1-Exercise Stroke P1

ARTICLES

Exercise Capacity Early After StrokeMarilyn J. MacKay-Lyons, PhD, Lydia Makrides, PhD

ABSTRACT. MacKay-Lyons MJ, Makrides L. Exercisecapacity early after stroke. Arch Phys Med Rehabil 2002;83:1697-702.

Objective: To evaluate exercise capacity of patients with apoststroke interval of less than 1 month.

Design: Prospective, cohort, observational study.Setting: Exercise testing laboratory in a tertiary care hospi-

tal.Participants: Twenty-nine patients (mean age � standard

deviation, 64.9�13.5y) with a poststroke interval of 26.0�8.8days.

Interventions: Not applicable.Main Outcome Measure: Peak exercise capacity (VO2peak)

was measured by open-circuit spirometry during maximal ef-fort treadmill walking with 15% body-weight support.

Results: Mean VO2peak was 14.4�5.1mL � kg�1 � min�1 or60%�16% of age- and sex-related normative values for sed-entary healthy adults.

Conclusions: Exercise capacity approximately 1 month afterstroke was compromised. Further research is needed to eluci-date the physiologic basis of this low capacity.

Key Words: Cerebrovascular disorders; Exercise; Hemiple-gia; Rehabilitation.

© 2002 by the American Congress of Rehabilitation Medi-cine and the American Academy of Physical Medicine andRehabilitation

CARDIOVASCULAR DISEASE is a major factor restrict-ing successful outcomes after stroke rehabilitation.1 As

many as 75% of patients poststroke also have heart disease.2 Infact, survivors of the acute phase of stroke are at greater risk ofdying from cardiac disease than from any other cause, includ-ing a second stroke.3 Whereas neurologic recovery after strokehas been extensively investigated, cardiovascular adaptationsto physical activity poststroke have received little attention.This situation is puzzling, given the high prevalence of cardiaccomorbidity and the observation that most of the variance indisability after stroke cannot be explained by neurologic im-pairment.4

Cardiovascular and neuromuscular impairments, togetherwith physical inactivity resulting from stroke, adversely affectexercise capacity—they limit the ability to respond to physio-logic stresses induced by prolonged physical effort. The detri-mental effects of low exercise capacity on functional mobilityand resistance to fatigue are compounded by the high metabolicdemand of hemiparetic gait, with energy costs as much as 3times higher than for subjects without neurologic impairmentwalking at the same speed.5,6 Exercise stress tests have shown

that individuals in the chronic poststroke period (�6mo) haveabnormally low exercise capacity.7-10 What has not been doc-umented is exercise capacity during the early poststroke period,the time during which physical rehabilitation usually takesplace and the potential for functional improvement is maxi-mized.11 Exercise testing during this period is critical to in-forming the clinician of the need for, and safe design of,cardiovascular exercise prescription.

Measurement of exercise capacity in the early poststrokeperiod has eluded researchers because balance and motor con-trol problems preclude use of standard exercise testing pro-tocols. The preferred mode of measuring maximal oxygenconsumption (V̇O2max), the definitive index of exercise capac-ity,12 is the treadmill. The potential to recruit sufficient musclemass to elicit a maximal metabolic response is much morelikely to be realized while walking than cycling, particularly indeconditioned populations.12 Recently, we devised a treadmillexercise protocol using partial body-weight suspension thatwould permit testing earlier poststroke than would otherwise befeasible. In a preliminary investigation13 of this protocol usinghealthy adults, we found that using 15% body-weight supportdid not affect the endpoints of the principal respiratory gasexchange variables of the exercise test and, thus, did notconfound interpretation of V̇O2max data. The main purpose ofthe present study was to measure exercise capacity early afterstroke by using a treadmill test protocol involving partialweight suspension. We selected VO2peak as the measure ofexercise capacity because the rigorous criteria for V̇O2maxoften cannot be met by deconditioned or elderly individuals,14

which would include most patients with stroke.

METHODS

Participants

Men or women who had a primary diagnosis of first, unilat-eral, ischemic stroke, confirmed by both clinical and radio-graphic means, and admitted to the acute stroke service of atertiary health care facility were consecutively screened foreligibility. Included were patients who were �18 years of age,whose stroke occurred within the prior month, who showed noevidence of dementia (as indicated by a score �24 of 30 on theMini-Mental State Examination),15 and who had greater thanstage 3 of Chedoke-McMaster Stages of Recovery of the LegAssessment.16 This assessment is used to rate motor impair-ment after stroke by observing the patient performing increas-ingly complex motor tasks. The measure has been shown tohave good reliability and validity.17 Stage 1 is assigned whenflaccid paralysis is present, stage 3 when active voluntarymovement is limited to stereotyped synergistic patterns, andstage 7 when movement is normal.16 Patients with stage 3 orless require physical assistance to advance the affected legwhile walking, thus precluding valid VO2peak measurement.Exclusion criteria were the contraindications for exercise test-ing outlined by the American College of Sports Medicine(ACSM).18 Prospective subjects who met the criteria weregiven a detailed explanation of the study and were asked to signthe consent form approved by the hospital research ethicscommittee.

From the School of Physiotherapy, Dalhousie University (MacKay-Lyons) andHealth and Wellness Institute (Makrides), Halifax, NS, Canada.

Supported by the Heart and Stroke Foundation of Canada.The authors have chosen not to select a disclosure statement.Reprint requests to Marilyn J. MacKay-Lyons, PhD, Schl of Physiotherapy,

Dalhousie University, 5869 University Ave, Halifax, NS B3H 3J5, Canada, e-mail:[email protected].

0003-9993/02/8312-7243$35.00/0doi:10.1053/apmr.2002.36395

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Arch Phys Med Rehabil Vol 83, December 2002

The clinical history of each subject was recorded, notingsmoking habits and comorbidities such as hypertension, diabe-tes mellitus, chronic obstructive pulmonary disease, and coro-nary artery disease (CAD), the latter indicated by the presenceof at least 1 of the following: myocardial infarction by historyor electrocardiogram, angina pectoris, or coronary artery by-pass graft surgery.19 The Barthel Index was used to evaluatefunctional ability by assessing 10 activities of self-care andmobility, yielding 1 combined score, ranging from 0 to 100.20

The Physical Activity Questionnaire (PAQ) was used as ageneral measure of the premorbid physical activity level ofeach subject.21 This questionnaire involves asking the subjectsto indicate the frequency and duration of their participationover the past year in 11 forms of physical activity. A score foreach activity is derived from the product of the length of timeof participation per session (in hours), the number of sessionsper week, and the number of seasons of participation per year.A total activity score is the sum of the individual scores and canbe categorized as a score greater than 18, very active; 1 to 18,active; and 0, inactive.

Exercise TestingWithin 1 week before exercise testing, each subject visited

the exercise testing laboratory for orientation to weight-sup-ported treadmill walking and identification of the initial tread-mill speed for the testing protocol. The subject practicedbreathing through a mouthpiece with headgear and nose clip inplace. A vest, similar to a parachute harness, was securedaround the torso and attached to the supporting frame posi-tioned over the treadmill. The subject walked on the treadmillat a self-selected, comfortable speed with 15% of body massvertically displaced through the overhead support.

In preparation for the exercise test, subjects were requestedto avoid food and smoking for at least 2 hours, to refrain fromdrinking caffeinated beverages for at least 6 hours, and to avoidheavy exertion or exercise for 12 hours. Medication scheduleswere not altered. The methods for data collection have beenpreviously described.13 In brief, a symptom-limited gradedexercise test was performed on a calibrated motorized tread-milla with 15% of body mass suspended using the PneuweightUnweighting System.b A patient-specific protocol, similar tothat described by Macko et al,22 was used because physicallimitations precluded application of a standardized protocol(table 1). Individualized protocols have been previously vali-dated for testing exercise capacity of untrained, sedentary in-dividuals.23,24 Fingertip contact of the handrail was permitted.The warm-up was limited to 1 minute because of the rapidonset of fatigue in some patients. During the initial 2 minutesof testing, the subject walked at the self-selected speed identi-fied in the orientation session and 0% treadmill grade, followedby a 2.5% increase in grade every 2 minutes until an incline of

10% was reached, and, thereafter, a .05m/s increase in speedevery 2 minutes, until test termination and a 2-minute cool-down.

Exercise time, the time from the initiation to termination ofthe exercise protocol excluding the warm-up and cool-down,was recorded. Subjective exertion on the treadmill was noted atthe end of each 2-minute stage and at peak exercise by usingthe rating of perceived exertion on a scale of 0 (nothing at all)to 10 (very, very hard).25 Subjects were instructed to usemaximal effort and to display the thumb-down signal whenthey wished to terminate the test. Termination of testing fol-lowed ACSM guidelines.18 For subjects with a history ofpulmonary disease, arterial oxygen saturation was monitoredusing a Nellcor NPB-40 pulse oximeter.c Saturation less than85% was a criterion for termination of testing.26

Expired gas was analyzed via open-circuit spirometry byusing a SensorMedics 2900 Metabolic Measurement Cartd todetermine oxygen consumption (V̇O2), carbon dioxide produc-tion, minute ventilation, respiratory exchange ratio (RER), andtidal volume. Volume calibration and calibration of gases byusing standard gases were done before each test. The subjectwore a nose clip and breathed room air though a 1-way direc-tional valve system attached to a mouthpiece. Peak values forexercise parameters were the averages of values recorded dur-ing the last 30 seconds of the test.

A 10-lead electrocardiogram provided continuous monitor-ing of heart rate and cardiac electrical activity. Resting heart-rate was determined after a 5-minute rest period. Peak heartrate (HRpeak) was the average heart rate during the last 30seconds of exercise and was expressed as a percentage ofage-predicted maximal heart rate ([220�age]/100).18 This for-mula was adapted for those patients on �-blocker medication toadjust for its heart rate–lowering effect (predicted maximalheart rate�85%[220�age]).27 Peak oxygen pulse in millilitersof oxygen per beat was calculated ([1000�VO2peak]/HRpeak).Right brachial artery systolic (SBP) and diastolic blood pres-sure (DBP) were measured by using a calibrated mercurysphygmomanometer at rest, every 2 minutes during exercise, andevery minute during recovery until returning to baseline. Rate-pressure product was calculated ([heart rate�SBP]/100).18

Criteria for attainment of V̇O2max included: (1) increase in V̇O2less than 150mL in the final minute of exercise—a “V̇O2plateau,” (2) peak RER greater than 1.0, (3) peak SBP greaterthan 200mmHg, and (4) HRpeak within 15 beats per minute ofpredicted maximal heart rate.14

To check the reliability of the testing protocol, we conducteda test-retest study of a subsample of subjects performing 2exercise tests with a 3- to 4-day interval between tests. Beingmindful of the physical and emotional stresses confrontingpatients in the early poststroke period, we delayed reliabilitytesting until 2 months after stroke.

Data Analysis

Descriptive statistics were used to characterize the subjectsand exercise test results. Univariate statistics (ie, t tests, Mann-Whitney U test, �2) were used to compare characteristics ofparticipants and nonparticipants. The independent t test forunequal sizes was applied to compare VO2peak data of subjectswith and without CAD. An � level of .05 was set.

Factorial analysis of variance (ANOVA) was performed tocompare VO2peak values of subgroups of subjects with BarthelIndex scores (� or �90). This analysis was repeated to com-pare VO2peak values of subgroups classified by their scores onthe PAQ (ie, inactive, active, very active) as well as subgroupsclassified by their Chedoke-McMaster Stage of Recovery of the

Table 1: Symptom-Limited Graded Exercise Test Protocol

Warm-up 1min at 60%–70% self-selected speed and noincline

Stages 2min each with 15% of body mass suspendedStage 1 Self-selected treadmill speed with no inclineStages 2–5 Self-selected treadmill speed maintained and

2.5% increase in incline at each stageStages �6 10% incline maintained and .05m/s increase in

treadmill speed at each stageCool-down 2min at 60%–70% self-selected speed and no

incline

1698 EXERCISE CAPACITY EARLY AFTER STROKE, MacKay-Lyons


Leg (ie, stages 4, 5, 6). Multiple linear regression was used toexamine the effects of independent variables (ie, age, BarthelIndex, Stage of Recovery of the Leg, PAQ) on VO2peak, withage treated as a forced variable because of its strong correlationwith VO2peak. The level of significance was set at .01. Least-square regression lines were calculated for V̇O2 and heart rateagainst exercise time for test-retest reliability data. The intra-class correlation coefficient (ICC3,1) was calculated for theslopes and intercepts of the regression lines as well as for theVO2peak and HRpeak. Analyses were performed with Micro-soft Excel, version 5.0,e and StatView®, version 4.01.f

RESULTSOf the 44 patients who met the screening criteria, 34 gave

consent to enter the study. Five of these patients who providedconsent were not tested because of early discharge from hos-pital (n�3) and progression of the neurologic status (n�2).Comparison of demographic and clinical characteristics of the29 participants and 15 nonparticipants revealed significantdifferences in age of participants and nonparticipants(64.9�13.5y vs 71.3�11.4y, P�.01) and sex distribution (22men, 7 women vs 5 men, 10 women, P�.01). Characteristics ofthe participants are in table 2. The percentages of patients withhistory of CAD or diabetes are consistent with previous re-ports.28,29 Of the 15 participants taking �-blocker medications,13 were on �1-selective blockers (metoprolol, atenolol) and 2were on nonselective (propranolol, labetalol). Of the 18 pa-tients with a history of smoking, 8 had quit prior to the time oftheir stroke. Eight (28%) participants were mildly affected withhemiparetic gait and did not require an assistive device, 12(41%) used a single cane, 6 (21%) used a quad cane, and 3(10%) used a walker.

No adverse events occurred during or after the tests. Patientsconsistently reported that the body-weight support vest wascomfortable and reduced anxiety related to fear of falling.Mean walking speed at initiation of testing was .39�.12m/sand at the last completed stage was .54�.30m/s. Arterial ox-ygen saturation did not fall below 85% during testing for the 5patients monitored. Twenty-four (83%) subjects terminatedtesting of their own volition, the most common reasons fortermination being generalized fatigue and shortness of breath.In the remaining 5 cases, termination was investigator-initiatedbecause the upper limit of blood pressure (ie, SBP�250mmHg � DBP �115mmHg)17 had been reached.Twenty-two (76%) subjects achieved 1 or more of the V̇O2maxcriteria. The RER and HRpeak criteria were attained by 18 and16 individuals, respectively, whereas the peak SBP and V̇O2plateau criteria were attained by 8 and 5 individuals, respec-tively.

Physiologic measurements at peak exercise intensity aresummarized in table 3. Mean VO2peak values were 60%�16%of age- and sex-related normative values by using nomogramsof sedentary individuals.18 Mean VO2peak values of male andfemale subjects differed significantly (15.5�5.3mL � kg�1 �min�1 vs 10.9�1.7mL � kg�1 � min�1, P�.01), in keeping withthe finding that VO2max values for women are approximately77% of that for men.30 In addition, mean VO2peak valuesfor patients with and without CAD were 12.9�3.1mL �kg�1 � min�1 and 16.0�5.2mL � kg�1 � min�1, respectively,the difference being significant (P�.05). Differences in meanpeak oxygen pulse of subjects taking �-blockers comparedwith those not taking �-blockers (ie, 10.1�3.5mL/beat vs9.1�3.2mL/beat) were not statistically significant. Mean rate-pressure product increased from 109.3�17.3 at rest to224.0�65.6 at peak exercise. Mean peak tidal volume andminute ventilation averaged 61% and 56%, respectively, ofage- and sex-related normative values.31

Figure 1 illustrates the differences in VO2peak values ofsubjects grouped according to the Barthel Index, premorbidphysical activity level, and Chedoke-McMaster Stage of Re-covery of the Leg, respectively. Factorial ANOVA revealed asignificant difference in VO2peak values of the subgroup withBarthel Index scores less than 90 (n�18) compared with thesubgroup with Barthel Index scores greater than 90 (n�11).Although there was a trend of increasing VO2peak values withincreasing levels of prestroke physical activity levels and in-creasing Stages of Recovery of the Leg; the differences werenot statistically significant. Multiple linear regression analysisgave similar results (table 4). The Barthel Index was found to

Table 2: Subject Characteristics

Age (y) 64.9�13.5Sex (men/women) 22/7Time poststroke (d) 26.0�8.8Side of stroke 18 right: 11 leftBarthel Index 76.7�12.6Chedoke-McMaster Stage of Leg, 1–7 5.3�0.7CAD 17/29 (59%)�-blocker medication 15/29 (52%)Diabetes mellitus 7/29 (24%)Chronic obstructive pulmonary disease 5/29 (17%)History of smoking 18/29 (62%)

NOTE. Values are mean � standard deviation (SD) or n (%).

Table 3: Physiologic Variables at Peak Exercise Intensity

VO2 (mL � kg�1 � min�1) 14.4�5.1V̇O2 (L/min) 1.2�0.50RER 1.00�0.06Heart rate (beats/min) 123.1�18.9% of predicted HRmax 84.9�8.2O2 pulse (mL/beat) 9.6�3.3SBP (mmHg) 182�33DBP (mmHg) 98�15Rate-pressure product 224.0�65.6Minute ventilation (L/min) 42.1�16.4Tidal volume (L) 1.4�0.53Exercise duration (min) 8.7�4.6

NOTE. Values are mean � SD.

Fig 1. Comparison of mean VO2peak values for subjects classifiedby Barthel Index, premorbid physical activity level, and Chedoke-McMaster Stages of Recovery. Error bars indicate 1 standard error(SE). *Significant difference in mean VO2peak between subjectswith Barthel Index <90 and >90 (P<.01).

1699EXERCISE CAPACITY EARLY AFTER STROKE, MacKay-Lyons


be significant in predicting both relative and absolute values ofVO2peak, whereas the PAQ scores and the Stages of Recoveryof the Leg were not significant factors.

Six subjects (4 men, 2 women) volunteered to participate inthe reliability substudy conducted at 2 months poststroke. TheICC3,1 for the VO2peak, and the slopes and intercepts of re-gression lines of V̇O2 against exercise time were .94, .96, and.92, respectively. The ICC3,1 for the HRpeak and the slopes andintercepts of regression lines of heart rate against exercise timewere .93, .88, and .92, respectively; these findings are consis-tent with reports of high reliability of exercise test results inhealthy subjects32 and subjects long after stroke.10

DISCUSSIONThis study is the first, to our knowledge, to report the response

of patients in the early poststroke period to symptom-limitedtreadmill exercise. As anticipated, not all subjects attained theminimum criteria for V̇O2max, reinforcing the notion that attainingV̇O2max in deconditioned and elderly subjects is often an unreal-istic goal.14 Nevertheless, the percentage of predicted maximumheart rate and the peak rate-pressure product achieved by thesubjects (84.9%�8.2% and 224.0�65.6, respectively) were sim-ilar to values reported for patients postmyocardial infarction(85%�8% and 230�48, respectively),33 which suggests compa-rable physical effort. The mean VO2peak at 26.0�8.8 days afterstroke was 14.4�5.1mL � kg�1 � min�1 or 60%�16% of that pre-dicted from age- and gender-adjusted normative values for sed-entary individuals. The finding of such low exercise capacity isclinically meaningful. Values for V̇O2max less than 84% of nor-mative values are interpreted as being pathologic,34 and the min-imum VO2peak to meet the physiologic demands of independentliving is 15mL � kg�1 � min�1.35 Further, exercise capacity hasbeen used as a predictor of mortality among patients with CAD(59% of our subjects had CAD)—those with VO2peak levels lessthan 21mL � kg�1 � min�1 have been designated as a high mortal-ity group.36 Cardiac rehabilitation strategies have proven effectivein increasing exercise capacity of patients in the chronic poststrokeperiod.7,8,10 What remains to be investigated is the extent to whichexercise capacity can be modified earlier after stroke.

The comparability of our data on exercise capacity withpublished VO2peak data is limited because previous studiesinvolved patients with longer poststroke intervals. In all ofthese studies,7-10 mean VO2peak baseline values were between1.0 and 2.5mL � kg�1 � min�1 higher than in our study, aftercorrecting for differences in the distribution of men and womenin the samples. This finding suggests a possible increase inexercise capacity over time poststroke, support for whichwould require longitudinal investigation. The percentage ofpredicted maximal heart rate attained during testing is anindication of the relative level of physical exertion—a variablethat can confound VO2peak results. In the treadmill exercisestudy by Macko et al,22 the percentage of predicted maximalheart rate attained (84%�10%) by patients more than 2 yearspoststroke was comparable to our study. Potempa et al10 re-ported the highest mean percentage of predicted maximal heart

rate (approximately 87%) despite using the cycle ergometertest protocol, a method that typically yields lower HRpeakvalues than the treadmill.37

The observation that �-blocking agents did not significantlyalter VO2peak and exercise duration is in accord with otherstudies of untrained, sedentary individuals.27,38 However, incontrast to the reported increase in peak oxygen pulse tocompensate for the dampening of the heart rate response duringexercises,38 the difference in peak oxygen pulse between sub-jects taking and not taking �-blocking agents in our study didnot reach statistical significance.

Our individualized protocol of incremental increases intreadmill grade, followed by incremental increases in speed,was well tolerated by the subjects. The reliability substudyprovided evidence that data collected using this protocol arehighly reproducible, which is consistent with findings of highreliability for exercise testing of healthy subjects32 and ofsubjects in the chronic poststroke period.10 As expected, themaximal speed attained, .54�.30m/s, was substantially slowerthan the speed of 1.3m/s that we had applied previously to testhealthy subjects in the same age range.13 The constant velocityprotocol used by Macko22 to measure HRpeak of patients in thechronic poststroke period involved treadmill speeds rangingfrom of .22 to 1.1 m/s. We did not encounter adverse incidentsduring testing, in contrast to previous speculation that cardio-respiratory responses such as hypotension and cardiac dys-rhythmia might occur during exercise testing of patients lessthan 6 months poststroke.22 Continuous electrocardiogrammonitoring and frequent blood pressure monitoring in ourprotocol reduced the possibility of these untoward events. Theuse of body-weight support mitigated against the possibility offalls during treadmill.

The mechanisms underlying the reduction in exercise capacitypoststroke cannot be ascertained from this study. Cardiovascular,respiratory, and neuromuscular impairments could contribute tothe poor adaptive responses to physical activity. The observationthat VO2peak values of the subjects in our study are equal to thelow end of the reported values for patients with CAD as a primarydiagnosis suggests that cardiovascular impairments may contrib-ute substantially to reduced aerobic capacity poststroke. Individ-uals with CAD have exercise capacities that are 60% to 70% ofhealthy, sedentary people,39 which is consistent with the finding of60% of normative values in our sample. The mean VO2peak value(13.8�3.8mL � kg�1 � min�1) in 90 patients after myocardial in-farction who were comparable to our sample in terms of age, sex,and time since onset approximated the mean VO2peak in ourstudy.40 In another study41 involving 50 men 1 month after myo-cardial infarction, the mean VO2peak was 19mL � kg�1 � min�1,which is slightly higher than the mean age- and sex-adjusted valuefor our sample of 17mL � kg�1 � min�1. A previous investigation42

of the effect of cardiac involvement on responses to submaximalexercise poststroke reported evidence of greater use of anaerobicprocesses during exercise in patients with cardiac comorbidity.

Respiratory function after hemispheric stroke is often onlymodestly affected, notwithstanding the relatively high occur-

Table 4: Multivariate Prediction of VO2peak

Variables Coefficient SE t P R2 Adjusted R2 Multivariate P

VO2peak (mL � kg�1 � min�1) Age �.200 .053 �3.76 .001 .475 .435 .0002BI .150 .056 2.67 .013

VO2peak (L/min) Age �.022 .004 �4.49 .0001 .563 .530 �.0001BI .016 .005 3.18 .0038

Abbreviation: BI, Barthel Index.



rence of acute respiratory complications.43 Thus, although thepeak minute ventilation and tidal volumes of our subjects weresubstantially lower than normative values, it is unlikely thatrespiratory dysfunction was a primary factor limiting exercisecapacity. The contribution of neurologic impairment to de-creased exercise capacity is attributed to a reduction in motorunit recruitment during physical work, the extent of whichdepends on the location and severity of the cerebrovascularlesion.44 In our study, regression analysis showed a significantrelationship between VO2peak and Barthel Index, the latterindirectly reflecting the level of neuromuscular involvement.Alterations in muscle metabolism and fiber type recruitmentpattern during dynamic exercise have been documented inhemiparetic patients.45

The results of our study must be interpreted with cautionbecause of the small sample size, differences in age and sexdistribution of the participants and nonparticipants, and the useof a nonstandardized, patient-specific testing protocol. Differ-ences in the level of physical effort exerted by the subjects mayhave confounded VO2peak measurements.

CONCLUSION

In this first investigation of exercise capacity of patientsearly after stroke, we have provided evidence that cardiovas-cular adaptations to strenuous physical exercise in this popu-lation are limited. Mean VO2peak at 1 month poststroke wascomparable to previously reported age-adjusted VO2peak at 1month after myocardial infarction and only 60% of the norma-tive values for sedentary healthy individuals. Further researchis required to elucidate the physiologic basis for the lowcapacity. The relative contributions of cardiovascular, neuro-muscular, and respiratory impairments to reduce aerobic ca-pacity also remain to be clarified. In addition, there is a clinicalneed to define longitudinally the cardiovascular responses toexercise over the course of recovery. A pattern of sustained lowVO2peak values could have significant implications for strokerehabilitation. The extent to which exercise capacity can bemodified during rehabilitation remains an important unan-swered question, deserving of further investigation.

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Suppliersa. Model 18-60; Quinton Fitness Equipment, 3303 Monte Villa Pkwy,

Bothel, WA 98021-8906.b.Pneumex Inc, 804 Airport Wy, Sandpoint, ID 83864.c. Nellcor, 4280 Hacienda Dr, Pleasanton, CA 94588.d.SensorMedics, 22705 Savi Ranch Pkwy, Yorba Linda, CA 92687.e. Microsoft Corp, One Microsoft Wy, Redmond, WA 98052.f. SAS Institute Inc, SAS Campus Dr, Cary, NC 27513.



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