ORIGINAL ARTICLE

John P. McCarthy áMarcas M. BammanJanice M. Yelle áAdrian D. LeBlanc áRoger M. RoweMichael C. Greenisen áStuart M.C. LeeElisabeth R. Spector áSuzanne M. Fortney

Resistance exercise training and the orthostatic response

Accepted: 17 January 1997

Abstract Resistance exercise has been suggested to in-crease blood volume, increase the sensitivity of the car-otid baroreceptor cardiac re¯ex response (BARO), anddecrease leg compliance, all factors that are expected toimprove orthostatic tolerance. To further test these hy-potheses, cardiovascular responses to standing and topre-syncopal limited lower body negative pressure(LBNP) were measured in two groups of sedentary menbefore and after a 12-week period of either exercise(n = 10) or no exercise (control, n = 9). Resistanceexercise training consisted of nine isotonic exercises, foursets of each, 3 days per week, stressing all major musclegroups. After exercise training, leg muscle volumes in-creased (P < 0.05) by 4±14%, lean body mass increased(P = 0.00) by 2.0 (0.5) kg, leg compliance and BAROwere not signi®cantly altered, and the maximal LBNPtolerated without pre-syncope was not signi®cantly dif-ferent. Supine resting heart rate was reduced (P = 0.03)without attenuating the heart rate or blood pressureresponses during the stand test or LBNP. Also, bloodvolume (125I and 51Cr) and red cell mass were increased(P < 0.02) by 2.8% and 3.9%, respectively. These®ndings indicate that intense resistance exercise increasesblood volume but does not consistently improve ortho-static tolerance.

Key words Blood volume áCarotid barore¯exesLeg compliance áBlood pressure áMuscle mass

Introduction

Resistance exercise has been proposed as a counter-measure to prevent muscle atrophy and strength reduc-tions during long-duration space¯ight (Greenleaf et al.1989; Tipton 1983). In ambulatory subjects, resistanceexercise has also been proposed to improve orthostaticresponses, such as heart rate or blood pressure changesduring standing, and to improve orthostatic tolerance.Suggested mechanisms for these resistance exercise ef-fects include increased blood volume (Ploutz et al. 1993),reduced leg compliance (Convertino et al. 1988, 1989;Lightfoot et al. 1994), and an increased slope of thecarotid baroreceptor cardiac re¯ex response (BARO)(Tatro et al. 1992). At this time, however, only twostudies (Lightfoot et al. 1994; Tatro et al. 1992) haveassessed the e�ect of chronic resistance exercise pro-grams on orthostatic tolerance using lower body nega-tive pressure (LBNP) to simulate an orthostaticchallenge. The ®ndings of these two studies were con-¯icting: Tatro et al. (1992) reported no signi®cant e�ectof resistance exercise training on LBNP tolerance, andLightfoot et al. (1994) reported a positive e�ect.

The purpose of this study was to determine whetheran intensive program of whole-body resistance exercisewould reduce orthostatic heart rate and blood pressureresponses and increase orthostatic tolerance, as esti-mated by a pre-syncopal limited LBNP test. We hy-pothesized that possible contributing mechanisms forimprovements in orthostatic responses and tolerancefollowing whole-body resistance training include: in-creased resting blood volume, increased slope, operatingpoint, and range of the BARO, and/or reduced legcompliance.

Eur J Appl Physiol (1997) 76: 32 ± 40 Ó Springer-Verlag 1997

J.P. McCarthy á J.M. Yelle áM.C. Greenisen á S.M. FortneyNASA Johnson Space Center,Medical Life Sciences Division (SD/3) Houston, TX 77058, USA

M.M. Bamman á S.M.C. Lee áE.R. SpectorKRUG Life Sciences Inc., 1290 Hercules, Suite 120,Houston, TX 77058, USA

A.D. LeBlanc áR.M. RoweBaylor College of Medicine, 6550 Fannin St.,Houston, TX 77030, USA

J.P. McCarthy (&)12 North Rural Street, Chippewa Falls, WI 54729, USA

Methods

Subjects

Nineteen healthy, sedentary, normotensive men volunteered toparticipate as either exercise or control subjects. Because vascular¯uid volumes were important dependent variables in this inves-tigation and the menstrual cycle a�ects these volumes, only maleswere studied. All subjects passed a physical examination to ensurethat they were free from any cardiovascular or musculoskeletaldisorders that would prevent activity or interfere with proceduresof this study. Subjects did not exercise regularly (one or less thanone exercise session, on average, per week) for at least 3 monthsbefore the start of the study. Participants gave informed consent,and the protocol was approved by the Human Research Policy andProcedures Committee of NASA Johnson Space Center. Initialgroup characteristics [(mean (SD)] for the exercise (n = 10) andcontrol (n = 9) groups were 34 (5) and 29 (5) years of age, 77.8(10.5) and 78.9 (7.8) kg body mass, and 176.0 (8.0) and 182.1(7.8) cm height respectively.

Overall research design

This study followed a repeated-measures design in which bodycomposition, muscle volume, and strength tests were performedpre- and post-training to verify the e�ectiveness of the resistancetraining program. A control, non-exercising group was tested at thesame time intervals.

Blood volume, BARO, leg compliance, stand and LBNP testswere performed during a 2-week interval before, and within 1 weekafter the 12-week resistance training program or control period.Exercise was prohibited for at least 36 h, and ca�eine and alcoholwere prohibited for at least 24 h before testing. All testing sessionsfor a given measurement were performed at the same time of day.

Whole-body resistance exercise program

Exercise subjects trained on Mondays, Wednesdays, and Fridaysfor 12 weeks. The intensity, frequency, and duration of the trainingwere designed to induce marked improvements in strength andmuscle mass (MacDougall et al. 1980; McCarthy et al. 1995). Theresistance training regimen stressed all major muscle groups andconsisted of nine exercises, each performed for one warm-up setand three maximal e�ort sets. The exercises performed using bar-bells included parallel squat, bench press, and standing curl. Re-sistance exercise machines (Cybex Strength Systems, Ronkonkoma,N.Y., USA) were used for the remaining movements: horizontal legpress, leg curl, wide grip lat pulldown, shoulder press, inclined heelraise, and seated heel raise. A sequential progression in load wasincorporated within each week of training: session one, 11 repeti-tion maximum (11 RM) (range 10±12 RM); session two, 7 RM(range 6±8 RM); and session three, 5 RM (range 4±6 RM). When aset was performed outside the desired range of repetitions, the loadof subsequent sets was adjusted accordingly. Warm-up sets wereperformed with approximately 67% of the load lifted in the ®rstmaximal e�ort set for each exercise. Rest periods between exercisesets were limited to 90 s. Training sessions were closely supervisedand monitored by the investigators. Subjects completed an averageof 34.6 out of a possible 36 sessions (96% adherence). No injuriesoccurred during this study and missed sessions were due toscheduling con¯icts.

Testing protocols for cardiovascular and leg compliancemeasurements

On the same day, and always in the following order, BARO, standtest, LBNP, and leg compliance assessments were performed. Thefollowing assessments were made three times: a familiarization

session to acquaint each subject with the measurements and pro-cedures, a pre-training data session (pre-test) and a post-trainingdata session (post-test) for the exercise group. Controls were testedat the same three time intervals.

Subjects reported to the laboratory at 0730 hours and ingested500 ml of water to ensure adequate hydration. They then rested inthe supine position for 30 min before the BARO assessment. Aftera further 10 min of supine rest, this test was followed by the standtest. After the stand test, subjects rested in the supine position for30 min before the LBNP test. After lunch, subjects returned to thelaboratory and rested in the supine position for 30 min before theleg compliance assessment.

Vascular ¯uid volumes were measured on a separate day.Subjects reported to the laboratory in the morning in a post-ab-sorptive state, ingested 500 ml of water, and then rested in thesupine position for 30 min before the plasma volume (PV) and redcell mass (RCM) measurements were made.

BARO assessment

Non-invasive measurement of the BARO was achieved as describedby Fritsch et al. (1992). At the end of a normal expiration, a se-quence of R-R wave-triggered 15-mmHg (where 1 mmHg =0.133 kPa) pressure changes (from +40 to )65 mmHg) was de-livered to a neck chamber. The R-R intervals were measured fromthe electrocardiogram. Resting arterial blood pressure was mea-sured at the brachial artery using sphygmomanometry immediatelybefore the protocol. A test session consisted of seven successfulapplications of the neck pressure sequence. The average R-R in-terval at each pressure step was plotted against carotid distendingpressures (systolic blood pressure ) neck chamber pressure) toexamine various characteristics of the BARO. The BARO wasde®ned from the average of each seven trial sequences of responses.The responses were reduced to the following variables: range of R-R intervals, maximum slopes, and operational points (Fritsch et al.1991). Maximum slopes were identi®ed by applying a linear re-gression analysis to each set of three consecutive pairs of data onthe stimulus-response relationship. The operational points werede®ned as: [(R-R intervals at 0 mmHg neck pressure ) minimumR-R intervals)/R-R interval range] á 100%. The operational pointis a measure of the relative BARO bu�ering capacity for pressuresabove and below resting levels.

Stand tests

Cardiovascular responses were assessed during the stand test.Manual blood pressure measurements were obtained from the leftarm using standard sphygmomanometry once each minute. After6 min of supine resting measurements, subjects were assisted to afree-standing position where they remained for 10 min. The manualblood pressure and heart rate data were averaged over the ®nal3 min of supine rest, and over minutes 3±5 and 8±10 of standing.

Pre-syncopal-limited LBNP tests

LBNP was used to produce a central hypovolemia, thus simulatinga severe orthostatic challenge. LBNP tolerance was de®ned as thelevel of negative pressure ()mmHg) a subject could tolerate for atleast 1 min without the appearance of well-de®ned pre-syncopalsigns or symptoms, which included a sudden drop in heart rate(>15 beats/min), sudden fall in systolic blood pressure(>25 mmHg/min), a systolic blood pressure of less than 70 mmHg,or severe nausea.

The LBNP protocol consisted of 30 min of supine rest followedby sequential 3-min levels of LBNP until pre-syncope. The LBNPstages began with 3 min at )20 mmHg, 3 min at )40 mmHg, andthen continued in )10-mmHg steps every 3 min until pre-syncope.During each LBNP test, the subject rested on a padded saddle andwas instructed to remain relaxed and avoid tensing his legs. Thiswas assessed by viewing a continuous output from a mercury strain

33

gauge positioned around the left calf. During each LBNP test,®nger blood pressure (Ohmeda Model 2300 Finapres, Englewood,Colo., USA) and heart rate (Physiocontrol, Model VSM 4, Red-mond, Wash., USA) were monitored continuously, and manualblood pressure was obtained from the arm, once each minute.LBNP tolerance was assessed for each test in three ways: ®rst, asthe maximal LBNP tolerated for at least 1 min without pre-syn-copal signs; second, as the duration of LBNP (s); and third, as theLuft's cumulative stress index (CSI) which is the sum of the totalminutes at each LBNP stage multiplied by the stage pressure (Luftet al. 1976).

Leg compliance and blood ¯ow measurements

Leg compliance and blood ¯ow were each measured using thighocclusion and a mercury strain gauge, as previously described(Melchior and Fortney 1993). During both measurements subjectsrested in the supine position on a horizontal bed at room temper-ature (20±23°C) with the right leg suspended at an angle of 15°. Amercury-in-silastic strain gauge was positioned over the mid-calf,an occlusion cu� was placed around the ankle, and a contouredcu� was positioned around the mid-thigh. The leg remained in thisposition for 30 min before measurements were begun.

To measure leg blood ¯ow, the ankle cu� was in¯ated to200 mmHg at least 1 min before readings. The thigh cu� was in-¯ated to 50 mmHg and held for 6 s while the increase in leg cir-cumference was measured using the strain gauge. Measurementswere taken every 30 s and repeated ®ve times. Leg blood ¯ow wascalculated as the change in leg circumference versus time bydrawing a tangent line to the slope of the strain gauge record. Theaverage value of the ®ve measurements was used for the calculationof leg blood ¯ow.

Three minutes after the blood ¯ow measurements were obtainedand the ankle cu� removed, leg compliance measurements werebegun. The thigh cu� was in¯ated to successive occlusion pressuresof 20, 30, 50, 70, and 80 mmHg. The changes in calf circumferencebetween baseline and each occlusion pressure were used to producea curve of the change in leg area (A), in cm2, versus the occlusionpressure. Since a strength training program may increase leg size,we considered it inappropriate to compare changes in leg circum-ference during the occlusion pressures in terms of a percentage areaincrease [100(DA)/A] as carried out by most investigators. Thepercentage area increase could vary because of a change in baselinerather than a change in compliance. Therefore, the compliancecurves were expressed as the absolute area increase (cm2) relative tothe changes in thigh occlusion pressure.

Vascular ¯uid volumes

The RCM and PV were measured by the chromium labeled (i.e.,[51 Cr]-labelled) red cell and iodine-labeled (i.e., [125I]-labeled) hu-man serum albumin methods, respectively, as described by Johnsonet al. (1971). The only modi®cation to these methods was that forthe determination of PV, where one blood sample was taken20 min after injection of the 125I rather than two blood samples atseparate time intervals. We currently use the single blood samplemethod since we ®nd no signi®cant di�erence in PV calculationsusing the two methods. Blood volumes were calculated as the sumof RCM and PV. Total body hematocrit (HCTTB) was calculatedfrom the radioisotope data as HCTTB = RCM á (RMC + PV))1,and peripheral hematocrit was measured in duplicate (microcen-trifuge technique). F-cell ratios were calculated by dividing theHCTTB by the peripheral venous hematocrit (not corrected fortrapped plasma), as described by Sawka et al. (1992).

Body composition

Measurements were obtained by dual-energy X-ray absorptiometry(DEXA) using a QDR 2000 Whole Body Densitometer (HologicWaltham, Mass., USA). All scans were performed using the whole-

body pencil-beam scan mode, following the manufacturer'sguidelines for subject positioning. A single operator performed allscans and scan analyses in order to reduce inter-operator di�er-ences as a source of error. A Hologic tissue calibration bar wasscanned simultaneously with each subject. The calibration bar iscomposed of six di�erent solid sections representing lean-equiva-lent and fatty-equivalent material, calibrated by the manufacturerto known fat/lean standards. The tissue calibration bar is intendedto ensure intra-machine accuracy for each whole-body scan. Scanswere analyzed using the manufacturer's routine whole-body anal-ysis software (version 5.60). Body mass (kg) was compartmentali-zed into lean body mass (LBM) fat mass, and bone mineralcontent. A study of test-retest reliability was conducted using theQDR 2000 on 21 subjects, each tested three times, separated by anaverage of 7 days (Spector et al. 1995). Coe�cients of variationwere 0.68% for body mass, 0.87% for LBM, 1.71% for fat mass,and 0.63% for bone mineral content.

Skeletal muscle volume

Muscle volumes of the right quadriceps, hamstrings, adductors(including the gracilis and sartorius), plantar ¯exors, and anteriorcalf musculature were determined using magnetic resonanceimaging techniques (LeBlanc et al. 1988). All imaging was per-formed using a 1.5-Tesla Siemens magnet using a whole-body coil.Subjects were recumbent for a minimum of 10±15 min before thestart of data acquisition, and the order in which the measurementswere made was consistent for each test. The feet were positioned ina holder to minimize movement during image acquisition and toensure repositioning. The portion of the limb being imaged wassuspended while the non-imaged portion was supported with linen.A radio frequency shield was positioned caudally to the imagedportion of the leg, and thigh and calf muscle images were obtained.A total of 32 contiguous images was acquired using a 256 ´ 256pixel matrix with a repetition time of 1.5 s and an echo time of22 ms, and each slice was 1 cm thick. A phantom was imaged tocorrect for any changes in pixel size. Each image analysis wasperformed by the same individual who was unaware as to the ex-perimental status of each subject (i.e. exercise or control). Matchingof the extremity slices from pre- to post-testing was accomplishedby comparing the marrow area, as described previously (LeBlancet al. 1988).

Voluntary muscle strength

After completion of all other pre-tests, subjects were tested for1 RM strength in a horizontal leg press, a leg curl, a bench press,and an incline heel raise (using the same order of testing during pre-and post-tests). Then, 2 or 3 days before 1 RM pre-testing, subjectsreceived a light training session to familiarize themselves with theprocedures and motor patterns involved in these tests. For eachexercise, after three progressive warm-up sets, sets of one repetition(separated by 2±3 min) were completed with increasing loads untiltwo consecutive unsuccessful trials occurred at a given weight. Thelast successful load to be lifted correctly was deemed the criterionscore. For pre-testing, subjects were evaluated twice on two sepa-rate days. Five to seven days separated the two pre-tests to allowrecovery from delayed-onset muscle soreness. The greatest loadlifted in either of the testing sessions was accepted as the pre-testmaximum. Then, 1 RM strength was measured again following the12-week training period. Post-testing occurred during the second-to-last training session for the exercise subjects. Because of thepotential for resistance exercise to alter vascular ¯uid volumes andinduce muscle soreness in untrained subjects, post-testing of allother variables preceded the 1 RM testing in the controls.

Statistical analyses

In this study the control and exercise groups were assessed bymeasurement of several dependent variables before and after a 12-

34

week period. Thus, the study design can be characterized as``groups by trials''. The objectives of the statistical analyses for thisstudy are: (1) to determine whether a change from pre- to post-testing occurred within each group and (2) to determine whetherthe change in the dependent variables between pre- and post-testingwas di�erent between the two groups. With regard to the ®rstobjective, paired t-tests were used to determine whether within-group changes occurred. Regarding the second objective, inferencesconcerning possible di�erences between the post-treatment meansof the two groups could be confounded by the groups not beinginitially equivalent. For that reason group di�erences were inves-tigated using analysis of covariance (ANCOVA) with the pre-testvalues as the covariable. For leg compliance, each subject's datawere ®t with a second-order polynomial �y � ax2 � bx� c�. Thenthe estimates of the a, b, and c, coe�cients for each subject weretreated as dependent variables in a ``groups by trials'' design andanalyzed statistically as above.

In addition, for the heart rates and blood pressures obtainedduring stand tests and during LBNP, a third objective was to assessintra-group di�erences for time or pressure. This was performed byadding a repeated measures contrast for stand test times or LBNPpressures in the ANCOVA. When a signi®cant di�erence wasfound, post-hoc analysis was performed using a Tukey honestsigni®cant di�erence Test. For all statistical hypothesis tests, analpha level of 0.05 was used.

Results

LBNP

Tolerance

There was a signi®cant di�erence in the pre-testing LBNPtolerances of the two groups. For the control group, themaximum pre-testing LBNP pressure tolerated averaged82 (4) mmHg, compared to 98 (5) mmHg for the exercisegroup, and the LBNP duration time was 282 shorter(Fig. 1). The pre-testing CSI values for the two groupswere 1028 (96) mmHg á min for the controls, comparedto 1465 (141) mmHg á min for the exercise group.

LBNP tolerance did not change signi®cantly in eithergroup between pre- and post-testing; for controls, thepost-testing maximum LBNP pressure after training was83 (4) mmHg and the CSI was 1005 (97) mmHg á min.For the exercise group, the post-training maximum

LBNP pressure was 98 (7) mmHg and the CSI averaged1516 (197) mmHg á min.

Subtolerance responses

The heart rate and blood pressure responses to LBNPwere compared for all LBNP stages between 0 and)70 mmHg LBNP. There were no signi®cant group ortraining e�ects for any variable (Table 1).

Stand tests

All subjects completed the 10-min stand test during pre-and post-testing sessions without syncopal symptoms.The exercise group tended to have (P < 0.06) a higherpre-testing supine resting heart rate compared to thecontrol group (Fig. 2). The post-testing heart rate wasreduced signi®cantly in the exercise group both at restand during standing, so that the post-testing heart ratesof the two groups were similar.

No signi®cant group or pre- to post-test di�erenceswere found for systolic, diastolic, mean arterial or pulse

Fig. 1 Lower body negative pressure (LBNP) duration (s) for control(n = 9) and exercise (n = 10) subjects. Values are means (SE). There was a signi®cant di�erence in the pre-testing (PRE) LBNPduration of the two groups (P < 0.05). LBNP duration did notchange signi®cantly in either group between pre-testing and post-testing (POST)

Table 1 Subtolerance responsesat )70 mmHg Lower body ne-gative pressure. Values aremeans (SE). (LBNP Lowerbody negative pressure, fc heartrate, MAP mean arterial pres-sure, PP pulse pressure, PREpre-test, POST post-test)

LBNPstage

fc (beats min)1) MAP (mmHg) PP (mmHg)

PRE POST PRE POST PRE POSTn = 10 n = 10 n = 10 n = 10 n = 10 n = 10

Exercise group

Rest 63 61 91 91 41 40(4) (4) (3) (2) (2) (2)

)70 mmHg 94 87 91 87 27 28(4) (8) (3) (1) (3) (2)

Control group

Rest 57 57 91 90 43 45(4) (3) (2) (2) (2) (3)

)70 mmHg 99 93 90 89 25 32(8) (6) (2) (2) (4) (3)

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pressures at rest or during standing. For controls, pre-testing blood pressures (systolic/diastolic) during thestand test were (mmHg) 119 (3)/74 (2) (supine) and 112(3)/78 (2) (after 10 min of standing). Post-testing, bloodpressures were (mmHg) 116 (4)/72 (2) (supine) and 108(3)/77 (3) (after 10 min of standing). For the exercisegroup, pre-testing blood pressures during the stand testwere (mmHg) 117 (3)/79 (2) (supine) and 109 (4)/79 (3)(after 10 min of standing). Post-testing, blood pressureswere (mmHg) 115 (2)/74 (2) (supine) and 111 (3)/81 (3)(after 10 min of standing).

Vascular ¯uid volumes

For the exercise group, small signi®cant elevations inblood volume (2.8%; P = 0.001) and RCM (3.9%; P =0.02) were noted following training (Table 2). Changes inPV showed a similar trend (2.2% increase) that was notstatistically signi®cant (P = 0.13). When expressed asml á kg LBM)1, the post-training increases in blood vol-ume and RCM were not signi®cant. No changes werefound for post-trainingHCTTB, peripheral hematocrit, orF-cell ratio. For controls, no signi®cant changes were seenin any variable between pre- and post-testing.

BARO assessment

Signi®cant di�erences were found between the con-trols and exercise groups for the pre-testing slope andrange, but not for the operational point of the BARO(Table 3). Neither group showed any pre- to post-testingchanges.

Leg blood ¯ow and leg compliance

Leg circumference was similar for the two groups anddid not change pre- to post-testing (Table 4). In addi-tion, leg blood ¯ow (in cm3 á 100 cm3 tissue á min)1) didnot di�er signi®cantly between groups or change pre- topost-testing (Table 4). The leg compliance curves for thetwo groups were similar, with no signi®cant pre- to post-testing change for either group (Fig. 3).

Fig. 2 Heart rate (beats á min)1) response to stand test. Values aremeans (SE). There were no signi®cant di�erences (P > 0.05) betweenexercise (n = 10) and control (n = 9) groups, pre- or post-training.The heart rate signi®cantly decreased (P < 0.05) pre- to post-testingin the exercise group while at rest and standing

Table 2 Vascular ¯uidresponses to resistance training.(LBM Lean body mass, PVplasma volume, HCTTB totalbody hematocrit)

Exercise (n = 10) Control (n = 9)

PRE POST PRE POST

Erythrocyte volume(ml) 2017 (84) 2091 (77)*,** 2105 (102) 2088 (111)(ml á kg LBM)1) 34.8 (1.2) 34.9 (1.2) 35.7 (1.4) 35.1 (1.3)

PV(ml) 3133 (129) 3203 (139) 3152 (92) 3177 (102)(ml á kg LBM)1) 53.4 (2.0) 52.5 (1.7) 53.6 (1.2) 53.5 (0.8)

Blood volume(ml) 5150 (168) 5294 (174)*,** 5257 (168) 5264 (201)(ml á kg LBM)1) 87.7 (2.4) 86.9 (1.9) 89.2 (2.0) 88.6 (1.7)

HCTTB 39.2 (1.2) 39.6 (1.2) 39.9 (1.0) 39.5 (0.8)F-cell ratio 0.89 (0.01) 0.89 (0.00) 0.90 (0.01) 0.90 (0.01)

*Signi®cant di�erence (P < 0.05) pre- to post-testing, **Signi®cantly di�erent (P < 0.05) fromcontrols

Table 3 Carotid baroreceptorcardiac re¯ex responses to re-sistance training. Values aremeans (SE)

Exercisse (n = 10) Control (n = 9)

PRE POST PRE POST

Slope (ms á mmHg)1) 4.3 (0.6)* 4.0 (0.8) 3.9 (0.8) 3.8 (0.7)Range (ms) 253 (40)* 238 (5) 194 (38) 184 (29)Operational point (%) 14.2 (4.5) 16.1 (4.5) 17.8 (10.0) 9.7 (5.1)

*Signi®cantly di�erent (P < 0.05) from controls

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Body composition

Body mass and total bone mineral content did notchange in either group from pre- to post-testing (Ta-ble 5). The LBM increased by 3.4% (P = 0.002) and fatmass decreased by 12.0% (P = 0.016) in the exercisegroup, while no signi®cant changes were noted in thecontrol group.

Voluntary strength

The resistance training regimen induced marked im-provements in 1 RM strength (Table 6) for all exercises

tested (P � 0.001): leg press increased by 9.4%, leg curlby 7.8%, bench press by 18.9%, and heel raise by14.8%. No signi®cant changes occurred between pre-and post-testing in the control group.

Muscle volumes

Resistance training increased the muscle volume of thequadriceps by 14.4% (P < 0.001), the hamstrings by5.4% (P < 0.001), the adductors by 8.2% (P < 0.015),and the plantar ¯exors by 3.8% (P = 0.01) (Table 6).The anterior calf musculature was not a�ected by thetraining. The pre- and post-testing skeletal muscle vol-umes of the controls were not signi®cantly di�erent inany compartment.

Discussion

In agreement with earlier investigators, the resistanceexercise protocol used in this study produced substantialincreases in 1 RM strength (Kraemer et al. 1995;McCarthy et al. 1995), LBM (Katch and Drumm 1986)and leg muscle volume (MacDougall et al. 1980). Wealso found a small increase in blood volume. Despitethese adaptations to resistance exercise, no improvementin LBNP tolerance, cardiovascular responses to stan-ding, or LBNP were found.

Resistance training and orthostatic tolerance

There have been only two other studies (Lightfoot et al.1994; Tatro et al. 1992) in which the investigators ex-amined the e�ect of resistance exercise on orthostatictolerance, and both used pre-syncopal LBNP to simulatean orthostatic stress. The study by Lightfoot et al. (1994)demonstrated a positive e�ect of whole-body resistance

Table 4 Leg circumference andblood ¯ow responses to re-sistance training. Values aremeans (SE)

Exercise (n = 10) Control (n = 9)

PRE POST PRE POST

Leg circumference (cm) 36.7 (0.8) 36.7 (0.8) 35.3 (0.8) 35.3 (0.8)Blood ¯ow(cm)3 á 100 cm)3 tissue á min)1)

2.23 (0.30) 1.98 (0.22) 1.97 (0.16) 1.53 (0.15)

Fig. 3 Leg compliance curves. Values are means (SE). There were nosigni®cant di�erences (P > 0.05) between exercise (n = 10) andcontrol (n = 9) groups pre- or post-training. Neither were there anysigni®cant changes (P > 0.05) pre- to post-testing in exercise orcontrol groups

Table 5 Body composition be-fore and after a resistance-training program. Values aremeans (SE). (BMC Bone mi-neral content)

Exercise �n � 10� Control �n � 9�

PRE POST PRE POST

Body mass (kg) 77.8 (3.3) 77.9 (3.3) 78.9 (2.6) 79.7 (2.5)BMC (kg) 2.854 (0.087) 2.838 (0.089) 2.811 (0.091) 2.819 (0.087)LBM (kg) 59.1 (2.4) 61.1 (2.3)*,** 59.0 (1.6) 59.4 (1.7)Fat mass (kg) 15.9 (1.3) 14.0 (1.3)*,** 17.2 (2.4) 17.5 (2.3)%Fat 20.4 (1.2) 17.7 (1.2)*,** 21.3 (2.6) 21.5 (2.6)

*Signi®cant di�erence �P < 0:05� pre- to post-testing**Signi®cantly di�erent �P < 0:05� from controls

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training on LBNP tolerance, while the study of Tatroet al. (1992) reported no signi®cant exercise e�ect.Lightfoot et al. (1994) attributed the inconsistent resultsto di�erences in resistance training protocols in the twostudies. The subjects in the study of Tatro et al. (1992)trained twice a week with a protocol that stressed onlythe legs. The protocol of Lightfoot et al. (1994) em-ployed a more severe whole-body training programwhich was performed three times a week. The whole-body resistance training protocol used in our study ismost closely matched with that of Lightfoot et al. (1994),yet our results do not support their positive ®ndings.

Our study and that of Lightfoot et al. (1994) bothemployed 12- week rigorous programs of upper- andlower-body isotonic exercise. Our regimen employednine exercises of 6±11 RM, performed for one warm-upset and three maximal e�ort sets. Lightfoot et al. (1994)had a similar regimen that included 12 isotonic exerciseswith 5±8 RM of four to ®ve sets of maximal exercise.Although in both studies an isotonic regimen was usedfor training, Lightfoot et al. (1994) used an isokinetictesting mode while we employed an isotonic mode, thusmaking direct comparisons of strength improvementsbetween the studies inappropriate (Morrissey et al.1995).

Although there were minor di�erences in the pre-syncopal LBNP protocols and termination criteria be-tween our study and that of Lightfoot et al. (1994), it isunlikely that they could have accounted for our di�eringLBNP tolerance results. In our paper, LBNP tolerancewas de®ned as the ®nal LBNP stage that could be tol-erated for at least 60 s without pre-syncopal symptoms.We have found that this criterion improves the repeat-ability of tolerance assessment. Also, there was a slightdi�erence in the LBNP ramp protocols between the twostudies, but such a slight di�erence in pressure stepswould not be expected to a�ect tolerance.

A major di�erence between our two studies was thepre-training LBNP tolerances. The average pre-trainingLBNP tolerance of the exercise subjects in Lightfoot'sinvestigation was approximately 78 mmHg, comparedto a mean value of 98 mmHg in our study. The toler-

ances of our untrained exercise subjects were similar tothose observed in a group of chronic-resistance-trainedathletes in Lightfoot's study, who had a mean LBNPtolerance of 93 mmHg. In our study, the baseline LBNPtolerance of the exercise group were unusually high.From previous experience in testing over 100 healthyyoung men with our protocol, a normal LBNP toleranceis usually approximately 70±80 mmHg. For some un-known reason, the subjects who volunteered to be in theexercise group in our study had unusually high LBNPtolerances. The e�ectiveness of resistance exercise toalter LBNP tolerance may depend upon the pre-traininglevel of tolerance, where subjects with a high LBNPtolerance are less likely to exhibit an improvement fol-lowing an intervention.

Similarly, our subtolerance cardiovascular responsesto LBNP were not altered after the resistance exerciseregimen. Since LBNP simulates an orthostatic challenge,each subject was also exposed to an actual orthostaticstress: a 10-min stand test. These results also failed toreveal a signi®cant e�ect of resistance exercise trainingon the heart rate or blood pressure responses to stan-ding.

Role of blood volume on orthostatic tolerance

The ability of chronic aerobic exercise to expand PV iswell documented (Convertino 1987); however, little isknown about the ability of resistance exercise to altereither PV or RCM. Acute resistance exercise decreasesPV in relation to the severity of the exercise stimulus(Collins et al. 1989; Knowlton et al. 1987). As with en-durance exercise, however, the decline in PV is followedby a 20% overshoot above pre-exercise levels after 24 hof recovery (Ploutz et al. 1993). In a study comparing thechronic e�ects of resistance exercise on blood volume,Epperson et al. (1982) reported a 6.9% increase in bloodvolume after 12 weeks of whole-body resistance exercise.Since an important in¯uence of blood volume on or-thostatic responses has been well-documented (Con-vertino 1987) we proposed, in this study, that if whole-

Table 6 1 RM strength andskeletal muscle volumes beforeand after a resistance-trainingprogram. Values are means(SE)

Exercise (n = 10) Control (n = 9)

PRE POST PRE POST

1 RM strength (kg)

Leg press 153.8 � 5.9 168.3 � 5.4*,** 133.6 � 8.1 135.1 � 8.8Leg curl 79.9 � 4.5 86.2 � 4.8*,** 78.7 � 4.0 79.1 � 4.1Bench press 67.1 � 3.2 79.8 � 3.3*,** 66.0 � 8.6 68.0 � 9.2Heel raise 201.9 � 8.1 231.8 � 10.6*,** 194.5 � 8.2 191.5 � 6.6

Skeletal muscle volumes (cm3)

Quadriceps 1165 � 84 1334 � 95*,** 1161 � 82 1180 � 89Hamstrings 554 � 40 584 � 40*,** 547 � 35 560 � 42Adductors 525 � 37 569 � 49*,** 529 � 65 532 � 67Plantar ¯exors 799 � 72 829 � 72* 672 � 31 679 � 31Anterior calf 582 � 60 584 � 56 460 � 13 463 � 14

*Signi®cant di�erences(P < 0.05) pre- to post-testing,**Signi®cantly di�erent(P < 0.05) from controls

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body resistance training could successfully expand bloodvolume this could contribute to an increase in LBNPtolerance. We found a small, 2.8% (144 ml), increase inblood volume in this study which was not su�cient toinduce a detectable improvement in LBNP tolerance orstand test responses.

A secondary objective of this study was to determinewhether the F-cell ratio is altered following a program ofresistance training. The F-cell ratio represents the ratiobetween the HCTTB and peripheral venous hematocrit.Sawka et al. (1992) have shown that aerobically ®tsubjects, who have a relatively expanded PV comparedto sedentary subjects, had similar F-cell values, indicat-ing no change in the vascular distribution of ery-throcytes between large and small vessels. In our study,in which resistance training increased RCM, we alsofound no change in the F-cell ratio. This information isuseful for future investigations, supporting the use ofperipheral hematocrit and PV measurements only tocalculate blood volume, without the need for directRCM measurement.

Role of the BARO on orthostatic responses

Tatro et al. (1992) suggested that resistance training mayimprove LBNP tolerance by increasing the sensitivityand/or resetting the BARO. After their 19 week resis-tance exercise program, the exercise group exhibited asigni®cant increase in the maximum slope of the R-Rinterval to carotid distending pressure relationship (neckpressure/suction technique), and a reduction in thebaseline resting systolic blood pressure. This alterationin BARO function provided no measurable improve-ment in LBNP tolerance. Hill et al. (1989) also found asigni®cant reduction in systolic blood pressure in menafter whole-body resistance training, which they hy-pothesized may have been due to changes in the baro-re¯ex function. In contrast, Lightfoot et al. (1994) foundan improvement in LBNP tolerance after resistance ex-ercise, but without signi®cant change in the BARO re-sponse. In a cross-sectional study, Smith et al. (1988)compared the Dheart rate/Dblood pressure ratio duringLBNP, and the heart rate response to graded phenyl-ephrine infusion, as indicators of the overall barore¯exfunction. They reported no signi®cant di�erences inthese responses between sedentary, endurance-trained,and weight-trained athletes. In our study, prior totraining the exercise group had a signi®cantly greatersensitivity and range of their BARO accompanied by agreater LBNP tolerance than the controls, supporting apossible association between BARO function and or-thostatic tolerance. Our ®ndings support those of Smithet al. (1988) and Lightfoot et al. (1994) in that we foundno evidence that whole-body resistance training altersBARO function. This result disagrees with that of Tatroet al. (1992) who found increases in BARO function withleg-only resistance training. Therefore, the e�ect of re-sistance training on BARO function is still unclear.

Role of muscle mass on leg complianceand orthostatic responses

With exposure to an orthostatic stress, the ability tomaintain cardiac output and arterial pressure is depen-dent upon the amount of blood pooled in the lowerextremities and its subsequent e�ect on venous return.Convertino et al. (1988, 1989) suggested that leg com-pliance is lower when there is a large muscle mass pro-viding mechanical compression of the veins. Increases inmuscle mass may resist venous stretching and reduceblood pooling. Convertino et al. (1989) suggested thatthe orthostatic intolerance associated with bed rest isrelated to the decline in calf muscle mass, which wouldo�er less structural support to prevent blood pooling inthe leg vasculature during an orthostatic stress. Light-foot et al. (1994) hypothesized that resistance exercise,by increasing muscle mass, may decrease leg complianceand improve LBNP tolerance. In their study, at a givenlevel of LBNP a smaller increase in leg circumferenceduring LBNP occurred after resistance training. At tol-erance, the percentage change in leg circumference wassimilar pre- and post-training. suggesting that pre-syn-copal symptoms are provoked after a certain degree ofblood pooling in the lower body.

Our ®ndings would argue against a major role forincreases in muscle mass of the leg after resistancetraining to decrease passive leg compliance. Despite in-creases in leg muscle volume and strength, we found nochange in leg compliance, as determined with the thighocclusion-mercury strain gauge method. Our leg com-pliance technique was not comparable to that ofLightfoot et al. (1994), where leg compliance was as-sessed by measuring changes in leg circumference duringLBNP, and no assessment of muscle mass was made.Our study assessed leg compliance under conditions ofpassive ®lling. In the study of Lightfoot et al. (1994), leg®lling may be opposed by the vaso- and venoconstrictorre¯exes induced by the central blood volume shifts andregional changes associated with LBNP. Their resultswould suggest that resistance training improves the ef-fectiveness of such vasomotor re¯exes and contributesto an increase in LBNP tolerance. Our results suggestthat increases in leg muscle mass due to resistancetraining do not reduce leg compliance or alter LBNPtolerance.

In conclusion the e�ectiveness of this whole-bodyresistance training protocol was evident from the signi-®cant increase in LBM, leg muscle volume, and upper-and lower-body strength. Of the proposed mechanismsby which resistance exercise might improve orthostatictolerance, a slight (3%) increase in blood volume oc-curred, but there were no signi®cant changes in legcompliance or BARO. In conclusion, this intense resis-tance-exercise program did not improve orthostatic re-sponses or increase LBNP tolerance. The ®ndings of thisstudy should be extrapolated to the general populationwith caution because of the high pre-training LBNPtolerance of our resistance-exercise subjects.

39

Acknowledgements The authors express thanks to World Gym ofHouston, Tex. Who donated the use of their facility and equip-ment; Dr. John Gilbert, Je�rey Crouch, and Mark Guilliams fortheir assistance with training and testing; Dr. Dick Calkins forstatistical consultation; Theda Driscoll, CNMT for technical helpwith the isotope tests; Jackie Reeves for editorial help; and thesubjects for their participation. This work was supported through agrant from the National Aeronautics and Space Administration,Research and Technology Objectives and Planning Grant 199-26-11-29.

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