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* From the School of Health Sciences (Dr. Vogiatzis and Mr. Williamson), University of Sunderland, and the Departments of Physiotherapy (Ms. Miles) and Respiratory Medicine (Dr. Taylor), Sunderland Royal Hospital, Sunderland, UK.
Correspondence to: Ioannis Vogiatzis, PhD, University of Athens Medical School, Department of Pulmonary and Critical Care Medicine, Eugenidion Hospital, 2nd Floor, 20 Papandiamantopoulou Str 115–28, Ilisia, Athens, Greece; e-mail: vogiatzis{at}hotmail.com
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Abstract |
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 TOP Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Participants: Sixty patients with COPD (38 men) with a mean ± SD FEV1 % predicted of 55.1 ± 19.8 (range, 0.51 to 2.99). All patients performed identical incremental symptom-limited cycle ergometer testing before and after a 12-week study period.
Measurements and results: After 12 weeks, the patients demonstrated a significant (p < 0.05) increase in the peak values for work rate (WR; 77 ± 30 vs 91 ± 36 W) and oxygen uptake (1.14 ± 0.45 vs 1.20 ± 0.52 L/min). Furthermore, at a given WR during incremental symptom-limited cycle ergometer testing, there were significant (p < 0.05) reductions in minute ventilation (42.4 ± 16.1 vs 37.0 ± 13.6 L/min), carbon dioxide output (1.13 ± 0.49 vs 1.03 ± 0.42 L/min), ventilatory equivalent for oxygen (37.6 ± 8.1 vs 36.0 ± 6.3), and heart rate (135 ± 15 vs 128 ± 16 beats/min). None of the observed physiologic changes correlated with FEV1 % predicted.
Conclusions: A pulmonary rehabilitation program performed twice weekly with moderate exercise workloads can lead to a physiologic training response irrespective of the degree of airflow limitation.
Key Words: COPD • exercise training • pulmonary rehabilitation
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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While the above studies provide substantial evidence of physiologic training effects over a wide objective spectrum of airflow limitation, these were achieved in small groups of patients. Recent studies10 11 12 have clarified previous uncertainty that twice-weekly pulmonary rehabilitation sessions were adequate to produce significant gains in exercise performance, as assessed simplistically by walking tests. However, the possibility of inducing training effects on measured objective physiologic exercise responses by the implementation of an exercise program featuring fewer than three sessions per week remains uncertain. In view of the cost and resource effort involved in conducting a rehabilitation program, we were particularly interested in designing and implementing an exercise regimen of moderate frequency and intensity that could be sufficient to induce measurable physiologic exercise responses and improvements in exercise tolerance. We therefore undertook a trial of pulmonary rehabilitation in 60 patients with a wide spectrum of airflow limitation who participated in a 12-week outpatient program that featured twice-weekly moderately intense exercise training sessions. While our primary outcome measure was the evaluation of physiologic training effects in these patients, by comparison we also report data in a smaller control group of 15 patients who did not participate in any training sessions.
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Materials and Methods |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Pulmonary Function Tests: Pulmonary function evaluation was carried out 10 min after actuation from a metered-dose inhaler of two inhalations of both ipratropium bromide, 40 µg, and salbutamol, 200 µg. With the patients in a sitting position, spirometry was performed using an autolink spirometer (Transfer Test SN 293; P.K. Morgan; Haverhill, MA). The patients were required to perform three satisfactory spirometric techniques within 5% of each other by FVC; from the best of these maneuvers, FEV1 and FVC were determined. The transfer factor for carbon monoxide was determined via the single breath method; in contrast to the spirometric data, the results of three maneuvers were averaged. Pulmonary function data of the 60 patients in the training group at the outset and termination of the study are detailed in Table 2 . Additionally, comparable data from the 15 patients in the nontraining control group are shown in Table 2 .
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O2),
carbon dioxide output (CO2), minute
ventilation (E), and the ventilatory equivalent for
oxygen (E/O2) were
determined at intervals of 15 s by a respiratory mass spectrometer
featuring a mixing chamber (Airspec QP9000; Case; Kent, UK). Gas
exchange and respired minute volume were measured using the
concentration of injected argon at a rate of 600 mL/min into the
expirate upstream of the mixing chamber, while the resulting
composition downstream was used to deduce the mass flows of all its
components.13
The anaerobic threshold (AT) was determined
from a plot of CO2 vs
O2 by the modified gas exchange V-slope
technique described by Sue and coworkers.14
The
identification of the AT was made blindly and independently by two
observers from duplicate copies of the data. We recently reported 15
a significant agreement between the V-slope
technique 14
and another noninvasive gas exchange method
(plots of E and
E/O2 vs
O2) for the determination of the AT in
COPD patients with a high interobserver agreement. Heart rate (HR) was
recorded every minute by a monitor (PE 4000 Sports Tester Transmitter;
Polar; Kempele, Finland) and arterial oxygen saturation
(SaO2) was measured using a pulse oximeter
(Biox 3760; Datex-Ohmeda; Louisville, CO). The patients performed an incremental symptom-limited cycle ergometer test that included a 3-min rest period and 3 min of unloaded pedaling, followed by an increase in work rate (WR) of 10 W every minute from a starting work rate of 20 W until exhaustion was apparent from the inability to maintain the pedaling cadence above 40 revolutions/min. The peak WR was defined as the highest work level reached and maintained for a full minute.
Rehabilitation Program
The rehabilitation strategy was a comprehensive program that
included modalities of exercise training, breathing control techniques,
disease education, and instruction in the use of medication. There was
no weight training component. The exercise training component consisted
of the following sequence: (1) cycling on a calibrated cycle ergometer
(824E; Monark; ); (2) walking on level ground; and finally (3)
walking on an inclined nonmotorized treadmill (Woodway; Waukesha,
WA) for a total of 60 min (including periods of rest) twice
weekly for 12 consecutive weeks. The exercise training protocol is
shown in Figure 1
. Monitoring during exercise sessions was conducted by a physiotherapist
and involved measurements of HR and
SaO2.
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80% of the maximal age-predicted
HR or SaO2 < 85%) were exceeded
earlier. At subsequent sessions, this same WR was applied until the
patient could sustain it for 20 min. The exercise prescription was revised weekly by a physiologist. Once an individual could exercise at the prescribed work level for 20 min, the WR was increased by approximately 25%, and again this level was continued until it could be sustained for 20 min. Following the completion of cycling exercise, the patients walked on the horizontal for 10 min at a training intensity that was targeted at the highest pace that could be tolerated by each individual patient. The targeted walking speed was gauged to result in a HR of approximately 70% of the maximal age-predicted HR. Walking on the horizontal was subsequently followed by five 1-min bouts on a treadmill with 10% inclination at a speed of 3.0 km/h, unless the previously described symptomatic or physiologic end points were exceeded earlier. The patients who were unable at the beginning of the program to exercise for a full minute were allowed to stop before attempting again. Each 1-min bout was followed by 1 min of rest. The walking exercise prescription was kept constant throughout the 12 weeks. The patients exercised at a fairly steady WR for the entire duration of the three exercise modes, with only 5 min of cool-down periods on the bicycle ergometer at a low pedaling frequency, and three 5-min rest periods in between the remaining exercise modes (Fig 1) .
Statistical Analysis
Prior to statistical analysis, normality frequency plots were
performed to examine the data distribution. Data are presented as means
± SD, unless otherwise indicated. Percentage differences in
physiologic variables before and after the training intervention were
calculated according to the following formula: (poststudy mean
value-prestudy mean value/prestudy mean value) x 100. Comparisons
between baseline and outcome measurements in the training group were
made using paired t tests. Additionally, within the training
group, comparisons for a number of physiologic variables were evaluated
as a function of baseline airway function (FEV1
> 40% predicted vs < 40% predicted) by unpaired t
tests. Correlations between measured physiologic variables and airway
function were assessed by Pearson’s correlation coefficient.
As secondary outcome assessments, physiologic measurements between the training and nontraining control groups were compared using Student’s unpaired t tests at the beginning of the study prior to the training intervention; between-group mean differences are presented with 95% confidence intervals. Additionally, paired t test comparisons were made at baseline and at 12 weeks for a number of physiologic variables within the nontraining control group. The level of significance was set at p < 0.05.
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Results |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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There was significant improvement in exercise tolerance as assessed by
the incremental cycle ergometer test within the training group. Peak WR
increased by a mean of 18%; this was accompanied by significantly
higher peak values for O2,
CO2, E, and
HR (Table 2
; Fig 2 ). By contrast, none of these variables significantly changed in the
nontraining control group (Table 2
; Fig 2
).
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E (13%),
CO2 (9%),
O2 (8%),
E/O2 (4%),
and HR (5%) were found (Table 3
). Furthermore, the AT as detected by the V-slope
technique14
significantly increased by 10% following
training (Table 3
; Fig 2
). Changes in
CO2 were significantly
correlated with changes in E at a given exercise WR
(r = 0.63; p = 0.002). Significant changes in the above physiologic
variables within the nontraining control group were not observed (Fig 2) .
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CO2, E, and
HR at an identical WR during the incremental test were comparable and
independent of baseline pulmonary dysfunction (Table 4
).
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Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The improvements in exercise tolerance were manifest not only by
attainment of higher peak exercise responses (in WR,
E, and O2),
but also by reduced ventilatory requirement at a given level of
exercise. Furthermore, the magnitude of improvement in exercise
tolerance was comparable over a spectrum of airflow limitation.
There is considerable evidence (approaching 40 studies)17 that documents the benefits of exercise regimens in pulmonary rehabilitation strategies. However, there are only a minority of exercise programs3 8 9 18 19 20 21 22 23 that have been specifically designed to elicit as primary outcome measures the physiologic changes within the exercising muscles and other organ systems. The present training program design differed importantly from other programs 3 8 9 18 19 20 in two respects. First, it featured only two exercise training sessions per week; second, it incorporated multimodality lower limb exercises. It may be argued that the variety of different exercises incorporated into the present program renders the interpretation of training improvements to be perhaps more problematic in contrast to those programs in which the training interventions were solely restricted to cycle ergometer activities.3 8 9 20 However, we believe that the diversity of the training modalities selected were more realistic and functionally more relevant to the daily activities of our study population.
Although the duration of this entire program (12 weeks) and the duration of the individual exercise training sessions (60 min) were well within the recommendations for exercise training programs,24 this study is notable not only for the number of patients studied in comparison to other recently published data,3 8 9 in which physiologic variables were used as primary outcome measures to assess the effects of training, but also by the wide spectrum of airflow limitation encompassed within the large study population.
The target training intensity of bicycle exercise in this program (50%
of the baseline peak WR) was lower than comparative
studies3
9
that featured target training intensities
equivalent to 80% of the baseline peak WR. However, it has been
previously shown that training intensity is often difficult to
interpret because actual training loads may differ from the training
prescription.8
20
The majority of patients in the current
study were able to exceed their initial training prescription by up to
25%. Nevertheless, the relatively moderate training frequency and
intensity employed in the present program possibly explain why
improvements in exercise tolerance (peak WR by 18% and peak
O2 by 5%) were smaller than
those previously reported by Casaburi et al9
(increased
peak WR and O2 by 35% and
16%, respectively), although patient demographics and training
schedules were not directly comparable. In relation to other
comparative studies,3
8
20
training improvements seen in
this study were greater than those seen in a low WR (50% peak WR) and
moderately obstructed training cohort,3
and were
comparable to the improvements documented by Maltais et
al20
(increases in peak WR and peak
O2 by 14% and 9%,
respectively), albeit in a more severely impaired group of patients
with COPD (training three times weekly for 12 weeks at an average
exercise intensity equivalent to 50% of baseline WR).
In contrast to the improvements in exercise tolerance seen within the
training cohort, peak values for WR, E, and
O2 within the nontraining
control group were largely unchanged when reassessed after 12 weeks
(Table 2 ; Fig 2
). We are aware however, that a major limitation of this
study was the lack of prospective randomization into the training and
nontraining control groups. Allowing for the disparity in numbers, the
two groups nevertheless were well matched, although the nontraining
control cohort were younger (Table 1)
, with the implicit acceptance
that age may be an important factor in disease progression.
Furthermore, although the nontraining control group that was used may
have been biased by patients who declined rehabilitation because of
lack of motivation, the principal reason for the failure to participate
was time constraint. Despite these limitations, we have included
comparative data from the nontraining control cohort (Table 2)
,
recognizing that statistical and clinical interpretation may be
difficult.
Further evidence of training effects that were induced by the present
exercise program can be seen from the physiologic responses to a given
level of exercise. At an identical WR during the incremental exercise
test, E,
CO2,
E/O2, and
HR were all significantly lower after 12 weeks of training (Table 3)
.
Moreover, we observed increases in the AT after training, implying that
the training program might have induced functional changes in the
exercising muscles, most notably allowing them to increase their
capacity for aerobic work and forestall the onset of lactic acidosis.
Indeed, recent evidence obtained by comparable exercise programs has
demonstrated that training improved cellular bioenergetics and resulted
in increased levels of aerobic enzymes within the leg muscles of
patients with severe COPD8
22
; these adaptations were
associated with reduced exercise-induced lactic acidosis. Reduced
lactic acidosis could benefit patients with COPD by removing, at least
in part, some of the acid stimulus to breathe, thereby lowering the
ventilatory requirement at a given exercise level.3
The
reduction in E (13%) is in a good agreement with
two previous studies of Casaburi et al3
9
(12% and 9%,
respectively), and is considerably greater than in two further
comparative studies by Maltais et al8
20
(5% and 6%,
respectively). Reductions in
O2 at identical levels of
exercise seen in this study were also comparable (8%) to previously
reported data.3
We are aware however that the reduction in E could
be multifactorial and could relate to diverted substrate utilization or
diminished catecholamine production, or that it could be due to the
increased efficiency of peripheral muscle oxygen extraction, with lower
resultant lactate and CO2 generation from
bicarbonate buffering.25
Although the significant
correlation (r = 0.63) that was found between changes in
E and CO2
suggests that a considerable component of the reduction in
E is related to decreased
CO2 after training, we also
cannot exclude the possibility of a more efficient breathing pattern
(reduced physiologic dead space/tidal volume ratio) and decreased
hyperinflation following a training program being
contributory.9
In the absence of physiologic dead
space/tidal volume ratio measurements, we cannot confirm the previous
observations.9
There are several other potential explanations for the reduction in
E following training. First, there may be a reduced
metabolic requirement for a given exercise task, as evidenced by the
lower O2 at an identical WR.
Second, since CO2 decreased to
the same extent as O2 (from 8
to 9%; Table 3
), the enhanced mechanical efficiency may also have
contributed to the fall in the ventilatory requirement. However, at WRs
above the AT, physiologic training is associated with reduced lactate
production and, in turn, lower
O2 requirements (up to
approximately 10%) and lower bicarbonate-elevated
CO2.26
27
In
contrast to a comparative study,3
we did not evaluate
serum lactate.
A review17
of many pulmonary rehabilitation programs
identified only one program that featured a variable training frequency
of two or fewer sessions per week.28
While peak
O2 and submaximal exercise
performance improved following rehabilitation,28
there was
no evidence of a lower ventilatory requirement at a given WR. Recently,
studies10
11
12
featuring twice-weekly exercise
rehabilitation sessions for 7 to 12 weeks reported significant
improvements in exercise performance assessed by simple walking
tests. The current study confirms the effects of twice-weekly
training programs on enhancing exercise performance, not only in terms
of objectively measured peak physiologic responses, but that such
effects are accompanied by a reduced ventilatory requirement at a
submaximal level of exercise.
The design of the initial training prescription in the present study was similar to that described by Niederman et al,16 who exercised 33 patients with a wide spectrum of airflow limitation (FEV1 range, 0.33 to 3.8 L) three times a week for 9 weeks. It was shown that changes in maximal and submaximal exercise performance on a bicycle ergometer were not related to the magnitude of airflow impairment quantified as % predicted FEV1.16 In the present study, we were able to develop these observations in a larger cohort of patients but with a comparable wide spectrum of airflow limitation (FEV1 range, 0.51 to 2.99 L). Our data show that training benefits are unrelated to and independent of underlying airflow limitation; comparable benefits were observed for patients with % predicted FEV1 < 40% and for those whose FEV1 exceeded this threshold (Table 4) . Interestingly, in contrast to previous studies,4 5 6 7 there was a significant but very modest clinical impact on dynamic and static lung volumes. Even though the exercise program did not include weight training as a component, it is difficult to attribute the improvements in ventilatory capacity to the training schedule per se. A more likely explanation relates to indirectly derived educational benefits in the use of inhaled medication.
Primary outcome measures in pulmonary rehabilitation strategies include assessments of quality of life and psychosocial performance, quantification of domestic functional activity, in addition to the physiologic benefit derived from aerobic training. This study further emphasizes the important role of aerobic submaximal exercise training in patients with chronic pulmonary morbidity. Although the magnitude of the physiologic benefits observed in reducing ventilatory requirements may be considered small, they were nevertheless achieved irrespective of the degree of airflow limitation, and this has significant implications for clinical practice. We are unable to quantify which particular aspect of the exercise strategy is more important; additionally, we are unable to state with certainty whether or not the observed physiologic gains are directly extrapolatable to improved functional daily activity, since this was not our primary outcome measure. It is nevertheless likely, however, that in patients limited by dyspnea, peripheral muscle weakness and increased susceptibility to lactic acidosis, enhancement of exercise tolerance, and reduction in ventilatory and cardiovascular requirements at a defined level of exercise will extrapolate to improved domestic functioning. Of note, a recent study by Singh et al29 did demonstrate objective improvements in domestic function following a rehabilitation strategy that resulted in improved exercise tolerance.
In summary, these data expand on the physiologically based principles of exercise prescription for patients with chronic airflow limitation and endorses the benefit of such strategies. We have shown that submaximal aerobic exercise training of moderate intensity performed twice weekly for 12 weeks in a large cohort of patients has significant potential benefits on a number of physiologic responses irrespective of the severity of the underlying obstructive pulmonary disease. The implications for clinical practice are tangible and compelling.
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Acknowledgements |
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Footnotes |
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CO2 = carbon dioxide output;
E = minute ventilation;
E/O2 = ventilatory
equivalent for oxygen; O2 = oxygen
uptake; WR = work rate Supported by a grant from the Northern and Yorkshire NHS Executive for Research and Development.
Received for publication November 9, 1998. Accepted for publication May 26, 1999.
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References |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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This article has been cited by other articles:
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  I. Vogiatzis, S. Nanas, and C. Roussos Interval training as an alternative modality to continuous exercise in patients with COPD Eur. Respir. J., July 1, 2002; 20(1): 12 - 19. [Abstract] [Full Text] [PDF]
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 E. Clini, K. Foglio, L. Bianchi, R. Porta, M. Vitacca, and N. Ambrosino In-Hospital Short-term Training Program for Patients With Chronic Airway Obstruction Chest, November 1, 2001; 120(5): 1500 - 1505. [Abstract] [Full Text] [PDF]
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 British Thoracic Society Standards of Care Subcomm Pulmonary rehabilitation Thorax, November 1, 2001; 56(11): 827 - 834. [Full Text] [PDF]
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 L. R. Johnson, J. W. E. Rush, J. R. Turk, E. M. Price, and M. H. Laughlin Short-term exercise training increases ACh-induced relaxation and eNOS protein in porcine pulmonary arteries J Appl Physiol, March 1, 2001; 90(3): 1102 - 1110. [Abstract] [Full Text] [PDF]
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) and nontraining control (
)
groups. *p < 0.05; comparisons are within, not between, group.