Importance of physical exercise training in asthmatics [see comment].
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Biomedical subjects
Publications and source records attributed to A Varray.
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The occurrence of a late reaction following exercise induced asthma is questionable and its relationship with the non specific bronchial hyperreactivity is poorly known. In this study, nine patients (age 15-21 years) underwent an exercise challenge in order to (a) determine the incidence of immediate and late phase reaction and (b) analyse the modifications of non specific bronchial hyperreactivity. Study design was a follow; day-3: determination of bronchial responsiveness to metacholine; day 0: control day with FEV1 measurements every hour for 11 hours; day 1: exercise challenge followed by a careful observation of change in FEV1; day 2: new determination of bronchial responsiveness to metacholine. An immediate exercise induced bronchial obstruction was observed in 5 patients. A late phase reaction (6th hour) with a fall of FEV1 equal to or more than 20% has been demonstrated in two patients. For the former, the change in FEV1 did not differ from the value of the control day. For the second, the FEV1 changed spontaneously during the control day so that decreases of FEV1 during control and challenge days were parallel. Thus, no late phase reaction were observed (F = 0.46; ns). There was no modification of bronchial responsiveness to metacholine (pre-exercise: 1,784 +/- 1,970 [SD]; post-exercise 1,827 +/- 2,231 micrograms [SD]). The lack of true late phase reaction when the post-exercise change in FEV1 is compared to the one of a control day and the absence of modification of non specific bronchial hyperreactivity weaken the hypothesis of an inflammatory mechanism of exercise induced asthma.
The time-course of heart rate, blood lactate, and ventilatory gas exchange was studied during an incremental exercise test on cycloergometer in order to ascertain whether heart rate deflection occurred at the same load as the second lactate S[La]2) and ventilatory (SV2) thresholds. Twelve moderately trained subjects, 22 to 30 years old, participated in the study. The initial power setting was 30 W for 3 min with successive increases of 30 W every min except at the end of the test where the increase was reduced to 20 and 10 W.min-1. Ventilatory flow (VE), oxygen uptake (VO2), carbon dioxide production (VCO2, ventilatory equivalents of O2 (EO2 = VE/VO2) and CO2 (ECO2 = VE/VCO2), and heart rate (HR) were determined during the last 20 s of every min. Venous blood samples were drawn at the end of each stage of effort and analyzed enzymatically for lactate concentration ([La]). The HR deflection, S[La]2, and SV2 were represented graphically by two investigators using a double blind procedure. Following the method proposed by Conconi et al. 1982, the deflection in HR was considered to begin at the point beyond which the increase in work intensity exceeded the increase in HR and the linearity of the work rate/HR relationship was lost. S[La]2 corresponded to the second breaking point of the lactate time-course curve (onset of blood lactate accumulation) and SV2 was identified at the second breaking point in the increase in VE and ventilatory equivalent for O2 uptake accompanied by a concomitant increase in ventilatory equivalent for CO2 output. We observed that the deflection point in HR was present only in 7 subjects. The work load, VO2, HR, and [La] levels at which heart rate departed from linearity did not differ significantly from those determined with S[La]2 ans SV2. The VO2 and HR values at HR deflection point were significantly correlated with those measured at S[La]2 and SV2. It is concluded that deflection in heart rate does not always occur, and when it does, it coincides with the second lactate and ventilatory gas exchange thresholds. It can thus be used for the determination of optimal intensity for individualized aerobic training.
Despite current discussions promoting physical and sports activities in asthmatics, no studies have yet been done on the possible pathophysiological justifications for rehabilitation by sports programs. Consequently asthmatics are retrained in an empirical fashion and the assessment of these programs is subjective. The aim of this article is thus to review the different studies concerning the adjustment of asthmatics to muscular exercise and to deduce from these what could or should be the pathophysiological objectives of reconditioning protocols. The principal ideas which emerge from this study derive from three fundamental facts: 1) the training of asthmatics should be based on an individual approach since clinical severity leads to very unequal adaptations during muscular exercise; 2) it is advisable to strive against the declining physical fitness of the asthmatics, which is responsible for the accelerated functional deterioration, disturbances of psychomotor development and an increased risk of exercise-induce asthma; 3) the decrease of excessive exercise hyperventilation is, from the evidence, the greatest priority among the pathophysiological objectives, because hyperventilation is a principal cause implicated in the disturbance of cardiovascular adjustments to effort by heart-lung interaction.
The aim of this study was to investigate the effect of growth on ventilation and breathing pattern during maximal exercise oxygen consumption (VO2max) and their relationships with anthropometric characteristics. Seventy six untrained schoolboys, aged 10.5-15.5 years, participated in this study. Anthropometric measurements made included body mass, height, armspan, lean body mass, and body surface area. During an incremental exercise test, maximal ventilation (VEmax), tidal volume (VTmax), breathing frequency (fmax), inspiratory and expiratory times (tImax and tEmax), total duration of respiratory cycle (tTOTmax), mean inspiratory flow (VT/tImax), and inspiration fraction (tI/tTOTmax) were measured at VO2max. A power function was calculated between anthropometric characteristics and ventilatory variables to determine the allometric constants. The results showed firstly, that VEmax, VTmax, tImax, tEmax, tTOTmax, and VT/tImax increased with age and anthropometric characteristics (P less than 0.001), fmax decreased (P less than 0.001), and tI/tTOTmax remained constant during growth; secondly that lean body mass explained the greatest percentage of variance of VEmax (62.1%), VTmax (76.8%), and VT/tImax (70.6%), while anthropometric characteristics explained a slight percentage of variance of fmax and timing; and thirdly that VEmax, VTmax, and VT/tImax normalized by lean body mass did not change significantly with age. We concluded that at VO2max there were marked changes in ventilation and breathing pattern with growth. The changes in VEmax, VTmax, and VT/tImax were strongly related to the changes in lean body mass.
This software program adds two very interesting data to the usual results of exercise testing: an estimation of cardiac output according to the most recent validations and a reliable estimation of alveolar ventilation. The main advantage of this additional ventilatory and cardiovascular information using the same data: end-tidal PCO2.
The diagnosis of smoking-related chronic obstructive pulmonary disease (COPD) is often made too late. Could the study of breathing pattern during exercise testing help in earlier detection. In order to test this hypothesis, we studied 34 asymptomatic smokers (S) compared to 55 nonsmoking controls (NS). The subjects, divided into 3 age groups (30-60 yr), were comparable in terms of anthropometric and spirometric characteristics. The smokers from 30-50 yr had a lower VO2max than the controls (p less than 0.01) whereas the older smokers (50-60 yr) had a VO2max comparable to that of the controls. The study of breathing pattern indicated rapid, shallow breathing by all smokers. Thus exercise testing, and the abnormalities observed in breathing pattern, would seem to help in early detection of COPD in asymptomatic smokers.
There have been few works studying the effects of training in asthmatics and there does not yet exist any study utilising the idea of the individualization of training. This is why the aim of this study was to assess the value of the effects of individualised aerobic training on cardio-respiratory aptitude in the asthmatic child. This study was carried out on two populations of asthmatics, swimmers and non-swimmers matched for age, height, degree of bronchial obstruction during a remission and baseline of physical fitness. Each child in the swimming group was trained to a metabolic level corresponding to the ventilatory threshold. After a period of 3 months a second cardio-respiratory evaluation was carried out. A clear cut improvement (20%) of VO2 max was observed as well as a proportional elevation of the ventilatory threshold in the swimming group. The VE max, the VT max, the VT/Timax, the FC max and the maximal oxygen uptake were also recorded. On the other hand aerobic training seems to be without effect on resting pulmonary function, even if the clinical state of the children improved. In conclusion this study shows that aerobic training closely adapted to the level of each child, obtains an important and rapid gain in cardio-respiratory fitness which leads to a better exercise adaptation. In addition the progression of the ventilatory threshold implies an increased capacity for work without the appearance of hyperventilation. This enables an understanding of how aerobic training is generally accompanied in the asthmatic with a better respiratory comfort and argues in favour of the perfect efficacy of this type of reconditioning in the re-adaptation to effort in these patients.