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  Hirofumi Tanaka, Christopher A. DeSouza and Douglas R. Seals Absence of Age-Related Increase in Central Arterial Stiffness in Physically Active Women Print ISSN: 1079-5642. Online ISSN: 1524-4636 Copyright © 1998 American Heart Association, Inc. All rights reserved.Greenville Avenue, Dallas, TX 75231is published by the American Heart Association, 7272  Arteriosclerosis, Thrombosis, and Vascular Biology doi: 10.1161/01.ATV.18.1.1271998;18:127-132  Arterioscler Thromb Vasc Biol. World Wide Web at: The online version of  this article, along with updated information and services, is located on the at: is online  Arteriosclerosis, Thrombosis, and Vascular Biology Information about subscribing to Subscriptions: Information about reprints can be found online at: Reprints:  document. AnswerPermissions and Rights Question andunder Services. Further information about this process is available in thepermission is being requested is located, click Request Permissions in the middle column of the Web page whichCopyright Clearance Center, not the Editorial Office. Once the online version of the published article for can be obtained via RightsLink, a service of the  Arteriosclerosis, Thrombosis, and Vascular Biology in Requests for permissions to reproduce figures, tables, or portions of articles srcinally published Permissions:  by guest on April 16, 2014 Downloaded from by guest on April 16, 2014 Downloaded from   Absence of Age-Related Increase in Central ArterialStiffness in Physically Active Women Hirofumi Tanaka, Christopher A. DeSouza, Douglas R. Seals  Abstract   —Increased arterial stiffness is thought to contribute to the increased incidence of cardiovascular disease with age.Little, however, is known about the influence of aging on central and peripheral arterial stiffness in females. Moreover, itis unknown whether physical activity status influences age-related increases in arterial stiffness in females. Arterial pulsewave velocity (PWV) and augmentation index (AI, applanation tonometry) were measured in 53 healthy females,including 10 premenopausal (Pre-S) and 18 postmenopausal (Post-S) sedentary women, and 9 premenopausal (Pre-PA)and 16 postmenopausal (Post-PA) physically active women. In the sedentary women, there were no age-related differencesin arterial blood pressure, but aortic PWV and carotid AI (measures of central arterial stiffness) were higher ( P   .01) inPost-S versus Pre-S (1065  110 versus 690  80 cm/sec and 16.5%  1.8% versus 0.3%  1.6%, respectively); however,there were no significant differences in leg and arm PWV (measures of peripheral arterial stiffness). Systolic and meanarterial blood pressures were higher ( P   .05) in Post-PA versus Pre-PA. Despite this and in contrast to the sedentarywomen, aortic PWV and AI were not different in Post-PA versus Pre-PA. Stepwise multiple regression indicated thatmaximal oxygen consumption, plasma total cholesterol, and plasma LDL-cholesterol were significant independentpredictors and together explained up to 50% of the variability in central arterial stiffness. We concluded that (1) central,but not peripheral, arterial stiffness increases with age in sedentary healthy females in the absence of age-related increasesin arterial blood pressure; (2) significant age-related increases in central arterial stiffness are not observed in highly physicallyactive women; and (3) aerobic fitness and plasma total cholesterol and LDL-cholesterol levels are significant independentphysiological correlates of central arterial stiffness in this population.  (  Arterioscler Thromb Vasc Biol . 1998;18:127-132.)Key Words:  exercise    aging    pulse wave velocity    augmentation index    arterial compliance T he stiffness of the “central” arteries (eg, aortic, carotid)increases with age in males, 1–3 as indicated by an increase inPWV or earlier pressure wave reflections (ie, increased AI). 1–3 These increases in arterial stiffness are thought to contribute toage-related increases in the incidence of cardiovascular disease. 4,5 Much less is known about the influence of aging on arterialstiffness in females. A recent report from the Baltimore Longitu-dinal Study of Aging (BLSA) 2 found that aortic PWV and carotidAIincreasedprogressivelywithagein50healthyfemales(26to96 years) in whom only modest age-related increases in bloodpressure were observed. No data are available, however, regardingthe effects of aging on peripheral arterial stiffness in healthyfemales. This is noteworthy in that the elastic properties of arteriesare not necessarily uniform, 3 and aging has been reported to havedifferent effects on the stiffness of peripheral (eg, brachial andradial) and central arteries in men. 6 Regular physical activity is associated with reduced risk of cardiovascular disease. 7,8 In the BLSA mentioned above, older adult males who performed endurance exercise on a regular basis demonstrated lower levels of aortic PWV and carotid AIthan their sedentary peers. 2 These observations suggest thathabitual aerobic exercise may delay or prevent age-associatedincreases in central arterial stiffness. However, the absence of data on corresponding endurance-trained young adults pre-cluded the ability to assess this possibility. Moreover, these dataon males cannot necessarily be generalized to females becausecertain unique age-associated factors, such as menopause andhormone supplementation, could independently affect theelastic properties of arteries.Accordingly, the aims of the present investigation were todetermine (1) if central and/or peripheral arterial stiffnessincreases with age in sedentary healthy females in the absenceof age-related increases in arterial blood pressure; (2) if theseincreases in arterial stiffness with age are not observed in highlyphysically active women; and (3) the key physiological corre-lates of central and peripheral arterial stiffness in healthy femalesvarying in age and physical activity status. Methods Subjects A total of 53 healthy women were studied. They were divided intotwo groups according to their physical activity status. The sedentary Received July 24, 1997; revision accepted October 3, 1997.Human Cardiovascular Research Laboratory, Center for Physical Activity, Disease Prevention, and Aging, Department of Kinesiology (H.T., C.A.D.,D.R.S.), University of Colorado at Boulder, and Department of Medicine, Divisions of Cardiology and Geriatric Medicine and Center on Aging (D.R.S.),University of Colorado Health Sciences Center, Denver.Correspondence to Hirofumi Tanaka, PhD, University of Colorado at Boulder, Department of Kinesiolog y, Campus Box 354, Boulder, CO 80309-0354.E-mail© 1998 American Heart Association, Inc. 127   by guest on April 16, 2014 Downloaded from   groups consisted of 10 Pre-S and 18 Post-S women, none of whomperformed regular exercise. The physically active groups consisted of 9 Pre-PA and 16 Post-PA women who had been performingendurance exercise training for at least the past 2 years (mean, 13  1 year), and were actively competing in running road races. On average,the endurance-trained women exercised for 6  1 h/wk. Pre-PA andPost-PA were matched for age-adjusted running performance (Mas-ters Age-Graded Tables, National Masters News, Van Nuys, CA) asdescribed previously. 9 All subjects were free of overt cardiovascular disease as assessed by medical history questionnaire and had plasmalipid and lipoprotein concentrations all within the normal range. 10 Postmenopausal women were further evaluated by physical examina-tion and by resting and maximal exercise ECGs. None of the subjectssmoked or took medications (other than hormone replacement). Allwomen in the postmenopausal groups were postmenopausal at least 2 years (mean, 10  1 year). All premenopausal women were eumenor-rheic as assessed by self-report of menstrual cycles, and were not takingoral contraceptives. Among the 34 postmenopausal women, 18 (10sedentary and 8 active) used hormone replacement and 16 (8 sedentaryand 8 active) did not. We observed no influence of hormonereplacement use. Therefore, the data were pooled and presentedtogether. Before participation, a verbal and written explanation of theprocedures and potential risks was provided. All subjects gave their written informed consent to participate. This study was reviewed andapproved by the Human Research Committee of the University of Colorado at Boulder. Measurements Measurement of arterial stiffness was conducted after an abstinence of caffeine and an overnight fast of at least 12 hours. Subjects werefamiliarized with all pertinent procedures before making the measure-ments. During the experimental session, each subject rested supine for at least 15 minutes in a quiet, temperature-controlled room. Bloodpressure was measured by auscultation over the brachial artery in thelast 5 minutes according to American Heart Association guidelines. 11 Determination of arterial stiffness began with arterial applanationtonometry, followed by pulse wave velocity measurement.  Arterial Applanation Tonometry The pressure waveform and amplitude were obtained from the rightcommon carotid artery with a pencil-type probe incorporating ahigh-fidelity strain-gauge transducer (model TCB-500, Millar Instru-ments), as previously described by Kelly et al. 3 This instrument wasbased on the principle of applanation tonometry as used in ocular tonometry for the measurement of intraocular pressure. In principle,the flattening or applanation of the curved surface of a pressure-containing structure under the detecting device allows direct mea-surement of arterial pressure pulse within the structure. This tonom-eter has been shown to register a pressure wave with harmonic contentthat does not differ from that of an intra-arterially recorded wave, andthe use of the tonometer on an exposed artery records a waveformidentical to that recorded intra-arterially. 12 Waveforms were recordedon a Gould recorder at a high speed of 100 mm/sec. All measurementswere performed by the same investigators. Recordings were takenonly when reproducible signals could be obtained with high-ampli-tude excursion. The peak of the R wave from the simultaneouslyrecorded ECG was used as a timing marker. A minimum of 20consecutively recorded pulse waves were analyzed and averaged aspreviously described. 3,13 All the analyses were performed manually bythe same investigator who was blinded to the group assignment. Themeasured pressure waveform consists of both a “forward” or “inci-dent” wave, and a “reflected” wave that is returning from a peripheralsite. The reflected wave is superimposed on the incident wave suchthat the pulse and systolic pressures are increased. This increase isdefined as a pressure pulse AI, and it is calculated as pressure waveabove its systolic shoulder (  P) divided by pulse pressure. 3,13 Theshoulder was defined as the first concavity on the upstroke of the waveand separates the initial systolic pressure rise from the late systolic peak.The carotid AI has been proposed as an indicator of the magnitude of wave reflections, which is closely linked to arterial stiffness. 3 In thepresent study, carotid AI was used as a measure of the stiffness of thecentral arteries. The reliability of the AI measurement in our labora-tory was established by sequential measurement on 8 adult men andwomen of varying age on two separate days. Carotid AI was5.0%  3.2% versus 4.8%  2.9% for trial 1 versus trial 2 (not signifi-cant); the mean coefficient of variation was 7%. PWV  PWV is measured from the foot of pressure waves recorded at twopoints along the path of the arterial pulse wave, and is calculated fromthe measurement of pulse transit time (or time delay) and the distancetraveled between two arterial recording sites. 14 Two identical trans-cutaneous Doppler flowmeters (model 810-A, Parks Medical) wereused to obtain the pulse wave (1) between the aortic arch and thefemoral artery (aortic PWV); (2) between the femoral and posterior tibial artery (leg PWV); and (3) between the brachial and radial artery(arm PWV), as previously described by Avolio et al. 1 Distance traveledby the pulse wave was assessed in duplicate with a random zero lengthmeasurement over the surface of the body with a nonelastic tapemeasure. The peak of the R wave from the simultaneously recordedECG was used as a timing marker. A minimum of 20 simultaneouslyrecorded waveforms were analyzed and averaged as described previ-ously. 1 All the analyses were performed by the same trained technicianwho was blinded to the group assignment. Aortic PWV was used as ameasure of the stiffness of the central arteries, whereas leg and armPWV were used as measures of peripheral arterial stiffness.Arterial pressure waves were digitized for off-line analysis withsignal-processing software (WINDAQ, Dataq Instruments). PWV wascalculated from distance (cm) divided by transit time (sec). Transittime was determined from the time delay between the proximal andthe distal foot waveforms. The foot of the wave was identified as thecommencement of the sharp systolic upstroke. The test-retest reliabil-ity of our PWV measurements was established using the experimentalapproach described for AI above. The mean PWV combined for threesites was 973  56 versus 956  54 cm/sec for trial 1 versus trial 2 (notsignificant). The coefficients of variation of aortic, arm, and leg PWVmeasurements were similar with mean values of 8% in each case. Potential Physiological Correlates of   Arterial Stiffness Body fat percentage was estimated from the hydrostatic weighingtechnique. Body mass index was calculated according to the formulaof body mass (kg)/height (m 2 ). Waist circumference was measured atthe narrowest part of the torso, and hip circumference was measuredat the maximal extension of the buttocks. V˙ O 2 max was assessed withon-line computer-assisted open-circuit spirometry during incrementaltreadmill exercise as described in detail previously. 9 Dietary sodiumintake was determined using 3-day food intake records, 15 and 24-hour urinary sodium excretion was determined with the use of flamephotometry. Fasting plasma concentrations of cholesterol, glucose,and insulin were performed in the clinical laboratory affiliated with theGeneral Clinical Research Center at the University of ColoradoHealth Sciences Center as described previously. 15 All measurements of metabolic variables on the premenopausal women were performedduring the early follicular phase of the menstrual cycle. Statistical Analyses The respective influences of aging and physical activity were assessedwith two-way ANOVA (age and physical activity). When indicated Selected Abbreviations and Acronyms AI   augmentation indexBMI   body mass indexPost-PA   postmenopausal physically active womenPost-S   postmenopausal sedentary womenPre-PA   premenopausal physically active womenPre-S   premenopausal sedentary womenPWV   pulse wave velocityV˙ O 2 max   maximal oxygen consumption 128   Aging, Exercise, Arterial Stiffness in Women  by guest on April 16, 2014 Downloaded from   by a significant F-value, a post-hoc test using Scheffe´’s method wasperformed to identify significant differences among group means.ANCOVA, using systolic blood pressure or body fatness as a covariate,was used to analyze the effect of age on arterial stiffness. Univariatecorrelation and regression analysis were performed to determine therelation between arterial stiffness measurements and selected physio-logical variables. Stepwise regression analyses were used to determinesignificant, independent physiological correlates for each of the arterialstiffness measurements. Age was not included in the regression analysesbecause it did not have a continuous distribution. All data are reportedas the mean  SE. Statistical significance was set at  P   .05 unlessindicated otherwise. Results Arterial Stiffness in Premenopausal versusPostmenopausal Sedentary Women Table 1 shows the physical characteristics and blood pressure atrest of the sedentary women. Body mass index, percent bodyfat, and waist-to-hip ratio were higher ( P   .01) in Post-Srelative to Pre-S. There were no differences in height, bodymass, fat-free mass, resting heart rate, or arterial blood pressurebetween the two groups. Post-S had a lower V˙ O 2 max( P   .001) than Pre-S.Aortic PWV and carotid AI were higher ( P   .01) in Post-Sthan in Pre-S (1060  58 versus 690  80 cm/sec and16.4%  1.4% versus 0.3%  1.6%, respectively) (Fig 1). WhenANCOVA was performed using either BMI, percent body fat,or waist/hip as a covariate, the difference between Post-S andPre-S remained statistically significant ( P   .05). In contrast,there were no significant differences in leg and arm PWV inthe two groups. Arterial Stiffness in Premenopausal versusPostmenopausal Physically Active Women Physical characteristics of the physically active women arepresented in Table 2. There were no significant differences inheight, body mass, fat-free mass, BMI, waist-to-hip ratio, andresting heart rate between Post-PA and Pre-PA. Post-PA hadhigher ( P   .01) percent body fat than Pre-PA. Although wellwithin the normotensive range, systolic and mean arterialblood pressure were higher ( P   .05) in Post-PA than inPre-PA whereas no significant difference was observed for diastolic blood pressure. Post-PA had a lower V˙ O 2 max( P   .001) than Pre-PA.In contrast to the sedentary women, there were no signifi-cant differences in either aortic PWV or carotid AI betweenPost-PA and Pre-PA (Fig 2). When ANCOVA was performedusing systolic blood pressure as the covariate, aortic PWV andcarotid AI were 671.5  56.0 and 611.8  37.9 cm/sec and6.4%  1.6% and 3.9%  2.3% in Post-PA and Pre-PA, respec-tively (both not significant). Importantly, aortic PWV andcarotid AI were  30% and 50% lower ( P   .01), respectively,in Post-PA versus Post-S. Physiological Correlates of Arterial Stiffness Univariate correlation analyses were performed to determinewhich physiological variables were most closely associated with TABLE 1. Physical Characteristics of the Sedentary Women Pre-S(n  10)Post-S(n  18) Age, y 28  2 59  2*Height, m 1.66  0.02 1.62  0.02Body mass, kg 62.5  4.2 69.7  2.8Fat free mass, kg 44.3  1.9 42.5  1.2BMI, kg/m 2 22.9  1.5 26.6  1.0*Body fat, % 28  3 38  2*Waist, cm 75.1  2.8 87.2  2.5*Waist/hip 0.75  0.01 0.82  0.02*SBP, mm Hg 111  2 118  2DBP, mm Hg 73  2 76  1MABP, mm Hg 86  2 90  1Resting HR, bpm 61  2 62  3V˙ O 2 max, mL    kg  1   min  1 33.8  2.1 22.3  1.1*Data are mean  SE. SBP indicates systolic blood pressure; DBP, diastolic bloodpressure; MABP, mean arterial blood pressure; and HR, heart rate.* P   .01 vs premenopausal group. TABLE 2. Physical Characteristics of the PhysicallyActive Women Pre-PA(n  9)Post-PA(n  16) Age, y 31  1 59  2*Height, m 1.65  0.01 1.66  0.01Body mass, kg 52.0  1.7 57.1  1.5Fat free mass, kg 44.2  1.5 43.0  1.0BMI, kg/m 2 19.0  0.5 20.7  0.4Body fat, % 15  2 24  1*Waist/cm 66.6  1.6 70.5  1.0Waist/hip 0.74  0.01 0.74  0.01SBP, mm Hg 106  3 118  2*DBP, mm Hg 70  2 76  1MABP, mm Hg 82  3 90  2*Resting HR, bpm 56  1 53  2V˙ O 2 max, mL    kg  1   min  1 54.3  1.6 36.6  2.0*Data are mean  SE. SBP indicates systolic blood pressure; DBP, diastolic bloodpressure; MABP, mean arterial blood pressure; and HR, heart rate.* P   .05 vs premenopausal group. Figure 1.  PWV and carotid AI of sedentary premenopausal andpostmenopausal women. *  P  .01 vs premenopausal women. Tanaka et al   129   by guest on April 16, 2014 Downloaded from 

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