menses (low estrogen, low progesterone) and the proliferative phase (high estrogen, low progesterone). Participants engaged in dynamic handgrip exercise (30 contactions/min) with a ramped increase in workload (0.5kg resistance/min) until task failure. Vascular velocity and diameter were measured during exercise in the brachial artery by Doppler ultrasound; heart rate and blood pressure were repeatedly recorded. The data demonstrate that MetS (25.3 years +1.58) have an attenuated conductance response (MetS 4.78×10^−3+0.7×10^−3 ml/min/mmHg/L, n=5) vs Control 9.4×10^−3+0.96 ml/min/mmHg/L, n=8)per forearm volume at high intensities(3kg) during early menses. During the proliferaive phase the MetS group increased conductance (6.6×10^−3+0.53×10^−3 mL/min/mmHg/L) at high intensity. Thus metabolically compromised women have reduced vascular conductance which is improved by estrogen. Supported by NM‐INBRE P20RR016480, P20GM103451