Exercise capacity early after stroke

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Exercise Capacity Early After Stroke Marilyn J. MacKay-Lyons, PhD, Lydia Makrides, PhD ABSTRACT. MacKay-Lyons MJ, Makrides L. Exercise capacity early after stroke. Arch Phys Med Rehabil 2002;83: 1697-702. Objective: To evaluate exercise capacity of patients with a poststroke interval of less than 1 month. Design: Prospective, cohort, observational study. Setting: Exercise testing laboratory in a tertiary care hospital. Participants: Twenty-nine patients (mean age ⫾ standard deviation, 64.9⫾13.5y) with a poststroke interval of 26.0⫾8.8 days. Interventions: Not applicable. Main Outcome Measure: Peak exercise capacity (VO2peak) was measured by open-circuit spirometry during maximal effort treadmill walking with 15% body-weight support. Results: Mean VO2peak was 14.4⫾5.1mL 䡠 kg⫺1 䡠 min⫺1 or 60%⫾16% of age- and sex-related normative values for sedentary healthy adults. Conclusions: Exercise capacity approximately 1 month after stroke was compromised. Further research is needed to elucidate the physiologic basis of this low capacity. Key Words: Cerebrovascular disorders; Exercise; Hemiplegia; Rehabilitation. © 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation ARDIOVASCULAR DISEASE is a major factor restricting successful outcomes after stroke rehabilitation. As C many as 75% of patients poststroke also have heart disease. In 1

2

fact, survivors of the acute phase of stroke are at greater risk of dying from cardiac disease than from any other cause, including a second stroke.3 Whereas neurologic recovery after stroke has been extensively investigated, cardiovascular adaptations to physical activity poststroke have received little attention. This situation is puzzling, given the high prevalence of cardiac comorbidity and the observation that most of the variance in disability after stroke cannot be explained by neurologic impairment.4 Cardiovascular and neuromuscular impairments, together with physical inactivity resulting from stroke, adversely affect exercise capacity—they limit the ability to respond to physiologic stresses induced by prolonged physical effort. The detrimental effects of low exercise capacity on functional mobility and resistance to fatigue are compounded by the high metabolic demand of hemiparetic gait, with energy costs as much as 3 times higher than for subjects without neurologic impairment walking at the same speed.5,6 Exercise stress tests have shown

From the School of Physiotherapy, Dalhousie University (MacKay-Lyons) and Health 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$35.00/0 doi:10.1053/apmr.2002.36395

that individuals in the chronic poststroke period (⬎6mo) have abnormally low exercise capacity.7-10 What has not been documented is exercise capacity during the early poststroke period, the time during which physical rehabilitation usually takes place and the potential for functional improvement is maximized.11 Exercise testing during this period is critical to informing the clinician of the need for, and safe design of, cardiovascular exercise prescription. Measurement of exercise capacity in the early poststroke period has eluded researchers because balance and motor control problems preclude use of standard exercise testing protocols. The preferred mode of measuring maximal oxygen ˙ O2max), the definitive index of exercise capacconsumption (V ity,12 is the treadmill. The potential to recruit sufficient muscle mass to elicit a maximal metabolic response is much more likely to be realized while walking than cycling, particularly in deconditioned populations.12 Recently, we devised a treadmill exercise protocol using partial body-weight suspension that would permit testing earlier poststroke than would otherwise be feasible. In a preliminary investigation13 of this protocol using healthy adults, we found that using 15% body-weight support did not affect the endpoints of the principal respiratory gas exchange variables of the exercise test and, thus, did not ˙ O2max data. The main purpose of confound interpretation of V the present study was to measure exercise capacity early after stroke by using a treadmill test protocol involving partial weight suspension. We selected VO2peak as the measure of ˙ O2max exercise capacity because the rigorous criteria for V often 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, unilateral, ischemic stroke, confirmed by both clinical and radiographic means, and admitted to the acute stroke service of a tertiary health care facility were consecutively screened for eligibility. Included were patients who were ⱖ18 years of age, whose stroke occurred within the prior month, who showed no evidence of dementia (as indicated by a score ⱖ24 of 30 on the Mini-Mental State Examination),15 and who had greater than stage 3 of Chedoke-McMaster Stages of Recovery of the Leg Assessment.16 This assessment is used to rate motor impairment after stroke by observing the patient performing increasingly complex motor tasks. The measure has been shown to have good reliability and validity.17 Stage 1 is assigned when flaccid paralysis is present, stage 3 when active voluntary movement is limited to stereotyped synergistic patterns, and stage 7 when movement is normal.16 Patients with stage 3 or less require physical assistance to advance the affected leg while walking, thus precluding valid VO2peak measurement. Exclusion criteria were the contraindications for exercise testing outlined by the American College of Sports Medicine (ACSM).18 Prospective subjects who met the criteria were given a detailed explanation of the study and were asked to sign the consent form approved by the hospital research ethics committee. Arch Phys Med Rehabil Vol 83, December 2002

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Table 1: Symptom-Limited Graded Exercise Test Protocol Warm-up Stages Stage 1 Stages 2–5 Stages ⱖ6 Cool-down

1min at 60%–70% self-selected speed and no incline 2min each with 15% of body mass suspended Self-selected treadmill speed with no incline Self-selected treadmill speed maintained and 2.5% increase in incline at each stage 10% incline maintained and .05m/s increase in treadmill speed at each stage 2min at 60%–70% self-selected speed and no incline

The clinical history of each subject was recorded, noting smoking habits and comorbidities such as hypertension, diabetes mellitus, chronic obstructive pulmonary disease, and coronary artery disease (CAD), the latter indicated by the presence of at least 1 of the following: myocardial infarction by history or electrocardiogram, angina pectoris, or coronary artery bypass graft surgery.19 The Barthel Index was used to evaluate functional ability by assessing 10 activities of self-care and mobility, yielding 1 combined score, ranging from 0 to 100.20 The Physical Activity Questionnaire (PAQ) was used as a general measure of the premorbid physical activity level of each subject.21 This questionnaire involves asking the subjects to indicate the frequency and duration of their participation over the past year in 11 forms of physical activity. A score for each activity is derived from the product of the length of time of participation per session (in hours), the number of sessions per week, and the number of seasons of participation per year. A total activity score is the sum of the individual scores and can be categorized as a score greater than 18, very active; 1 to 18, active; and 0, inactive. Exercise Testing Within 1 week before exercise testing, each subject visited the exercise testing laboratory for orientation to weight-supported treadmill walking and identification of the initial treadmill speed for the testing protocol. The subject practiced breathing through a mouthpiece with headgear and nose clip in place. A vest, similar to a parachute harness, was secured around the torso and attached to the supporting frame positioned over the treadmill. The subject walked on the treadmill at a self-selected, comfortable speed with 15% of body mass vertically displaced through the overhead support. In preparation for the exercise test, subjects were requested to avoid food and smoking for at least 2 hours, to refrain from drinking caffeinated beverages for at least 6 hours, and to avoid heavy exertion or exercise for 12 hours. Medication schedules were not altered. The methods for data collection have been previously described.13 In brief, a symptom-limited graded exercise test was performed on a calibrated motorized treadmilla with 15% of body mass suspended using the Pneuweight Unweighting System.b A patient-specific protocol, similar to that described by Macko et al,22 was used because physical limitations precluded application of a standardized protocol (table 1). Individualized protocols have been previously validated for testing exercise capacity of untrained, sedentary individuals.23,24 Fingertip contact of the handrail was permitted. The warm-up was limited to 1 minute because of the rapid onset of fatigue in some patients. During the initial 2 minutes of testing, the subject walked at the self-selected speed identified in the orientation session and 0% treadmill grade, followed by a 2.5% increase in grade every 2 minutes until an incline of Arch Phys Med Rehabil Vol 83, December 2002

10% was reached, and, thereafter, a .05m/s increase in speed every 2 minutes, until test termination and a 2-minute cooldown. Exercise time, the time from the initiation to termination of the exercise protocol excluding the warm-up and cool-down, was recorded. Subjective exertion on the treadmill was noted at the end of each 2-minute stage and at peak exercise by using the rating of perceived exertion on a scale of 0 (nothing at all) to 10 (very, very hard).25 Subjects were instructed to use maximal effort and to display the thumb-down signal when they wished to terminate the test. Termination of testing followed ACSM guidelines.18 For subjects with a history of pulmonary disease, arterial oxygen saturation was monitored using a Nellcor NPB-40 pulse oximeter.c Saturation less than 85% was a criterion for termination of testing.26 Expired gas was analyzed via open-circuit spirometry by using a SensorMedics 2900 Metabolic Measurement Cartd to ˙ O2), carbon dioxide producdetermine oxygen consumption (V tion, minute ventilation, respiratory exchange ratio (RER), and tidal volume. Volume calibration and calibration of gases by using standard gases were done before each test. The subject wore a nose clip and breathed room air though a 1-way directional valve system attached to a mouthpiece. Peak values for exercise parameters were the averages of values recorded during the last 30 seconds of the test. A 10-lead electrocardiogram provided continuous monitoring of heart rate and cardiac electrical activity. Resting heartrate was determined after a 5-minute rest period. Peak heart rate (HRpeak) was the average heart rate during the last 30 seconds of exercise and was expressed as a percentage of age-predicted maximal heart rate ([220⫺age]/100).18 This formula was adapted for those patients on ␤-blocker medication to adjust for its heart rate–lowering effect (predicted maximal heart rate⫽85%[220⫺age]).27 Peak oxygen pulse in milliliters of oxygen per beat was calculated ([1000⫻VO2peak]/HRpeak). Right brachial artery systolic (SBP) and diastolic blood pressure (DBP) were measured by using a calibrated mercury sphygmomanometer at rest, every 2 minutes during exercise, and every minute during recovery until returning to baseline. Ratepressure product was calculated ([heart rate⫻SBP]/100).18 ˙ O2max included: (1) increase in V ˙ O2 Criteria for attainment of V ˙ O2 less than 150mL in the final minute of exercise—a “V plateau,” (2) peak RER greater than 1.0, (3) peak SBP greater than 200mmHg, and (4) HRpeak within 15 beats per minute of predicted maximal heart rate.14 To check the reliability of the testing protocol, we conducted a test-retest study of a subsample of subjects performing 2 exercise tests with a 3- to 4-day interval between tests. Being mindful of the physical and emotional stresses confronting patients in the early poststroke period, we delayed reliability testing until 2 months after stroke. Data Analysis Descriptive statistics were used to characterize the subjects and exercise test results. Univariate statistics (ie, t tests, MannWhitney U test, ␹2) were used to compare characteristics of participants and nonparticipants. The independent t test for unequal sizes was applied to compare VO2peak data of subjects with and without CAD. An ␣ level of .05 was set. Factorial analysis of variance (ANOVA) was performed to compare VO2peak values of subgroups of subjects with Barthel Index scores (⬍ or ⱖ90). This analysis was repeated to compare VO2peak values of subgroups classified by their scores on the PAQ (ie, inactive, active, very active) as well as subgroups classified by their Chedoke-McMaster Stage of Recovery of the

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Leg (ie, stages 4, 5, 6). Multiple linear regression was used to examine the effects of independent variables (ie, age, Barthel Index, Stage of Recovery of the Leg, PAQ) on VO2peak, with age treated as a forced variable because of its strong correlation with VO2peak. The level of significance was set at .01. Least˙ O2 and heart rate square regression lines were calculated for V against exercise time for test-retest reliability data. The intraclass correlation coefficient (ICC3,1) was calculated for the slopes and intercepts of the regression lines as well as for the VO2peak and HRpeak. Analyses were performed with Microsoft Excel, version 5.0,e and StatView®, version 4.01.f RESULTS Of the 44 patients who met the screening criteria, 34 gave consent to enter the study. Five of these patients who provided consent were not tested because of early discharge from hospital (n⫽3) and progression of the neurologic status (n⫽2). Comparison of demographic and clinical characteristics of the 29 participants and 15 nonparticipants revealed significant differences in age of participants and nonparticipants (64.9⫾13.5y vs 71.3⫾11.4y, P⫽.01) and sex distribution (22 men, 7 women vs 5 men, 10 women, P⫽.01). Characteristics of the participants are in table 2. The percentages of patients with history of CAD or diabetes are consistent with previous reports.28,29 Of the 15 participants taking ␤-blocker medications, 13 were on ␤1-selective blockers (metoprolol, atenolol) and 2 were on nonselective (propranolol, labetalol). Of the 18 patients with a history of smoking, 8 had quit prior to the time of their stroke. Eight (28%) participants were mildly affected with hemiparetic 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. Patients consistently reported that the body-weight support vest was comfortable and reduced anxiety related to fear of falling. Mean walking speed at initiation of testing was .39⫾.12m/s and at the last completed stage was .54⫾.30m/s. Arterial oxygen saturation did not fall below 85% during testing for the 5 patients monitored. Twenty-four (83%) subjects terminated testing of their own volition, the most common reasons for termination being generalized fatigue and shortness of breath. In the remaining 5 cases, termination was investigator-initiated because the upper limit of blood pressure (ie, SBP ⬎250mmHg ⫾ DBP ⬎115mmHg)17 had been reached. ˙ O2max Twenty-two (76%) subjects achieved 1 or more of the V criteria. The RER and HRpeak criteria were attained by 18 and ˙ O2 16 individuals, respectively, whereas the peak SBP and V plateau criteria were attained by 8 and 5 individuals, respectively.

Table 3: Physiologic Variables at Peak Exercise Intensity VO2 (mL 䡠 kg⫺1 䡠 min⫺1) V˙O2 (L/min) RER Heart rate (beats/min) % of predicted HRmax O2 pulse (mL/beat) SBP (mmHg) DBP (mmHg) Rate-pressure product Minute ventilation (L/min) Tidal volume (L) Exercise duration (min)

14.4⫾5.1 1.2⫾0.50 1.00⫾0.06 123.1⫾18.9 84.9⫾8.2 9.6⫾3.3 182⫾33 98⫾15 224.0⫾65.6 42.1⫾16.4 1.4⫾0.53 8.7⫾4.6

NOTE. Values are mean ⫾ SD.

Physiologic measurements at peak exercise intensity are summarized in table 3. Mean VO2peak values were 60%⫾16% of age- and sex-related normative values by using nomograms of sedentary individuals.18 Mean VO2peak values of male and female subjects differed significantly (15.5⫾5.3mL 䡠 kg⫺1 䡠 min⫺1 vs 10.9⫾1.7mL 䡠 kg⫺1 䡠 min⫺1, P⫽.01), in keeping with the finding that VO2max values for women are approximately 77% of that for men.30 In addition, mean VO2peak values for patients with and without CAD were 12.9⫾3.1mL 䡠 kg⫺1 䡠 min⫺1 and 16.0⫾5.2mL 䡠 kg⫺1 䡠 min⫺1, respectively, the difference being significant (P⫽.05). Differences in mean peak oxygen pulse of subjects taking ␤-blockers compared with those not taking ␤-blockers (ie, 10.1⫾3.5mL/beat vs 9.1⫾3.2mL/beat) were not statistically significant. Mean ratepressure product increased from 109.3⫾17.3 at rest to 224.0⫾65.6 at peak exercise. Mean peak tidal volume and minute ventilation averaged 61% and 56%, respectively, of age- and sex-related normative values.31 Figure 1 illustrates the differences in VO2peak values of subjects grouped according to the Barthel Index, premorbid physical activity level, and Chedoke-McMaster Stage of Recovery of the Leg, respectively. Factorial ANOVA revealed a significant difference in VO2peak values of the subgroup with Barthel Index scores less than 90 (n⫽18) compared with the subgroup with Barthel Index scores greater than 90 (n⫽11). Although there was a trend of increasing VO2peak values with increasing levels of prestroke physical activity levels and increasing Stages of Recovery of the Leg; the differences were not statistically significant. Multiple linear regression analysis gave similar results (table 4). The Barthel Index was found to

Table 2: Subject Characteristics Age (y) Sex (men/women) Time poststroke (d) Side of stroke Barthel Index Chedoke-McMaster Stage of Leg, 1–7 CAD ␤-blocker medication Diabetes mellitus Chronic obstructive pulmonary disease History of smoking

64.9⫾13.5 22/7 26.0⫾8.8 18 right: 11 left 76.7⫾12.6 5.3⫾0.7 17/29 (59%) 15/29 (52%) 7/29 (24%) 5/29 (17%) 18/29 (62%)

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

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

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EXERCISE CAPACITY EARLY AFTER STROKE, MacKay-Lyons Table 4: Multivariate Prediction of VO2peak

VO2peak (mL 䡠 kg

⫺1

䡠 min

⫺1

)

VO2peak (L/min)

Variables

Coefficient

SE

t

P

R2

Adjusted R2

Age BI Age BI

⫺.200 .150 ⫺.022 .016

.053 .056 .004 .005

⫺3.76 2.67 ⫺4.49 3.18

.001 .013 .0001 .0038

.475

.435

.0002

.563

.530

⬍.0001

Multivariate P

Abbreviation: BI, Barthel Index.

be significant in predicting both relative and absolute values of VO2peak, whereas the PAQ scores and the Stages of Recovery of the Leg were not significant factors. Six subjects (4 men, 2 women) volunteered to participate in the reliability substudy conducted at 2 months poststroke. The ICC3,1 for the VO2peak, and the slopes and intercepts of re˙ O2 against exercise time were .94, .96, and gression lines of V .92, respectively. The ICC3,1 for the HRpeak and the slopes and intercepts of regression lines of heart rate against exercise time were .93, .88, and .92, respectively; these findings are consistent with reports of high reliability of exercise test results in healthy subjects32 and subjects long after stroke.10 DISCUSSION This study is the first, to our knowledge, to report the response of patients in the early poststroke period to symptom-limited treadmill exercise. As anticipated, not all subjects attained the ˙ O2max, reinforcing the notion that attaining minimum criteria for V ˙ O2max in deconditioned and elderly subjects is often an unrealV istic goal.14 Nevertheless, the percentage of predicted maximum heart rate and the peak rate-pressure product achieved by the subjects (84.9%⫾8.2% and 224.0⫾65.6, respectively) were similar to values reported for patients postmyocardial infarction (85%⫾8% and 230⫾48, respectively),33 which suggests comparable physical effort. The mean VO2peak at 26.0⫾8.8 days after stroke was 14.4⫾5.1mL 䡠 kg⫺1 䡠 min⫺1 or 60%⫾16% of that predicted from age- and gender-adjusted normative values for sedentary individuals. The finding of such low exercise capacity is ˙ O2max less than 84% of norclinically meaningful. Values for V mative values are interpreted as being pathologic,34 and the minimum VO2peak to meet the physiologic demands of independent living is 15mL 䡠 kg⫺1 䡠 min⫺1.35 Further, exercise capacity has been used as a predictor of mortality among patients with CAD (59% of our subjects had CAD)—those with VO2peak levels less than 21mL 䡠 kg⫺1 䡠 min⫺1 have been designated as a high mortality group.36 Cardiac rehabilitation strategies have proven effective in increasing exercise capacity of patients in the chronic poststroke period.7,8,10 What remains to be investigated is the extent to which exercise capacity can be modified earlier after stroke. The comparability of our data on exercise capacity with published VO2peak data is limited because previous studies involved patients with longer poststroke intervals. In all of these studies,7-10 mean VO2peak baseline values were between 1.0 and 2.5mL 䡠 kg⫺1 䡠 min⫺1 higher than in our study, after correcting for differences in the distribution of men and women in the samples. This finding suggests a possible increase in exercise capacity over time poststroke, support for which would require longitudinal investigation. The percentage of predicted maximal heart rate attained during testing is an indication of the relative level of physical exertion—a variable that can confound VO2peak results. In the treadmill exercise study by Macko et al,22 the percentage of predicted maximal heart rate attained (84%⫾10%) by patients more than 2 years poststroke was comparable to our study. Potempa et al10 reported the highest mean percentage of predicted maximal heart Arch Phys Med Rehabil Vol 83, December 2002

rate (approximately 87%) despite using the cycle ergometer test protocol, a method that typically yields lower HRpeak values than the treadmill.37 The observation that ␤-blocking agents did not significantly alter VO2peak and exercise duration is in accord with other studies of untrained, sedentary individuals.27,38 However, in contrast to the reported increase in peak oxygen pulse to compensate for the dampening of the heart rate response during exercises,38 the difference in peak oxygen pulse between subjects taking and not taking ␤-blocking agents in our study did not reach statistical significance. Our individualized protocol of incremental increases in treadmill grade, followed by incremental increases in speed, was well tolerated by the subjects. The reliability substudy provided evidence that data collected using this protocol are highly reproducible, which is consistent with findings of high reliability for exercise testing of healthy subjects32 and of subjects in the chronic poststroke period.10 As expected, the maximal speed attained, .54⫾.30m/s, was substantially slower than the speed of 1.3m/s that we had applied previously to test healthy subjects in the same age range.13 The constant velocity protocol used by Macko22 to measure HRpeak of patients in the chronic poststroke period involved treadmill speeds ranging from of .22 to 1.1 m/s. We did not encounter adverse incidents during testing, in contrast to previous speculation that cardiorespiratory responses such as hypotension and cardiac dysrhythmia might occur during exercise testing of patients less than 6 months poststroke.22 Continuous electrocardiogram monitoring and frequent blood pressure monitoring in our protocol reduced the possibility of these untoward events. The use of body-weight support mitigated against the possibility of falls during treadmill. The mechanisms underlying the reduction in exercise capacity poststroke cannot be ascertained from this study. Cardiovascular, respiratory, and neuromuscular impairments could contribute to the poor adaptive responses to physical activity. The observation that VO2peak values of the subjects in our study are equal to the low end of the reported values for patients with CAD as a primary diagnosis suggests that cardiovascular impairments may contribute substantially to reduced aerobic capacity poststroke. Individuals with CAD have exercise capacities that are 60% to 70% of healthy, sedentary people,39 which is consistent with the finding of 60% of normative values in our sample. The mean VO2peak value (13.8⫾3.8mL 䡠 kg⫺1 䡠 min⫺1) in 90 patients after myocardial infarction who were comparable to our sample in terms of age, sex, and time since onset approximated the mean VO2peak in our study.40 In another study41 involving 50 men 1 month after myocardial infarction, the mean VO2peak was 19mL 䡠 kg⫺1 䡠 min⫺1, which is slightly higher than the mean age- and sex-adjusted value for our sample of 17mL 䡠 kg⫺1 䡠 min⫺1. A previous investigation42 of the effect of cardiac involvement on responses to submaximal exercise poststroke reported evidence of greater use of anaerobic processes during exercise in patients with cardiac comorbidity. Respiratory function after hemispheric stroke is often only modestly affected, notwithstanding the relatively high occur-

EXERCISE CAPACITY EARLY AFTER STROKE, MacKay-Lyons

rence of acute respiratory complications.43 Thus, although the peak minute ventilation and tidal volumes of our subjects were substantially lower than normative values, it is unlikely that respiratory dysfunction was a primary factor limiting exercise capacity. The contribution of neurologic impairment to decreased exercise capacity is attributed to a reduction in motor unit recruitment during physical work, the extent of which depends on the location and severity of the cerebrovascular lesion.44 In our study, regression analysis showed a significant relationship between VO2peak and Barthel Index, the latter indirectly reflecting the level of neuromuscular involvement. Alterations in muscle metabolism and fiber type recruitment pattern during dynamic exercise have been documented in hemiparetic patients.45 The results of our study must be interpreted with caution because of the small sample size, differences in age and sex distribution of the participants and nonparticipants, and the use of a nonstandardized, patient-specific testing protocol. Differences in the level of physical effort exerted by the subjects may have confounded VO2peak measurements. CONCLUSION In this first investigation of exercise capacity of patients early after stroke, we have provided evidence that cardiovascular adaptations to strenuous physical exercise in this population are limited. Mean VO2peak at 1 month poststroke was comparable to previously reported age-adjusted VO2peak at 1 month after myocardial infarction and only 60% of the normative values for sedentary healthy individuals. Further research is required to elucidate the physiologic basis for the low capacity. The relative contributions of cardiovascular, neuromuscular, and respiratory impairments to reduce aerobic capacity also remain to be clarified. In addition, there is a clinical need to define longitudinally the cardiovascular responses to exercise over the course of recovery. A pattern of sustained low VO2peak values could have significant implications for stroke rehabilitation. The extent to which exercise capacity can be modified during rehabilitation remains an important unanswered question, deserving of further investigation. References 1. Roth E. Heart disease in patients with stroke. Part II: Impact and implications for rehabilitation. Arch Phys Med Rehabil 1994;75: 94-101. 2. Roth E. Heart disease in patients with stroke. Part 1: Classification and prevalence. Arch Phys Med Rehabil 1993;74:752-60. 3. Matsumoto N, Whisnant JP, Kurland LT, Okazaki H. Natural history of stroke in Rochester, Minnesota, 1955 through 1969: an extension of a previous study, 1945 through 1954. Stroke 1973; 4:20-9. 4. Roth EJ, Heinemann AW, Lovell LL, Harvey RL, McGuire JR, Diaz S. Impairment and disability: their relation during stroke rehabilitation. Arch Phys Med Rehabil 1998;79:329-35. 5. Hash D. Energetics of wheelchair propulsion and walking in stroke patients. Orthop Clin North Am 1978;9:372-4. 6. Corcoran PJ, Jebsen RH, Brengelmann GL, Simons BC. Effects of plastic and metal leg braces on speed and energy cost of hemiplegic ambulation. Arch Phys Med Rehabil 1970;51:69-77. 7. Macko RF, Smith GV, Dobrovolny CL, Sorkin JD, Goldberg AP, Silver KH. Treadmill training improves fitness reserve in chronic stroke patients. Arch Phys Med Rehabil 2001;82:879-84. 8. Fujitani J, Ishikawa T, Akai M, Kakurai S. Influence of daily activity on changes in physical fitness for people with post-stroke hemiplegia. Am J Phys Med Rehabil 1999;78:540-4. 9. Bachynski-Cole M, Cumming GR. The cardiovascular fitness of disabled patients attending occupational therapy. Occup Ther J Res 1985;5:233-42.

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10. Potempa K, Lopez M, Braun LT, Szidon P, Fogg L, Tincknell T. Physiological outcomes of aerobic exercise training in hemiparetic stroke patients. Stroke 1995;26:101-5. 11. Skilbeck CE, Wade DT, Hewer RL, Wood VE. Recovery after stroke. J Neurol Neurosurg Psychiatry 1983;46:5-8. 12. Rowell LB. Human cardiovascular adjustments to exercise and thermal stress. Physiol Rev 1974;54:75-103. 13. MacKay-Lyons M, Makrides L, Speth S. Effect of 15% body weight support on exercise capacity of adults without impairments. Phys Ther 2001;81:1790-800. 14. Howley ET, Bassett DR, Welch HG. Criteria for maximal oxygen uptake: review and commentary. Med Sci Sports Exerc 1995;27: 1292-301. 15. Tombaugh TN, McIntyre NJ. The Mini-Mental Status Examination: a comprehensive review. J Am Geriatr Soc 1992;40:922-35. 16. Gowland C, van Hullenaar S, Torresin W, et al. Chedoke-McMaster Stroke Assessment: development, validation, and administration manual. Hamilton (Ont): Chedoke-McMaster Hospitals and McMaster Univ; 1995. 17. Gowland C, Stratford P, Ward M, Moreland J, Torresin W, van Hullenaar S. Measuring physical impairment and disability with the Chedoke-McMaster Stroke Assessment. Stroke 1993;24:5863. 18. American College of Sports Medicine. Guidelines for exercise testing and prescription. 6th ed. Baltimore: Williams & Wilkins; 2000. 19. Roth EJ, Mueller K, Green D. Stroke rehabilitation outcome: impact of coronary artery disease. Stroke 1988;19:42-7. 20. Mahoney F, Barthel D. Functional evaluation: the Barthel Index. Md State Med J 1965;14:61-5. 21. Jagal SB, Krieger N, Darlington G. Past and recent physical activity and risk of hip fracture. Am J Epidemiol 1993;138:10718. 22. Macko RF, Katzel LI, Yataco A, et al. Low-velocity graded treadmill stress testing in hemiparetic stroke patients. Stroke 1997; 28:988-92. 23. Foster C, Crowe AJ, Daines E, et al. Predicting functional capacity during treadmill testing independent of exercise protocol. Med Sci Sports Exerc 1996;28:752-6. 24. Myers J, Buchanan N, Walsh D, Kraemer M, et al. Comparison of the ramp versus standard exercise protocols. J Am Coll Cardiol 1991;17:1334-42. 25. Borg GA. Psychophysical bases of perceived exertion. Med Sci Sports Exerc 1982;14:377-81. 26. Mengelkoch LJ, Martin D, Lawler J. A review of the principles of pulse oximetry and accuracy of pulse oximeter estimates during exercise. Phys Ther 1994;74:40-7. 27. Pollock ML, Lowenthal DT, Foster C, et al. Acute and chronic responses to exercise in patients treated with beta blockers. J Cardiopulm Rehabil 1991;11:132-44. 28. Rokey R, Rolak LA, Harati Y, Kutka N, Verani MS. Coronary artery disease in patients with cerebrovascular disease: a prospective study. Ann Neurol 1984;16:50-3. 29. Harvey RL, Roth EJ, Heinemann AW, Lovell LL, McGuire JR, Diaz S. Stroke rehabilitation: clinical predictors of resource utilization. Arch Phys Med Rehabil 1998;79:1349-55. 30. Bruce RA, Kusumi F, Hosmer D. Maximal oxygen intake and nomographic assessment of functional aerobic impairment in cardiovascular disease. Am Heart J 1973;85:546-62. 31. Blackie SP, Fairbarn MS, McElvaney NG, Wilcox PG, Morrison NJ, Pardy PL. Normal values and ranges for ventilation and breathing pattern at maximal exercise. Chest 1991;100:136-42. 32. Taylor HL, Buskirk E, Henschel A. Maximal oxygen uptake as an objective measure of cardiorespiratory performance. J Appl Physiol 1955;8:73-80. 33. Hsi WL, Lai JS. Exercise test in acute myocardial. Am J Phys Med Rehabil 1996;75:263-9. 34. Wasserman K, Hansen JE, Sue DY, Casaburi R, Whipp BJ. Principles of exercise testing and interpretation. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 1999. 35. Shephard RJ. Physical training in the elderly. Arch Environ Health 1986;5:515-33. Arch Phys Med Rehabil Vol 83, December 2002

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42. Iseri LT, Smith RV, Evans MJ. Cardiovascular problems and functional evaluation in rehabilitation of hemiplegic patients. J Chronic Dis 1968;21:423-34. 43. Vingerhoets F, Bogousslavsky J. Respiratory dysfunction in stroke. Clin Chest Med 1994;15:729-37. 44. McComas AJ, Sica RE, Upton AR, Aquilera N. Functional changes in motoneurones of hemiparetic patients. J Neurol Neurosurg Psychiatry 1973;36:183-93. 45. Landin S, Hagenfeldt L, Saltin B, Wahren J. Muscle metabolism during exercise in hemiparetic patients. Clin Sci Mol Med 1977; 53:257-69. Suppliers a. 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.