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1 Institute for Human Science and Biomedical Engineering, National Institute of Advanced Industrial Science and Technology (AIST), 1-1-1 Higashi, Tsukuba, Ibaraki 305-8566, Japan2 Division of Health Promotion and Exercise, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku, Tokyo 162-8636, Japan3 Department of Health and Sports Sciences, Kawasaki University of Medical Welfare, 288 Matsushima, Kurashiki, Okayama 701-0193, Japan4 Department of Health Sciences, Kurashiki University of Science and the Arts, 2640 Tsurajima, Kurashiki, Okayama 712-8505, Japan5 Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8574, Japan
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(Received 17 August 2005;
accepted after revision 4 January 2006; first published online 11 January 2006)
Corresponding author K. Hayashi: Institute for Human Science and Biomedical Engineering, National Institute of Advanced Industrial Science and Technology, 1-1-1 Higashi, Tsukuba, Ibaraki, 305-8566, Japan. Email: k-hayashi{at}aist.go.jp
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Introduction |
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Many studies have reported that hormone replacement therapy (HRT) effectively prevents and, in some cases, reverses the decreases in central arterial compliance seen in postmenopausal women (McGrath et al. 1998; Bui et al. 2002). McGrath et al. (1998) reported that carotid arterial distensibility in women with oestrogen treatment alone was greater than that in women with oestrogen plus progestin treatment. In addition, several reports could not identify any increases in arterial compliance in women receiving oestrogen and progesterone (Westendorp et al. 2000; Teede et al. 2001). These results suggest that progesterone seems to counteract the effects of oestrogen on arterial elasticity.
The effects of the menstrual cycle on arterial compliance also have never been conclusive. One study showed that carotid and femoral arterial distensibility and compliance did not change significantly during the menstrual cycle (Willekes et al. 1997). In contrast, it was reported that systemic arterial compliance, but not aortic pulse wave velocity increases in the late follicular phase and decreases after ovulation during the menstrual cycle (Williams et al. 2001). Changes in radial artery compliance were similar (Giannattasio et al. 1999). This discrepancy may be derived from differences in the evaluation of arterial elasticity and/or the method of identifying the menstrual cycle phase. In these two studies, however, measurements of arterial compliance around the time ovulation were not done even though blood oestradiol concentrations increase sharply prior to ovulation. Therefore, we decided to divide the menstrual cycle into phases in order to examine changes in the arterial elasticity in detail.
From previous studies, we hypothesized that carotid arterial compliance changes significantly during the menstrual cycle, probably in a manner that is synchronized with the balance between serum oestrogen and progesterone. To address this aim comprehensively, we determined the changes in central and peripheral arterial compliance and stiffness at five hormonal time points during the normal menstrual cycle in healthy young women.
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Methods |
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Ten healthy sedentary or recreationally active young women, ranging in age from 18 to 24 years old (20.6 ± 1.5 years old, mean ±S.D.), were examined. All subjects were normotensive, non-diabetic and non-smokers who did not take any form of oral contraception. Seven of the subjects jogged daily (1–2 h day–1, 3 or 4 days week–1) and three subjects were sedentary women. All subjects had regular menstrual cycles ranging between 25 and 32 days (mean, 28.3 days) in length for at least two menstrual cycles before experimentation. All subjects gave their written informed consent prior to participation. All procedures were approved by the Ethics Committee of the University of Tsukuba and conformed with the Declaration of Helsinki.
Study protocol
The changes in central and peripheral blood pressure, carotid arterial elasticities (carotid arterial compliance, distensibility coefficient and the ß-stiffness index), peripheral arterial stiffness (pulse wave velocity in the leg), and serum ovarian hormone (oestradiol and progesterone) concentrations were measured in five phases of the subject's menstrual cycles: menstrual phase (M; 2–4 days after the beginning of menstruation); follicular phase (F; the middle day between the day of measurement in the M phase and the predicted day of ovulation), ovulatory phase (O; the 3 day period beginning 2 days prior ovulation), early luteal phase (EL; 4–7 days after ovulation), and late luteal phase (LL; 11–13 days after ovulation). The day of ovulation was predicted on the basis of previous menstrual cycle length and the time of menstruation, using the assumption that the luteal phase duration was 14 days. Timing of ovulation was determined from the body temperature and a urinary ovulation kit (Rohto pharmaceutical Co., Ltd, Osaka, Japan). Subjects were enrolled randomly at different phases in the menstrual cycle to prevent examiner bias. To avoid potential diurnal variations, subjects were always tested at the same time of day (between 9.00 am and noon). Subjects fasted, abstaining from caffeine, for at least 12 h prior to each test. All haemodynamic and hormonal measurements were initiated by placing the subject in the supine position. Individuals were then fitted with an electrocardiogram and brachial blood pressure device. After a 20 min rest, brachial blood pressure, heart rate, pulse wave velocity of a peripheral (leg) artery, carotid arterial compliance, distensibility coefficient (DC) and the ß-stiffness index (assessed by ultrasound imaging and applanation tonometry) were measured. After another 15 min rest, blood was drawn for hormonal measurements.
Measurements
We combined ultrasound imaging of the common carotid artery with simultaneous applanation tonometry to obtain arterial pressure from the contralateral carotid artery. This technique permits the non-invasive determination of arterial compliance (Miyachi et al. 2004). Carotid artery diameter was measured from ultrasound images obtained using a high-resolution linear-array transducer. A longitudinal image of the cephalic portion of the common carotid artery was acquired 1–2 cm proximal to the carotid bulb. Computer images were digitized using a media converter and analysed using image analysis software (NIH image 1.62). The minimal and maximal lumen diameters were determined by scrolling through images acquired at 33 ms intervals. Both diameters measured the distance from the media–adventitia border of the near wall to the intima–lumen interface of the far wall. All image analyses were performed by a single investigator, who was blinded to the menstrual phase assignments.
Pressure waveforms and amplitudes were obtained from the common carotid artery using a pencil-type probe that incorporated a high-fidelity strain-gauge transducer (SPT-301, Millar Instruments, Houston, TX, USA; Miyachi et al. 2004). Since baseline carotid blood pressure levels are subjected to hold-down force, the pressure signals obtained by tonometry were calibrated by equating the carotid mean arterial and diastolic blood pressures to the values determined for the brachial artery as described by Armentano et al. (1995). Carotid arterial compliance, DC and the ß-stiffness index were calculated from the equation: (D12
–D02)/[2(P1–P0)], [(D12–D02)/D02]/[2(P1–P0)] and log(P1/P0)/[(D1–D0)/D0], respectively, where D1 and D0 are the maximum and minimum diameters of the vessel and P1 and P0 are the maximal and minimal blood pressures. As previously reported (Miyachi et al. 2004), the day-to-day coefficients of variation were 2 ± 1, 7 ± 3 and 5 ± 2% for carotid artery diameter, pulse pressure and arterial compliance, respectively.
Carotid artery intima–media thickness (IMT) was measured from ultrasound images obtained using a high-resolution linear array transducer as described by Miyachi et al. (2004). Ultrasound images were digitized using a video frame grabber and analysed using computerized image analysis software (NIH image 1.62). At least 10 IMT measurements were obtained at each segment; the mean values were used for analysis. Day-to-day coefficient of variation was 3 ± 1% for measurement of the carotid IMT (Miyachi et al. 2003).
Heart rate, brachial blood pressure, and the pulse wave velocity of a leg artery (leg PWV) during resting in the supine position were measured in triplicate using a semi-automated device (form PWV/ABI, Colin Medical Technology, Komaki, Japan). Brachial blood pressures were measured by the oscilometric method as previously described (Sugawara et al. 2005). To measure leg PWV, we simultaneously recorded pressure waveforms at the femoral and posterior-tibial arteries. Femoral arterial pressure waveforms were acquired by two multi-element tonometry sensors attached manually to the left femoral artery. Posterior-tibial arterial pressure waveforms were recorded by a cuff that was connected to a plethysmographic sensor wrapped around the left ankle. PWVs were calculated by dividing the distance between the two arterial recording sites by the time delay between the proximal and distal ‘foot’ waveforms as we have previously reported (Sugawara et al. 2004). Day-to-day coefficient of variation was 2.3 ± 0.6% for measurement of the leg PWV (Sugawara et al. 2004).
To measure serum oestradiol and progesterone concentrations in each menstrual phase, a 5 ml fasting blood sample was taken from the antecubital vein. Blood was centrifuged at 3000 r.p.m. (2000g) for 15 min. All serum samples were distributed into appropriate preservative tubes and stored at –80°C until analysis. Serum oestradiol and progesterone concentrations were measured by radioimmunoassay (Abraham et al. 1972) using commercially available kits. To minimize intra-assay variability, all samples were analysed together; intra-assay variability was < 5%. Body composition was determined using the previously described bioelectric impedance method (Houtkooper et al. 1992).
Statistical analysis
We performed a priori sample size calculation and it was decided that the number of subjects is sufficient, and our data were normally distributed. Differences across menstrual cycle phases in the parameters other than carotid arterial elastic properties were assessed by one-way analysis of variance (ANOVA) with repeated measures. For significant F values in ANOVA, a post hoc test using the Newman–Keuls method was used to identify significant differences between the mean values. We analysed for changes in arterial elastic properties (arterial compliance, distensibility coefficient and ß-stiffness index), with brachial mean arterial pressure as covariates (ANCOVA), because blood pressure level is a key determinant of arterial elasticity. Pearson's correlation and regression analyses were performed to determine the relationship between variables of interest. The level of significance was set at P < 0.05. All data are presented as the means ±S.D.
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Results |
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Across all subjects, carotid arterial compliance (r= 0.42, P < 0.05; Fig. 2), carotid arterial DC (r= 0.48, P < 0.05) and the carotid artery ß-stiffness index (r=–0.39, P < 0.05) correlated significantly with the E:P ratio. No other variables were significantly related to measurements of any carotid arterial elastic properties or leg PWV.
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Discussion |
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Williams et al. (2001) reported that whole body arterial compliance fluctuated significantly throughout the menstrual cycle. The method used to evaluate the arterial compliance throughout the whole body included both central (e.g. aorta and carotid arteries) and peripheral arteries (e.g. brachial and femoral). In this study, we separated central from peripheral measurements, demonstrating that carotid arterial compliance and stiffness fluctuated significantly, whereas leg arterial stiffness did not change significantly throughout the normal menstrual cycle. These results indicate that menstrual cycle phase only affects central arteries, whose cushioning function dampens the fluctuations in pressure and flow. This is the first study to suggest that central arterial compliance varies throughout the menstrual cycle in young women. The clinical significance of these fluctuations in central arterial elastic properties during the menstrual cycle in this population remains unclear.
In this study, the maximum difference in carotid arterial compliance was 25.1% (ovulatory versus late luteal phases). The fluctuations in central arterial elastic properties in healthy young women with normal menstrual cycles are probably greater than those seen in individuals following the menopause, because the menopause increases arterial stiffness by approximately 8–14% (Jonason et al. 1998; Staessen et al. 2001). In their examination of the effects of HRT on arterial elastic properties, Moreau et al. (2003) demonstrated that carotid arterial compliance was significantly higher, by approximately 33%, in postmenopausal women taking HRT than in age-matched women not receiving HRT. Although the changes in carotid arterial compliance throughout the menstrual cycle were smaller than those seen for HRT in the menopausal women, these differences depend on the time period of ovarian hormone encounter, with HRT administered for several months to several years and the menstrual cycle changing over several days. Regardless, our data indicate that it is necessary to control for menstrual phase when assessing central arterial elasticity in premenopausal women using these measures.
Carotid arterial compliance changed cyclically, increasing significantly from the M and F into the O phase (oestradiol high) and decreasing dramatically in the EL (oestradiol and progesterone high) and LL phases. This result is consistent with a previous report examining the variations in whole body arterial compliance throughout the menstrual cycle (Williams et al. 2001). Although oestrogen replacement therapy in postmenopausal women has been reported to increase arterial compliance (McGrath et al. 1998), the mechanisms by which hormonal fluctuations affect carotid arterial compliance are not well understood. Multiple studies, however, have documented that oestrogen can act as a both a vasodilator and as an anti-atherogenic agent. Since the changes in arterial compliance in this study occurred on a short time scale, it is likely that oestrogen rapidly modulates vascular properties by acting on either the vascular endothelium or smooth muscle cells (Orshal & Khalil, 2004). Oestrogen has been reported to enhance endothelial nitric oxide synthase (eNOS) activity, NO release (Knot et al. 1999; Geary et al. 2000), prostacyclin release (Geary et al. 2000) and the vasodilator activity of endothelial-dependent hyperpolarization factor (EDHF; Liu et al. 2001), and to decrease endothelin-1 production (Akishita et al. 1998). In addition, oestrogen inhibits Ca2+ influx into vascular smooth muscle cells (Murphy & Khalil, 2000). Sudhir et al. (1996) also demonstrated that endothelial function, evaluated by flow-mediated vasodilatation (FMD), improved in postmenopausal women following 8 weeks of oestradiol administration. Endothelial function in premenopausal women, evaluated by FMD, increased in the late follicular phase (O phase in this study, in which oestradiol is high) in comparison to that seen in the menstrual phase (in which oestradiol is low; Williams et al. 2001). Thus, the increase in carotid arterial compliance observed in the O phase probably results from the vasodilatory effects of oestrogen.
In the EL phase, carotid arterial compliance fell and stiffness rose, despite similar oestradiol levels to those seen in the O phase. The physiological mechanisms underlying these increases in arterial stiffening during the luteal phase remain poorly understood. Although progesterone levels, as well as oestrogen levels, increase during the luteal phase, the influence of progesterone on arterial functions may be complex. In animal studies, Miller & Vanhoutte (1991) reported that acetylcholine-induced relaxations in canine coronary arteries were greater in the oestrogen-treated group than in the group given both oestrogen and progesterone. Williams et al. (1998) reported that medroxy progesterone acetate antagonized oestrogen-mediated increases in acetylcholine-induced endothelial-dependent vasodilation in atherosclerotic monkeys. These data suggest that progesterone inhibits the endothelial-dependent vasodilatory actions of oestrogen. Recent studies, however, have indicated that progesterone also possesses vasodilatory activity, which may be mediated by modulation of Ca2+ channel open probabilities (Barbagallo et al. 2001; Minshall et al. 2002). Thus, increases in serum progesterone concentrations may not necessarily decrease arterial compliance. Other potential mechanisms may be related to decreases in carotid arterial compliance during the luteal phase. Minson et al. (2000) reported that resting muscle sympathetic nervous activity and plasma noradrenaline concentrations were higher in the midluteal phase than in the early follicular phase. Progesterone also affects fluid retention (Minson et al. 2000; Stachenfeld et al. 2003; Stachenfeld & Taylor, 2004), probably decreasing the amount of water in vascular smooth muscle cells to decrease arterial compliance (Hanke et al. 1996). In addition, the renin–angiotensin system and aldosterone, which are capable of altering arterial characteristics, are upregulated in the luteal phase compared with the follicular phase of the menstrual cycle (Chapman et al. 1997). We speculate that the additive interaction of these factors results in the decreases in carotid arterial compliance seen in the luteal phase.
We observed that the changes in carotid arterial compliance were synchronized with the balance between serum oestradiol and progesterone concentrations (E:P ratio). Although significant, these correlations were not strong. Basal individual differences in arterial compliance may influence these weak correlations, especially in the phases with a low E:P ratio. Other possible confounding factors included differences in individual efficacy of oestradiol and progesterone, and the interaction of these hormones in the regulation of arterial elasticity. Recent studies demonstrated that oestrogen receptor 
polymorphisms are associated with arterial morphology (Lehtimaki et al. 2002a) and function (Lehtimaki et al. 2002b). Further study examining the interindividual differences in ovarian hormonal action on arteries will be necessary.
In our subjects, elevations of serum progesterone levels in the early luteal phase were somewhat low. The reason why progesterone levels were low might be that a substantial number of the studied women had corpus luteum deficiency but not anovular menstruation, because all the subjects had clear elevations of progesterone levels in the early luteal phase (at least > 5 nmol l–1). In this regard, we should emphasize the significant change of central arterial compliance even if elevations of progesterone concentrations in the luteal phase were less than that of mature females.
In summary, this study examined the changes in young women in central and peripheral arterial elasticity at five distinct time points in the menstrual cycle. Carotid arterial compliance varied cyclically, increasing significantly from the menstrual and follicular phases into the ovulatory phase and decreasing sharply in the early and late luteal phases, but the PWV of the peripheral artery (leg) did not exhibit any significant changes throughout the menstrual cycle. Although the physiological mechanisms underlying these alterations remain unclear, these findings suggest that the menstrual cycle phase affects central, but not peripheral, arterial elasticity. Thus, it is necessity to consider the phase of the menstrual cycle when interpreting the cardiovascular disease risk of premenopausal women using carotid arterial compliance.
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
P < 0.05 versus EL and LL phases. Values are means ±S.D.