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Individualized Aerobic and High Intensity Training for Asthmatic Children in an Exercise Readaptation Program*
Individualized Aerobic and High Intensity Training for Asthmatic Children in an Exercise Readaptation Program* Is Training Always Helpful for Better Adaptation to Exercise? Alain L. Varray, Ph.D.; jacques G. Mercier; M.D.; Claude M. Terral, M.D.; and Christian G. Prefaut, M.D.
In order to de6ne the role of individualized training intensity in a conditioning program for asthmatic children, we have trained seven asthmatics (age 11.4± 1.8 years) at their ventilatory threshold (VTh) intensity level for a threemonth period (aerobic training) and at maximal intensity also for three months (high intensity training). VTh is the point at which a nonlinear increase of VE occurs. Another group of seven asthmatics (age = 11.4 ± 1.5) served as control subjects. Cardiopulmonary 6tness was determined on a cycle ergometer before and after each training session. This study demonstrated that aerobic training, correctly
adapted to the child's physical ability, induces the following: (I) a rapid and marked cardiovascular OtDess increase; and (2) a decrease in VE over a given work range so that VTh is increased. This is of great importance because hyperventilation is a major determinant of exercise-induced bronchospasm. In contrast, even if high intensity training is well tolerated in an indoor swimming pool, the long-term effects are unsuitable for asthmatic children because the decrease of VTh will involve an increase of hyperventilation, even when exercise is performed at submaximal intensity. (Che.t 1991; 99:579-86)
spite of the aerobic fitness limitation described in I nasthmatic children,l-4 there are surprisingly few
MATERIAL AND METHODS
=
studies on the retraining of these patients. In the earliest studies, attention was focused on the asthmogenic character of various sports. 5 According to subsequent studies, there was some evidence that if the levels of ventilation and inspired air conditions were matched, the asthmogenic degree of all sports would be the same.&9 Thus, in order to control the level of hyperventilation during exercise, monitoring of the training characteristics (duration, intensity) has become necessary. However, the description of training programs is still insufficient. The major problem in previous studies has been the absence ofa fundamental notion used in modern training techniques: the individualization of training. This oversight could explain the discrepancies among the results of these studies. 16-16 This study was designed to determine the impact of different individualized training intensities on cardiorespiratory fitness, and beyond that, on the underlying disease in children with asthma. Two types of conditioning programs were performed: aerobic and high intensity training.
*From the Hopital de rAiguelongue, Service d'Exploration Fonctionnelle Respiratoire, Montpellier, France. Manuscript received February 14; revision accepted August 6. Reprint requests: Dr. \fJfTay, Hopital AigtIelorigue, Seroice EFR, MontepeUier; France 34059
Subjects
This study was carried out with 14 atopic asthmatic children, during a six-month period. All the asthmatic subjects were known to have had recurrent reversible wheezing episodes and were required to fulfill at least three of the four following criteria: (1) clinical: family history of asthma and/or personal history of eczema, conjunctivitis or rhinitis caused by a known allergen; (2) allergic: all the children presented a cutaneous hypersensitivity to one or several allergens; (3) immunologic: blood IgE levels were determined by the paper radioimmunoabsorbent test (PRIST): any values above 150 UIIml were considered abnormal; and (4) functional: improvement of 15 percent, at least, in FEV 1 by inhaling a bronchodilator. The children were divided into two groups: control subjects (n = 7) and swimmers (n = 7). The two groups showed no significant differences concerning age, height, weight, lean body mass, airBows, regular physical practice, frequency ofacute attack ofasthma, and initial cardiorespiratory fitness. All patients were asymptomatic before testing. Basal medication (disodium cromoglycate, PI sympaticomimetics, and exceptionally, steroids) was not modified but was withdrawn at least 24 hours before each test. The anthropometric characteristics and the spirometric values of the asthmatic children are given in Tables 1 and 2. The patients took part in the study after informed consent was obtained from them and their parents. Measurements
The maximum expiratory flow-volume curves were performed on a digital spirometer (Datalink pulmochart). The lung function study included FVC, FEV.. maximal expiratory flow at 50 percent of FVC, and forced expiratory flow between 25 and 75 percent of FVC. The following values were then calculated: FEV/FVC and FEF25-751FVC. The predicted values were those of Zapletal et al l7 CHEST I 99 I 3 I MARCH, 1991
579
Table I-Anthropometric CharacteriBtica of the Control Group arad the StDimmirag Group Before PhflaictJl lraining No. Control group 1 2 3 4 5 6 7 Mean±SEM Swimming group 1 2 3 4 5 6 7 Mean±SEM Difference between groups*
Age, yrs
Sex
Height, cm
Weight, kg
Lean body mass, kg
12 10 9 12 11 13 13 11.4± 1.5
M M M F M M M
163 140 116 147 144 157 161 146.8± 16.1
48 33 22 49 33 44
39.48 28.71 19.65 35.09 30.14 37.84
13 13 9 11 9 13 12 11.4± 1.8
F M M M M M M
148 142 141 135 141 142 140 141.2±3.8
27 33 38 28 34.1 ±6.7
39.94 30.31 30.06 25.01 29.16 32.92 25.82 30.4±4.9
NS
NS
NS
NS
45.88
58
33.8±8.5
41±12.2 47 33
33
*NS, no significant difference. for MEF5O%FVC and Dickman et ailS for FVC, FEV., and FEF2575. The exercise test was performed on an electrically-braked cycle ergometer (Gauthier). Subjects breathed through a low resistance valve (Hans Rudolph, dead space = 90 ml). Inspiratory airflow was measured during exercise with a pneumotachograph (Fleich No.3) and a pressure transducer (Validyne) with a measuring range of ± 2 cm HtO. The pneumotachograph was placed on the inspiratory tubing in order to avoid problems due to water vapor. Calibration of the Row module was accomplished by introducing a calibrated volume of air at several Row rates. Expired gases were sampled in a mixing chamber (5 L) and analyzed for Ot with a polarographic
analyzer (Beckman OM 11) and for COt with an infrared analyzer (Cosma diamant 6000). Each gas analyzer was calibrated before and after each test with standard gases. The inspiratory airBow and the fractions of expired Ot and COt (FEOt and FECOJ were calculated by a computer from ten breath cycles. Averages were established for minute ventilation (VE L.min- I BTPS), 0t uptake (VOl L.min- I STPD), COt production (Veot L.min- I STPD), respiratory ratio (R), ventilatory equivalent for 0. (VE. VOt-I) and CO2 (VE. Veo2 -I), breathing frequency (f bpm), tidal volume (VT L. min -I BTPS), inspiratory duty cycle (fi/ftot), and mean inspiratory Bow (VT/li L.s-I). The heart rate was determined on an electrocardiogram continuously recording on a cardioscope (Simonsen and Weel).
Table 2-Spirometric Values of the Control Group arad the Swimming Group Before PhyaictJl TrainingNo. Control group 1 2 3 4 5 6 7 Mean SEM Swimming group 1 2 3 4 5 6 7 Mean SEM
FVC
FEVI
FEV/FVC
MEF50
FEF25-75
112 107 107 88 102 92 86 99 4
(3.25) (2.29) (1.37) (1.83) (2.34) (2.74) (2.79) (2.37) (0.23)
103 104 102 91 93 79 69 92 5
(2.63) (1.91) (1.08) (1.64) (1.83) (2.02) (1.91) (1.86) (0.17)
81 83 78 89 78 73 68 79 2
74 74 63 75 63 61 40 64 5
(2.97) (2.23) (1.12) (2.42) (2.05) (2.42) (1.67) (2.13) (0.22)
73 75 65 83 62 49 38 63 6
(2.55) (1.92) (1.11) (2.19) (1.67) (1.72) (1.41) (1.8) (0.18)
104 94 84 107 105 119 95 101 4
(3.16) (2.11) (1.86) (2.12) (2.32) (2.62) (2.03) (2.31) (0.17) NS
86 87 70 72 91 118 70 85 6
(2.26) (1.69) (1.33) (1.22) (1.73) (2.24) (1.28) (1.68) (0.16) NS
72 80 72
53 64 48 26 59 73 31 51 6
(2.04) (2.04) (1.49) (0.74) (1.86) (2.79) (0.93) (1.70) (0.26) NS
48 66 36 32 61 100 30 53 9
(1.72) (1.77) (0.95) (0.77) (1.62) (2.64) (0.77) (1.46) (0.26) NS
58
74 85 63 72 3 NS
FEF25-751FVC 78 83 81 119 72 63 50
78 8
54
84 51 36 70 100 38 62 9 NS
*FVC, forced vital capacity, L; FEV I, forced expiratory volume in one second, L; MEF5O%FVC, maximal expiratory 80w at 50% of FVC, L.see- I ; FEF25-75, forced expiratory Bow between 25 and 75% of FVC, L.s-I; The data are expressed in percent predicted values and in absolute value (between parentheses). NS, no Significant difference.
580
Individualized Aerobic and High Intensity Tn*1ing in Asthmatic ChiIdrwI MItt8Y.t aI)
Electrodes were placed in the CsM lead position. To account for interindividual differences in subjects, VE, VT, and VTffi were normalized by body weight; for the same reason, the V02 was expressed in ml.kg-I.min- I. The maximal exercise test started with a 3 min 30 W warm-up period. The work load was then increased by 30 W each minute (20 W for female subjects) until exhaustion. The observation of at least three of the four following criteria was necessary to consider that the subjects had reached their Vo2 max: (1) stability of HR at a value close to the theoretical maximal heart rate; (2) stability of oxygen uptake in spite of the increase of work load; (3) respiratory and (4) the inability of the subject to maintain a ratio ~1.10; pedaling rate of 50 rpm. The ventilatory threshold (VTh) was determined as the last point before an increase in VE.V02 -I plotted against a work rate without a concomitant VE.VC02-I increase. 19 The reading was effected independently by two observers. In the rare case of discordance, a third one was used to reach a consensus or to eliminate the subject (in this study a consensus was always reached). The maximal oxygen pulse (V02max/HRmax) was expressed in ml.kg- I. beat-I.
60
55
x o
E40
o
N
.>
35
II
l··············.. · · · · · :f~· · · ·
NS
· · · · · ·l
NS
---------1_
30.....----+--------.... TO T3 45
NS
40
II
T6
.09 (NS)
Protocol
The subjects were tested before training (To), after a three-month aerobic training period (T3), and one last time after three months of high intensity training (TJ. At the same times, the children of the control group were also tested. The entire evaluation included clinical examination, exercise testing, and flow-volume curves just before and 10 min after exercise. This laboratory evaluation allowed us to determine, for each subject, the training intensity to be used during the next training period. Evaluation of Functional VTh Swimming ~locity
During the To exercise test, we assessed VTh and the corresponding heart rate (HR at VTh). Following this, the children had to swim 400 m (crawl). Heart rate was continuously recorded on a sport tester PE 3000 (Pragmat), and the time needed to cover each 25 meter interval was regularly noted. The average performance time when the heart rate was steady and near the HR at VTh was used to define the VTh swimming velocity. During one aerobic training session, the children swam for 10 min, three times at their own VTh velocity (individualized training). The children were aware of their velocity by being informed of their swimming time every 25 m. It was thus possible for them to control their swimming speed. The duration of one session was one hour, and there were two different sessions per week. Training was supervised by a physical education teacher to be sure that the swimming speed was correct and by a physician in case of any medical problem and to control ventilatory function once per week. This kind ofconditioning allowed prolonged exercise performed at metabolic steady state. High Intensity 1raining
The second schedule of training consisted of a series of 25 m crawls performed at maximal speed in order to reach supramaximal intensities. The HR reached by the asthmatic children were markedly higher than the HR at VTh and near their maximal HR (± 5 percent oftheir maximal HR measured in laboratory). Recovery (1 min) was incomplete between repetitions in the same series (six repetitions of 25 m) and complete between two different series. A total session consisted of 12, 25-m crawl stimulations (2 x 6). The new intensity training was controlled in the same manner as previously described. The frequency and duration of the sessions was the same as for the aerobic training period. Clinical Benefit
This was assessed by a questionnaire, administered orally, which
r······································:r·····································1 20
+++
15""-----+--------.... ---------4TO TJ T6 FIGURE 1. Time course, between To, T3 and Ts of maximal Os uptake (V02max) and VTh in the swimming group (closed circles) and in the control group (open circles). The data are presented as mean ± SEM. Intergroup comparisons at each time (bottom of the figure): tt, p
The values are reported as mean ± SEM. The data collected on entry were compared for homogeneity between the two groups, using an unpaired Student t-test. Breathing pattern variables were compared at the same metabolic level in the swimming group by using a paired Student's t-test. The other data were analyzed for statistical significance using a two-way analysis of variance to test for between-group differences and using a one-way analysis of variance to test for within-group changes. fD An hortogonal contrast method was used at each time (To, T3 and TJ when the ANOVA F ratio was significant. lIO The limit for statistical significance was always set at p
Clinical Benefit
. All children completed the entire training program, which was well tolerated. The parents reported neither an improvement concerning the frequency of attacks nor a decreased need for regular medication. However, a major subjective clinical improvement was the marked decrease of the intensity of wheezing attacks. This was quickly observed at the beginning of CHEST I 99 I 3 I MARCH, 1991
581
75
2.1
II
1.1
NS
NS NS
70
0-
c
oX
....... .~ 1.7
NS
II
15
E
I:
......
E
-.1.5
.~
.................···································1
50
+
46
r···················!
1.3
NS
NS
1.1
TO
T3
TI
40
TO
T3
TI
70 42
II
t
·····
NS
·!····································1
··t·········
NS
1.....- -.....- - - - -.....---------4~
TO
FIGURE
····························r
•..•..........•.....•.............. ++
24
21
NS
,I
T3
TI
JO~--
NS
NS ....- - - - -.......- - - - - -.....TI T3 TO
2. TIme course between To, T3 and T 6 of ventilation divided by weight (VE BW)' respiratory frequency
(1), tidal volume divided by weight (VTBW), and mean inspiratory flow divided by weight (VTBJfi), at
maximal exercise, in the swimming group (closed circles) and in the control group (open circles). The data are reported as mean ± SEM. Intergroup comparisons at each time (bottom of the figure): t, p
the training sessions. Moreover, the parents pointed out that their children were sometimes able to prevent acute asthmatic attacks by practicing relaxation and breathing exercises; the children were also described as being less anxious than previousl)'. These observations were unlinked to the intensity of training. TIme Course of Lung Function
We observed no significant differences between the two groups throughout the stud)'. Effects of Aerobic Training
The Vo2 max (ml.kg-1.min- 1) was significantly higher (Fig 1) in the training group after aerobic training (p<0.001). At Vo2 max, the training group showed a significantly higher VE (VEmax) than control subjects (Fig 2, p
by 20 percent after aerobic training. Maximal heart rate (HRmax) was increased (Fig 3, p intragroup <0.05) but the difference between the two groups after aerobic training was at the limit of significance (p<0.06). At the same time, we observed a significant maximal O2 pulse increase after aerobic training (p intragroup and intergroup <0.(01). Effects of High Intensity Training
The Vo2 max (Fig 1) remained unchanged after high intensity training. However, the difference between the two groups was still significant (p
VTBwIfi* 34.43± 1.39 39.88±2.36 35.95±O.93 (mles-"kg- 1) t 4.75 -1.67 P <0.01 NS *VTBJIi, mean inspiratory flow normalized by body weight. Individualized Aerobic and High Intensity Training in Asthmatic Children (Varray et 8/)
erage baseline pulmonary function and clinical wellbeing was only partly affected.
210 NS
II
205
Clinical Benefit and Pulmonary Function
·e ""-
c:200
~ 115
.8 ~
1to
~
1115
I
180
!
••••••••••••••••••••••••••••••········r··············· .06 (NS)
NS
TO
...
0.3 +I
j 0.28 ""~'"
..
T6
TJ
II
NS
~0.26
E
.0.24
• 1-
tSO.22
l
I
0.2 O.18.!---~Tt-O
r···································1····································1 NS
+++ - - - - - - - T I -- - - - - -...T6 3
FIGURE 3. TIme course between To, T 3 and Ttl of maximal heart rate and O. pulse in the training group (closed circles) and in the control group (open circles). The data are expressed as mean ± SEM. Intergroup comparisons at each time (bottom of the figure): t, p
training. This decrease did not reach the limit of significance (p
In this study, we specifically wanted to assess the influence of exercise intensity, base4 on the subject's physical potential, in a population of asthmatic children. Our findings show that intensity training is of particular importance to the cardiorespiratory fitness variables, because it plays an important role in longterm adaptation to exercise. In contrast, our study failed to demonstrate significant modifications in av-
Though clinical evolution was not a specific feature of this work, and it was impossible to characterize the specific effects of the different training programs (season lability) on the underlying asthmatic disease, a subjective comparison with the previous year suggests a decrease in the intensity of wheezing attacks. However, no effects were found either on their frequency or on the reported change in need for regular medication. These results confirm those of a more specific previous report21 which described an improvement of symptoms in subjective reporting. The decrease of intensity of wheezing attacks could be explained by the following: (1) the regular practice of respiratory exercises during warm-up21 which probably leads the children to better control their respiratory muscles, and/or, (2) a decrease in anxiety due to physical activity. 22 The nonsignificant improvement ofpulmonary function supports the findings of previous studies. 10,15,16,23 However, all these studies were conducted over a short period (six weeks to six months). It would be particularly interesting to verify whether long-term investigation could show that physical activity offsets the rate of decline of lung function in asthmatics. 24
Effects of Aerobic Training After aerobic training, we observed a marked increase of two cardiorespiratory fitness variables: maximum O 2 uptake (Y02max) and VTh. The increase of Vo2max agrees with several previous studies 1G-13.15,16 but contrasts with others. 2,14 The results of our study show that this discrepancy might be explained by the lack of training individualization. Training in the previous studies was the same for all the subjects, and it is possible that some subjects could have been either insufficiently or too much stimulated. Aerobic training appears to have increased VTBWmax and VTBJIlmax in our training group, with a subsequent rise ofVEmax. Ramonatxo et al3 have suggested that children with moderate asthma have good neural compensation of their resistive load by using higher VTBW and lower respiratory frequencies, probably in order to avoid exaggerated turbulence. iS A complementary study carried out with more obstructed asthmatics· has shown that this adaptation could reach a limit, these asthmatics being unable to increase sufficiently their VTBW during an incremental exercise test. In this stud~ after the training period, the VTBW values were the same as those reported by Ramonatxo et al, 3 indicating a better ventilatory adaptation. After aerobic training, VTBwfIi was significantly increased at maximal exercise but also for the same metabolic CHEST I 99 I 3 I MARCH, 1991
583
rate (ie, at the same V02), thus, presumably for the same neural drive. This result probably indicates a decrease ofailWay resistance. 26 We observed a nonsignificant improvement in maximal flows in the trained group and we can hypothesize that VTBWIfi was more sensitive for showing a decrease in ailWay resistance than the maximal Hows. However, an alternative explanation may be proposed since Haas et a123 have shown that aerobic training induces an improvement of exercise-induced bronchodilation. Even if resting pulmonary function remains largely unchanged, our results indicate that aerobic training leads to an enhancement oflung function, at least during exercise, and to better ventilatory adaptation. The increase of maximal O 2 pulse indicates that aerobic training improves both cardiac adaptation and O 2 extraction. 27-29 This phenomenon is a common result of training and does not represent a particular adaptation of asthmatics. 30 Therefore, the interpretation of the increase of aerobic fitness remains difficult: either (1) it originates from the improvement of cardiac function and/or O 2 extraction capacity, and the increase of maximal O 2 pulse supports this hypothesis; or (2) the ventilatory limitation in asthmatics, described in our previous study,4 has partially disappeared, and this hypothesis is difficult to support since we have only an indirect indication of slight improvement in lung function. It seems reasonable that the final interpretation will combine elements of both hypotheses. Aerobic training can induce better ventilatory adaptation, thus permitting the full range of cardiac adaptation and O 2 extraction effects of training. A particularly interesting finding in this study is the increase in VTh (about 20 percent) because the ventilatory requirement, for the range intensities between the pretraining and posttraining VTh, is lower. It is now well established that the level of hyperventilation is a major determinant of exercise-induced bronchospasm.6-9 Thus, we can argue that, beyond cardiorespiratory fitness improvement, aerobic training increases the ability to perform submaximal exercise. In addition, the improvement of exercise-induced bronchodilation after aerobic training, described by Haas et a1, 23 linked to the increase ofVTh can explain why the physical fitness improvement is associated with a reduction of exercise-induced bronchospasm. 10,31
Effects of High Intensity Training High intensity exercises performed in an indoor swimming pool were well tolerated at least after an aerobic training program. High intensity training induced no effect on V02 max and decreased moderately the VTh in the swimming group (Fig 1), so that after this training, there was no longer any difference of VTh between the beginning and the end of the 584
whole training period. For an ethical reason, we did not use a crossover experimental design with one group beginning with aerobic exercises and the other with high intensity exercises. Indeed, these exercises pose the risk of exercise-induced asthma (hyperventilation and blood lactate concentrations,32,33 and it is hazardous to begin a training program with them. We thus cannot rule out the possibility that a bias occurred in the effects of the different training programs. In addition, the interpretation of our results remains problematic because there have been no other studies carried out on maximal intensity exercise in asthmatic children. However, we can point out that asthmatics seem to respond in much the same physiologic manner as do normal people practicing high intensity training. Indeed, it has been shown that this kind of training produces no adaptative improvement of cardiorespiratory function and muscle fiber characteristics. 34 According to the authors, this training decreases muscle respiratory capacity. Such a situation would reduce the relative work rate at which ATP resynthesis can be met by purely oxidative phosphorylation, and result in an earlier energy production via anaerobic glycolysis. 34 The stability ofV02 max can be explained by the structural changes in skeletal muscle tissue after high intensity training. 35 Indeed, it has been shown that this structural adaptation is clearly marked by a decrease of the volume density of mitochondria which is counterbalanced by a total muscle volume increase. Because of the lack of studies carried out on high intensity training, biochemical studies provide one of the few ways liable to explain its effects upon VTh, leading to an understanding of high intensity training metabolic consequences. Previous studies have shown that exercise of maximal intensity and 30-s duration (which corresponds approximately to the sprint time performed by the children during the high intensity training) requires essentially an anaerobic glycolysis contribution.36-38 Moreover, when several bouts of exercise are performed, an inhibition ofglycogenolysis occurs at the third and fourth exercise bouts. 38 Therefore, the muscle oxidative capacity is not solicited, and this can explain the moderate decrease of VTh, which would represent the muscle oxidative capacity.39,4O This assumption supports the findings of previous studies41 ,42 which have reported that a close correlation exists between VTh and the percentage of slow-twitch fibers. Moreover, it could be assumed that, above a training intensity which corresponds approximately to 85 percent ofV02 max, increasing the training load decreases the oxidative capacity of slow-twitch fibers. 43 This kind of training leads to a major problem because any decrease of VTh ,viII induce an exaggerated hyperventilation at submaximal exercise intensities, which represents for the asthmatic children, a Individualized Aerobic and High Intensity Training in Asthmatic Children (Varray at 81)
very bad long-term adaptation for the same reasons previously discussed. The results concerning the cardiovascular adaptations after high intensity training (Fig 3) show that the maximal heart rate increased in the training group, but the maximal O 2 pulse decreased slightly. These data suggest the following: 28 (1) a decrease of stroke volume mediated by decreasing myocardial contractibility; (2) a decrease of arteriovenous O2 difference, with the data concerning the reduction of muscle oxidative capacity and the decrease ofVTh supporting this hypothesis; or (3) a combination of the above. In the absence of direct measurement of each of these possibilities, any explanation remains speculative. In conclusion, our study shows that when intensity training is individualized, it is possible to markedly increase the cardiorespiratory fitness of asthmatic children by aerobic training. Subsequent high intensity training does not further contribute to increased fitness. It appears that the intensity of training is of great importance in regard to the development of cardiorespiratory fitness because it seems to involve important consequences upon the asthmatic-exercise "interface," since the asthmatics' major problem is to avoid any excessive hyperventilation during exercise. Furthermore, this study suggests that the control of VTh could be a good index for evaluating the correct compatibility of the subjects capacities and the trainFinall}; further studies involving other ing intensi~ intensities should be carried out in order to determine the optimal training intensity for asthmatic subjects. ACKNOWLEDGMENTS: The writers thank Pr F.B. Michel and his respiratory disease department for the recruitment of asthmatic children and his work concerning exercise readaptation in asthmatics.
REFERENCES 1 Friedman M, Kovitz KL, Miller SD, Marks M, Sackner MA. Hemodynamics in teenagers and asthmatic children during exercise. J Appl Physiol1979; 46:293-97 2 Vavra J, Macek M, Mrzena B, Spicak ~ Intensive physical training in children with bronchial asthma. Acta Prediatr Scand 1971; suppl,217:90-92 3 Ramonatxo M, Amsalem F, Mercier J, Jean R, Prefaut C. Ventilatory control during exercise in children with mild and moderate asthma. Med Sci Sports Exerc 1989; 21:11-17 4 Varray A, Mercier J, Ramonatxo M, Prefaut C. L'exercise physique maximal chez I'enfant asthmatique: limitation aerobie et compensation anaerobie? Sci Sports 1989; 4:199-207 5 Anderson SD, Silverman M, Konig ~ Godfrey S, Saltin B. Exercise-induced asthma. Br J Dis Chest 1975; 69: 1-39 JJ. 6 Deal EC, McFadden ER Jr, Ingram RH, Breslin FJ, Jae~er Airway responsiveness to cold air and hyperpnea in normal subjects and those with hay fever and asthma. Am Rev Respir Dis 1980; 121:621-28 7 Bundgaard A, Ingemann-Hansen T, Schmidt A, Halkjaer--Kristensen J. The importance of ventilation in exercise-induced asthma. Allergy 1981; 36:385-89 8 Bundgaard A, Ingemann-Hansen T, Schmidt A, Halkjaer-Kristensen J. Exercise-induced asthma after walking, running and
cycling. Scand J Clin Lab Invest 1982; 42: 15-18 9 Bundgaard A, Schmidt A, Ingemann-Hansen T, Halkjaer--Krisand tensen J, Bloch I. Exercise-induced asthma after swimmin~ bicycle exercise. Eur J Respir Dis 1982; 63:245-48 10 Arborelius M, Svenonius E. Decrease of exercise-induced asthma after physical training. Eur J Respir Dis 1984; 65(suppl, 136):25-31 11 Bundgaard A, Ingemann-Hansen T, Halkjaer-Kristensen J, Schmidt A, Bloch I, Andersen PK. Short term physical trainin~ in bronchial asthma. Br J Dis Chest 1983; 77:147-52 12 Bundgaard A, Ingemann-Hansen T, Halkjaer--Kirstensen J. Physical training in bronchial asthma. Int Rehabil Med 1984; 6:17982 13 Fitch KD, Morton AR, Blanksby BA. Effects of swimming training on children with asthma. Arch Dis Child 1976; 51:19094
14 Graff-Lonnevig ~ BevegArd S, Eriksson BO, Kraepelien S, Saltin B. Two years' follow-up of asthmatic boys participating in a physical activity programme. Acta Prediatr Scand 1980; 69:34752 15 Nickerson BG, Bautista DB, Namey MA, Richard ~ Keens TG. Distance running improves fitness in asthmatic children without pulmonary complications or changes in exercise-induced bronchospasm. Pediatrics 1983; 71:147-52 16 Svenonius E, Kautto R, Arborelius M. Improvement after training of children with exercise-induced asthma. Acta Prediatr Scand 1983; 72:23-30 17 Zapletal A, Motoyama EK, Van de Woestijne K~ Ilunt VR, Bouhuys A. Maximum expiratory flow-volume curves and airway conductance in children and adolescents. J Appl Physiol 1969; 26:308 18 Dickman ML, Schmidt CD, Gardner RM. Spirometric standards for normal children and adolescents (ages 5 years through 18 years). Am Rev Respir Dis 1971; 104:680-87 19 Wasserman K. Breathing during exercise. N Eng) J Med 1978; 298:780-85 20 Winner BJ. Statistical principles in experimental desiWl. New York: McGraw-Hill, 1971 21 Sly RM, Harper RT, Rousselot I. The effect of physical <.'onditioning upon asthmatic children. Ann AllerJO' 1972; 30:86-94 22 Martinsen EW The role of aerobic exercise in the treatment of depression. Stress Med 1987; 3:93-100 23 Haas F, Pasierski S, Levine N, Bishop M, Axen K, Pineda II, et a1. Effect of aerobic training on forced expiratory airflow in exercising asthmatic humans. J Appl Physiol 1987; 63:1230-35 24 Peat JK, Woolcock AJ, Cullen K. Rate of decline of lung function in subjects with asthma. Eur J Respir Dis 1987; 70:171-79 25 Hedstrand U. The optimal frequency of breathing in bronchial asthma. Scand J Respir Dis 1971; 52:217-21 26 Milic-Emili J, Aubier M. Some recent advances in the study of the control ofbreathing in patients with chronic obstructive lung disease. Anesthesia and Analgesia 1980; 59:865-73 27 Clausen JE Effects of physical training on cardiovascular adjustments to exercise in man. Physiol Rev 1977; 57:779-815 28 Scheuer J, TIpton CM. Cardiovascular adaptations to physical training. Ann Rev Physiol1977; 39:221-51 29 Cunningham DA, Paterson DH, Blimkie CJR, Donner A~ Development of cardiorespiratory function in circumpubertal boys: a longitudinal study. J Appl Physioll984; 56:302-07 30 Mercier J, Vago ~ Ramonatxo M, Bauer C, Prefaut C. Effect of aerobic training quantity on the Vo2 max of circumpubertal swimmers. Int J Sports Moo 1987; 8:26-30 31 Henriksen JM, Nielsen TI. Effect of physical trainin~ on exercise-induced bronchoconstriction. Acta Prediatr Scand 1983; 72:31-36 32 Arborelius M, Svenonius E. Decrease of exercise-induced asthma after physical training. Eur J Respir Dis 1984; 65(suppl. CHEST I 99 I 3 I MARCH, 1991
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136):25-31 33 Henriksen JM, Nielsen TI. Effect of physical training oil exercise-induced bronchoconstriction. Acta Pediatr Scand 1983; 72:31-36 34 Aitken Je, Bennet WM, Thompson J. The effects of high intensity training upon respiratory gas exchanges during fixed term maximal incremental exercise in man. Eur J Appl Physiol 1989; 58:717-21 35 LUthi JM, Howald H, Claassen H, Rosier Ie, Vock ~ Hoppeler H. Structural changes in skeletal muscle tissue with heavyresistance exercise. Int J Sports Moo 1986; 7:123-27 36 Jacobs I, Tesch PA, Bar-Or 0, Karlsson J, Dotan R. Lactate in human skeletal muscle after 10 and 30 s of supramaximal exercise. J Appl Physioll983; 55:365-67 37 McCartney N, Spriet LL, Heigenhauser GJF, Kowalchuk JM, Sutton JR, Jones NL. Muscle power and metabolism in maximal intermittent exercise. J Appl Physioll986; 60:1164-69 38 Cheetham ME, Boobis LH, Brooks S, Williams C. Human
39 40 41
42
43
muscle metabolism during sprint running. J Appl Physioll986; 61:54-60 Rusko H, Rahkila ~ Karvinen E. Anaerobic threshold skeletal muscle enzymes and fiber composition in young cross-country siders. Acta Physiol Scand 1980; 108:263-68 Gollniclc PD, Saltin B. Significance of skeletal muscle oxidative enzyme enhancement with endurance training. Clio Physiol 1982; 2:1-12 Ivy JL, Withers RT, Van Handel PJ, Elger DH, Costill DL. Muscle respiratory capacity and fiber type as determinants of the lactate threshold. J Appl Physioll980; 48:523-27 Aunola S, Rusko H. Aerobic and anaerobic thresholds determined from venous lactate or from ventilation and gas exchange in relation to muscle fiber composition. Int J Sports Med 1986; 7:161-66 DUdley GA, Abraham WM, Terjung RL. In8uence of exercise intensity and duration on biochemical adaptations in skeletal muscle. J Appl Physioll982; 53:844-50
Plan to Attend ACCP's
57th Annual Scientific Assembly San Francisco November 4-8, 1991
588
Individualized AerobIc and HIgh Inten8Ily Tt'IIinq In AIIhmaIic ChIldren ~
8t eI)
In order to de6ne the role of individualized training intensity in a conditioning program for asthmatic children, we have trained seven asthmatics (age 11.4± 1.8 years) at their ventilatory threshold (VTh) intensity level for a threemonth period (aerobic training) and at maximal intensity also for three months (high intensity training). VTh is the point at which a nonlinear increase of VE occurs. Another group of seven asthmatics (age = 11.4 ± 1.5) served as control subjects. Cardiopulmonary 6tness was determined on a cycle ergometer before and after each training session. This study demonstrated that aerobic training, correctly
adapted to the child's physical ability, induces the following: (I) a rapid and marked cardiovascular OtDess increase; and (2) a decrease in VE over a given work range so that VTh is increased. This is of great importance because hyperventilation is a major determinant of exercise-induced bronchospasm. In contrast, even if high intensity training is well tolerated in an indoor swimming pool, the long-term effects are unsuitable for asthmatic children because the decrease of VTh will involve an increase of hyperventilation, even when exercise is performed at submaximal intensity. (Che.t 1991; 99:579-86)
spite of the aerobic fitness limitation described in I nasthmatic children,l-4 there are surprisingly few
MATERIAL AND METHODS
=
studies on the retraining of these patients. In the earliest studies, attention was focused on the asthmogenic character of various sports. 5 According to subsequent studies, there was some evidence that if the levels of ventilation and inspired air conditions were matched, the asthmogenic degree of all sports would be the same.&9 Thus, in order to control the level of hyperventilation during exercise, monitoring of the training characteristics (duration, intensity) has become necessary. However, the description of training programs is still insufficient. The major problem in previous studies has been the absence ofa fundamental notion used in modern training techniques: the individualization of training. This oversight could explain the discrepancies among the results of these studies. 16-16 This study was designed to determine the impact of different individualized training intensities on cardiorespiratory fitness, and beyond that, on the underlying disease in children with asthma. Two types of conditioning programs were performed: aerobic and high intensity training.
*From the Hopital de rAiguelongue, Service d'Exploration Fonctionnelle Respiratoire, Montpellier, France. Manuscript received February 14; revision accepted August 6. Reprint requests: Dr. \fJfTay, Hopital AigtIelorigue, Seroice EFR, MontepeUier; France 34059
Subjects
This study was carried out with 14 atopic asthmatic children, during a six-month period. All the asthmatic subjects were known to have had recurrent reversible wheezing episodes and were required to fulfill at least three of the four following criteria: (1) clinical: family history of asthma and/or personal history of eczema, conjunctivitis or rhinitis caused by a known allergen; (2) allergic: all the children presented a cutaneous hypersensitivity to one or several allergens; (3) immunologic: blood IgE levels were determined by the paper radioimmunoabsorbent test (PRIST): any values above 150 UIIml were considered abnormal; and (4) functional: improvement of 15 percent, at least, in FEV 1 by inhaling a bronchodilator. The children were divided into two groups: control subjects (n = 7) and swimmers (n = 7). The two groups showed no significant differences concerning age, height, weight, lean body mass, airBows, regular physical practice, frequency ofacute attack ofasthma, and initial cardiorespiratory fitness. All patients were asymptomatic before testing. Basal medication (disodium cromoglycate, PI sympaticomimetics, and exceptionally, steroids) was not modified but was withdrawn at least 24 hours before each test. The anthropometric characteristics and the spirometric values of the asthmatic children are given in Tables 1 and 2. The patients took part in the study after informed consent was obtained from them and their parents. Measurements
The maximum expiratory flow-volume curves were performed on a digital spirometer (Datalink pulmochart). The lung function study included FVC, FEV.. maximal expiratory flow at 50 percent of FVC, and forced expiratory flow between 25 and 75 percent of FVC. The following values were then calculated: FEV/FVC and FEF25-751FVC. The predicted values were those of Zapletal et al l7 CHEST I 99 I 3 I MARCH, 1991
579
Table I-Anthropometric CharacteriBtica of the Control Group arad the StDimmirag Group Before PhflaictJl lraining No. Control group 1 2 3 4 5 6 7 Mean±SEM Swimming group 1 2 3 4 5 6 7 Mean±SEM Difference between groups*
Age, yrs
Sex
Height, cm
Weight, kg
Lean body mass, kg
12 10 9 12 11 13 13 11.4± 1.5
M M M F M M M
163 140 116 147 144 157 161 146.8± 16.1
48 33 22 49 33 44
39.48 28.71 19.65 35.09 30.14 37.84
13 13 9 11 9 13 12 11.4± 1.8
F M M M M M M
148 142 141 135 141 142 140 141.2±3.8
27 33 38 28 34.1 ±6.7
39.94 30.31 30.06 25.01 29.16 32.92 25.82 30.4±4.9
NS
NS
NS
NS
45.88
58
33.8±8.5
41±12.2 47 33
33
*NS, no significant difference. for MEF5O%FVC and Dickman et ailS for FVC, FEV., and FEF2575. The exercise test was performed on an electrically-braked cycle ergometer (Gauthier). Subjects breathed through a low resistance valve (Hans Rudolph, dead space = 90 ml). Inspiratory airflow was measured during exercise with a pneumotachograph (Fleich No.3) and a pressure transducer (Validyne) with a measuring range of ± 2 cm HtO. The pneumotachograph was placed on the inspiratory tubing in order to avoid problems due to water vapor. Calibration of the Row module was accomplished by introducing a calibrated volume of air at several Row rates. Expired gases were sampled in a mixing chamber (5 L) and analyzed for Ot with a polarographic
analyzer (Beckman OM 11) and for COt with an infrared analyzer (Cosma diamant 6000). Each gas analyzer was calibrated before and after each test with standard gases. The inspiratory airBow and the fractions of expired Ot and COt (FEOt and FECOJ were calculated by a computer from ten breath cycles. Averages were established for minute ventilation (VE L.min- I BTPS), 0t uptake (VOl L.min- I STPD), COt production (Veot L.min- I STPD), respiratory ratio (R), ventilatory equivalent for 0. (VE. VOt-I) and CO2 (VE. Veo2 -I), breathing frequency (f bpm), tidal volume (VT L. min -I BTPS), inspiratory duty cycle (fi/ftot), and mean inspiratory Bow (VT/li L.s-I). The heart rate was determined on an electrocardiogram continuously recording on a cardioscope (Simonsen and Weel).
Table 2-Spirometric Values of the Control Group arad the Swimming Group Before PhyaictJl TrainingNo. Control group 1 2 3 4 5 6 7 Mean SEM Swimming group 1 2 3 4 5 6 7 Mean SEM
FVC
FEVI
FEV/FVC
MEF50
FEF25-75
112 107 107 88 102 92 86 99 4
(3.25) (2.29) (1.37) (1.83) (2.34) (2.74) (2.79) (2.37) (0.23)
103 104 102 91 93 79 69 92 5
(2.63) (1.91) (1.08) (1.64) (1.83) (2.02) (1.91) (1.86) (0.17)
81 83 78 89 78 73 68 79 2
74 74 63 75 63 61 40 64 5
(2.97) (2.23) (1.12) (2.42) (2.05) (2.42) (1.67) (2.13) (0.22)
73 75 65 83 62 49 38 63 6
(2.55) (1.92) (1.11) (2.19) (1.67) (1.72) (1.41) (1.8) (0.18)
104 94 84 107 105 119 95 101 4
(3.16) (2.11) (1.86) (2.12) (2.32) (2.62) (2.03) (2.31) (0.17) NS
86 87 70 72 91 118 70 85 6
(2.26) (1.69) (1.33) (1.22) (1.73) (2.24) (1.28) (1.68) (0.16) NS
72 80 72
53 64 48 26 59 73 31 51 6
(2.04) (2.04) (1.49) (0.74) (1.86) (2.79) (0.93) (1.70) (0.26) NS
48 66 36 32 61 100 30 53 9
(1.72) (1.77) (0.95) (0.77) (1.62) (2.64) (0.77) (1.46) (0.26) NS
58
74 85 63 72 3 NS
FEF25-751FVC 78 83 81 119 72 63 50
78 8
54
84 51 36 70 100 38 62 9 NS
*FVC, forced vital capacity, L; FEV I, forced expiratory volume in one second, L; MEF5O%FVC, maximal expiratory 80w at 50% of FVC, L.see- I ; FEF25-75, forced expiratory Bow between 25 and 75% of FVC, L.s-I; The data are expressed in percent predicted values and in absolute value (between parentheses). NS, no Significant difference.
580
Individualized Aerobic and High Intensity Tn*1ing in Asthmatic ChiIdrwI MItt8Y.t aI)
Electrodes were placed in the CsM lead position. To account for interindividual differences in subjects, VE, VT, and VTffi were normalized by body weight; for the same reason, the V02 was expressed in ml.kg-I.min- I. The maximal exercise test started with a 3 min 30 W warm-up period. The work load was then increased by 30 W each minute (20 W for female subjects) until exhaustion. The observation of at least three of the four following criteria was necessary to consider that the subjects had reached their Vo2 max: (1) stability of HR at a value close to the theoretical maximal heart rate; (2) stability of oxygen uptake in spite of the increase of work load; (3) respiratory and (4) the inability of the subject to maintain a ratio ~1.10; pedaling rate of 50 rpm. The ventilatory threshold (VTh) was determined as the last point before an increase in VE.V02 -I plotted against a work rate without a concomitant VE.VC02-I increase. 19 The reading was effected independently by two observers. In the rare case of discordance, a third one was used to reach a consensus or to eliminate the subject (in this study a consensus was always reached). The maximal oxygen pulse (V02max/HRmax) was expressed in ml.kg- I. beat-I.
60
55
x o
E40
o
N
.>
35
II
l··············.. · · · · · :f~· · · ·
NS
· · · · · ·l
NS
---------1_
30.....----+--------.... TO T3 45
NS
40
II
T6
.09 (NS)
Protocol
The subjects were tested before training (To), after a three-month aerobic training period (T3), and one last time after three months of high intensity training (TJ. At the same times, the children of the control group were also tested. The entire evaluation included clinical examination, exercise testing, and flow-volume curves just before and 10 min after exercise. This laboratory evaluation allowed us to determine, for each subject, the training intensity to be used during the next training period. Evaluation of Functional VTh Swimming ~locity
During the To exercise test, we assessed VTh and the corresponding heart rate (HR at VTh). Following this, the children had to swim 400 m (crawl). Heart rate was continuously recorded on a sport tester PE 3000 (Pragmat), and the time needed to cover each 25 meter interval was regularly noted. The average performance time when the heart rate was steady and near the HR at VTh was used to define the VTh swimming velocity. During one aerobic training session, the children swam for 10 min, three times at their own VTh velocity (individualized training). The children were aware of their velocity by being informed of their swimming time every 25 m. It was thus possible for them to control their swimming speed. The duration of one session was one hour, and there were two different sessions per week. Training was supervised by a physical education teacher to be sure that the swimming speed was correct and by a physician in case of any medical problem and to control ventilatory function once per week. This kind ofconditioning allowed prolonged exercise performed at metabolic steady state. High Intensity 1raining
The second schedule of training consisted of a series of 25 m crawls performed at maximal speed in order to reach supramaximal intensities. The HR reached by the asthmatic children were markedly higher than the HR at VTh and near their maximal HR (± 5 percent oftheir maximal HR measured in laboratory). Recovery (1 min) was incomplete between repetitions in the same series (six repetitions of 25 m) and complete between two different series. A total session consisted of 12, 25-m crawl stimulations (2 x 6). The new intensity training was controlled in the same manner as previously described. The frequency and duration of the sessions was the same as for the aerobic training period. Clinical Benefit
This was assessed by a questionnaire, administered orally, which
r······································:r·····································1 20
+++
15""-----+--------.... ---------4TO TJ T6 FIGURE 1. Time course, between To, T3 and Ts of maximal Os uptake (V02max) and VTh in the swimming group (closed circles) and in the control group (open circles). The data are presented as mean ± SEM. Intergroup comparisons at each time (bottom of the figure): tt, p
The values are reported as mean ± SEM. The data collected on entry were compared for homogeneity between the two groups, using an unpaired Student t-test. Breathing pattern variables were compared at the same metabolic level in the swimming group by using a paired Student's t-test. The other data were analyzed for statistical significance using a two-way analysis of variance to test for between-group differences and using a one-way analysis of variance to test for within-group changes. fD An hortogonal contrast method was used at each time (To, T3 and TJ when the ANOVA F ratio was significant. lIO The limit for statistical significance was always set at p
Clinical Benefit
. All children completed the entire training program, which was well tolerated. The parents reported neither an improvement concerning the frequency of attacks nor a decreased need for regular medication. However, a major subjective clinical improvement was the marked decrease of the intensity of wheezing attacks. This was quickly observed at the beginning of CHEST I 99 I 3 I MARCH, 1991
581
75
2.1
II
1.1
NS
NS NS
70
0-
c
oX
....... .~ 1.7
NS
II
15
E
I:
......
E
-.1.5
.~
.................···································1
50
+
46
r···················!
1.3
NS
NS
1.1
TO
T3
TI
40
TO
T3
TI
70 42
II
t
·····
NS
·!····································1
··t·········
NS
1.....- -.....- - - - -.....---------4~
TO
FIGURE
····························r
•..•..........•.....•.............. ++
24
21
NS
,I
T3
TI
JO~--
NS
NS ....- - - - -.......- - - - - -.....TI T3 TO
2. TIme course between To, T3 and T 6 of ventilation divided by weight (VE BW)' respiratory frequency
(1), tidal volume divided by weight (VTBW), and mean inspiratory flow divided by weight (VTBJfi), at
maximal exercise, in the swimming group (closed circles) and in the control group (open circles). The data are reported as mean ± SEM. Intergroup comparisons at each time (bottom of the figure): t, p
the training sessions. Moreover, the parents pointed out that their children were sometimes able to prevent acute asthmatic attacks by practicing relaxation and breathing exercises; the children were also described as being less anxious than previousl)'. These observations were unlinked to the intensity of training. TIme Course of Lung Function
We observed no significant differences between the two groups throughout the stud)'. Effects of Aerobic Training
The Vo2 max (ml.kg-1.min- 1) was significantly higher (Fig 1) in the training group after aerobic training (p<0.001). At Vo2 max, the training group showed a significantly higher VE (VEmax) than control subjects (Fig 2, p
by 20 percent after aerobic training. Maximal heart rate (HRmax) was increased (Fig 3, p intragroup <0.05) but the difference between the two groups after aerobic training was at the limit of significance (p<0.06). At the same time, we observed a significant maximal O2 pulse increase after aerobic training (p intragroup and intergroup <0.(01). Effects of High Intensity Training
The Vo2 max (Fig 1) remained unchanged after high intensity training. However, the difference between the two groups was still significant (p
VTBwIfi* 34.43± 1.39 39.88±2.36 35.95±O.93 (mles-"kg- 1) t 4.75 -1.67 P <0.01 NS *VTBJIi, mean inspiratory flow normalized by body weight. Individualized Aerobic and High Intensity Training in Asthmatic Children (Varray et 8/)
erage baseline pulmonary function and clinical wellbeing was only partly affected.
210 NS
II
205
Clinical Benefit and Pulmonary Function
·e ""-
c:200
~ 115
.8 ~
1to
~
1115
I
180
!
••••••••••••••••••••••••••••••········r··············· .06 (NS)
NS
TO
...
0.3 +I
j 0.28 ""~'"
..
T6
TJ
II
NS
~0.26
E
.0.24
• 1-
tSO.22
l
I
0.2 O.18.!---~Tt-O
r···································1····································1 NS
+++ - - - - - - - T I -- - - - - -...T6 3
FIGURE 3. TIme course between To, T 3 and Ttl of maximal heart rate and O. pulse in the training group (closed circles) and in the control group (open circles). The data are expressed as mean ± SEM. Intergroup comparisons at each time (bottom of the figure): t, p
training. This decrease did not reach the limit of significance (p
In this study, we specifically wanted to assess the influence of exercise intensity, base4 on the subject's physical potential, in a population of asthmatic children. Our findings show that intensity training is of particular importance to the cardiorespiratory fitness variables, because it plays an important role in longterm adaptation to exercise. In contrast, our study failed to demonstrate significant modifications in av-
Though clinical evolution was not a specific feature of this work, and it was impossible to characterize the specific effects of the different training programs (season lability) on the underlying asthmatic disease, a subjective comparison with the previous year suggests a decrease in the intensity of wheezing attacks. However, no effects were found either on their frequency or on the reported change in need for regular medication. These results confirm those of a more specific previous report21 which described an improvement of symptoms in subjective reporting. The decrease of intensity of wheezing attacks could be explained by the following: (1) the regular practice of respiratory exercises during warm-up21 which probably leads the children to better control their respiratory muscles, and/or, (2) a decrease in anxiety due to physical activity. 22 The nonsignificant improvement ofpulmonary function supports the findings of previous studies. 10,15,16,23 However, all these studies were conducted over a short period (six weeks to six months). It would be particularly interesting to verify whether long-term investigation could show that physical activity offsets the rate of decline of lung function in asthmatics. 24
Effects of Aerobic Training After aerobic training, we observed a marked increase of two cardiorespiratory fitness variables: maximum O 2 uptake (Y02max) and VTh. The increase of Vo2max agrees with several previous studies 1G-13.15,16 but contrasts with others. 2,14 The results of our study show that this discrepancy might be explained by the lack of training individualization. Training in the previous studies was the same for all the subjects, and it is possible that some subjects could have been either insufficiently or too much stimulated. Aerobic training appears to have increased VTBWmax and VTBJIlmax in our training group, with a subsequent rise ofVEmax. Ramonatxo et al3 have suggested that children with moderate asthma have good neural compensation of their resistive load by using higher VTBW and lower respiratory frequencies, probably in order to avoid exaggerated turbulence. iS A complementary study carried out with more obstructed asthmatics· has shown that this adaptation could reach a limit, these asthmatics being unable to increase sufficiently their VTBW during an incremental exercise test. In this stud~ after the training period, the VTBW values were the same as those reported by Ramonatxo et al, 3 indicating a better ventilatory adaptation. After aerobic training, VTBwfIi was significantly increased at maximal exercise but also for the same metabolic CHEST I 99 I 3 I MARCH, 1991
583
rate (ie, at the same V02), thus, presumably for the same neural drive. This result probably indicates a decrease ofailWay resistance. 26 We observed a nonsignificant improvement in maximal flows in the trained group and we can hypothesize that VTBWIfi was more sensitive for showing a decrease in ailWay resistance than the maximal Hows. However, an alternative explanation may be proposed since Haas et a123 have shown that aerobic training induces an improvement of exercise-induced bronchodilation. Even if resting pulmonary function remains largely unchanged, our results indicate that aerobic training leads to an enhancement oflung function, at least during exercise, and to better ventilatory adaptation. The increase of maximal O 2 pulse indicates that aerobic training improves both cardiac adaptation and O 2 extraction. 27-29 This phenomenon is a common result of training and does not represent a particular adaptation of asthmatics. 30 Therefore, the interpretation of the increase of aerobic fitness remains difficult: either (1) it originates from the improvement of cardiac function and/or O 2 extraction capacity, and the increase of maximal O 2 pulse supports this hypothesis; or (2) the ventilatory limitation in asthmatics, described in our previous study,4 has partially disappeared, and this hypothesis is difficult to support since we have only an indirect indication of slight improvement in lung function. It seems reasonable that the final interpretation will combine elements of both hypotheses. Aerobic training can induce better ventilatory adaptation, thus permitting the full range of cardiac adaptation and O 2 extraction effects of training. A particularly interesting finding in this study is the increase in VTh (about 20 percent) because the ventilatory requirement, for the range intensities between the pretraining and posttraining VTh, is lower. It is now well established that the level of hyperventilation is a major determinant of exercise-induced bronchospasm.6-9 Thus, we can argue that, beyond cardiorespiratory fitness improvement, aerobic training increases the ability to perform submaximal exercise. In addition, the improvement of exercise-induced bronchodilation after aerobic training, described by Haas et a1, 23 linked to the increase ofVTh can explain why the physical fitness improvement is associated with a reduction of exercise-induced bronchospasm. 10,31
Effects of High Intensity Training High intensity exercises performed in an indoor swimming pool were well tolerated at least after an aerobic training program. High intensity training induced no effect on V02 max and decreased moderately the VTh in the swimming group (Fig 1), so that after this training, there was no longer any difference of VTh between the beginning and the end of the 584
whole training period. For an ethical reason, we did not use a crossover experimental design with one group beginning with aerobic exercises and the other with high intensity exercises. Indeed, these exercises pose the risk of exercise-induced asthma (hyperventilation and blood lactate concentrations,32,33 and it is hazardous to begin a training program with them. We thus cannot rule out the possibility that a bias occurred in the effects of the different training programs. In addition, the interpretation of our results remains problematic because there have been no other studies carried out on maximal intensity exercise in asthmatic children. However, we can point out that asthmatics seem to respond in much the same physiologic manner as do normal people practicing high intensity training. Indeed, it has been shown that this kind of training produces no adaptative improvement of cardiorespiratory function and muscle fiber characteristics. 34 According to the authors, this training decreases muscle respiratory capacity. Such a situation would reduce the relative work rate at which ATP resynthesis can be met by purely oxidative phosphorylation, and result in an earlier energy production via anaerobic glycolysis. 34 The stability ofV02 max can be explained by the structural changes in skeletal muscle tissue after high intensity training. 35 Indeed, it has been shown that this structural adaptation is clearly marked by a decrease of the volume density of mitochondria which is counterbalanced by a total muscle volume increase. Because of the lack of studies carried out on high intensity training, biochemical studies provide one of the few ways liable to explain its effects upon VTh, leading to an understanding of high intensity training metabolic consequences. Previous studies have shown that exercise of maximal intensity and 30-s duration (which corresponds approximately to the sprint time performed by the children during the high intensity training) requires essentially an anaerobic glycolysis contribution.36-38 Moreover, when several bouts of exercise are performed, an inhibition ofglycogenolysis occurs at the third and fourth exercise bouts. 38 Therefore, the muscle oxidative capacity is not solicited, and this can explain the moderate decrease of VTh, which would represent the muscle oxidative capacity.39,4O This assumption supports the findings of previous studies41 ,42 which have reported that a close correlation exists between VTh and the percentage of slow-twitch fibers. Moreover, it could be assumed that, above a training intensity which corresponds approximately to 85 percent ofV02 max, increasing the training load decreases the oxidative capacity of slow-twitch fibers. 43 This kind of training leads to a major problem because any decrease of VTh ,viII induce an exaggerated hyperventilation at submaximal exercise intensities, which represents for the asthmatic children, a Individualized Aerobic and High Intensity Training in Asthmatic Children (Varray at 81)
very bad long-term adaptation for the same reasons previously discussed. The results concerning the cardiovascular adaptations after high intensity training (Fig 3) show that the maximal heart rate increased in the training group, but the maximal O 2 pulse decreased slightly. These data suggest the following: 28 (1) a decrease of stroke volume mediated by decreasing myocardial contractibility; (2) a decrease of arteriovenous O2 difference, with the data concerning the reduction of muscle oxidative capacity and the decrease ofVTh supporting this hypothesis; or (3) a combination of the above. In the absence of direct measurement of each of these possibilities, any explanation remains speculative. In conclusion, our study shows that when intensity training is individualized, it is possible to markedly increase the cardiorespiratory fitness of asthmatic children by aerobic training. Subsequent high intensity training does not further contribute to increased fitness. It appears that the intensity of training is of great importance in regard to the development of cardiorespiratory fitness because it seems to involve important consequences upon the asthmatic-exercise "interface," since the asthmatics' major problem is to avoid any excessive hyperventilation during exercise. Furthermore, this study suggests that the control of VTh could be a good index for evaluating the correct compatibility of the subjects capacities and the trainFinall}; further studies involving other ing intensi~ intensities should be carried out in order to determine the optimal training intensity for asthmatic subjects. ACKNOWLEDGMENTS: The writers thank Pr F.B. Michel and his respiratory disease department for the recruitment of asthmatic children and his work concerning exercise readaptation in asthmatics.
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Plan to Attend ACCP's
57th Annual Scientific Assembly San Francisco November 4-8, 1991
588
Individualized AerobIc and HIgh Inten8Ily Tt'IIinq In AIIhmaIic ChIldren ~
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