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Abstract(s)
Asthma is a chronic inflammatory disorder of the
respiratory airways affecting people of all ages, and
constitutes a serious public health problem
worldwide (6). Such a chronic inflammation is
invariably associated with injury and repair of the
bronchial epithelium known as remodelling (11).
Inflammation, remodelling, and altered neural
control of the airways are responsible for both
recurrent exacerbations of asthma and increasingly
permanent airflow obstruction (11, 29, 34).
Excessive airway narrowing is caused by altered
smooth muscle behaviour, in close interaction with
swelling of the airway walls, parenchyma retractile
forces, and enhanced intraluminal secretions (29,
38). All these functional and structural changes are
associated with the characteristic symptoms of
asthma – cough, chest tightness, and wheezing –and
have a significant impact on patients’ daily lives, on
their families and also on society (1, 24, 29). Recent
epidemiological studies show an increase in the
prevalence of asthma, mainly in industrial countries
(12, 25, 37). The reasons for this increase may
depend on host factors (e.g., genetic disposition) or
on environmental factors like air pollution or contact
with allergens (6, 22, 29).
Physical exercise is probably the most common
trigger for brief episodes of symptoms, and is
assumed to induce airflow limitations in most
asthmatic children and young adults (16, 24, 29, 33).
Exercise-induced asthma (EIA) is defined as an intermittent narrowing of the airways, generally
associated with respiratory symptoms (chest
tightness, cough, wheezing and dyspnoea),
occurring after 3 to 10 minutes of vigorous exercise
with a maximal severity during 5 to 15 minutes after
the end of the exercise (9, 14, 16, 24, 33). The
definitive diagnosis of EIA is confirmed by the
measurement of pre- and post-exercise expiratory
flows documenting either a 15% fall in the forced
expiratory volume in 1 second (FEV1), or a ≥15 to
20% fall in peak expiratory flow (PEF) (9, 24, 29).
Some types of physical exercise have been
associated with the occurrence of bronchial
symptoms and asthma (5, 15, 17). For instance,
demanding activities such as basketball or soccer
could cause more severe attacks than less vigorous
ones such as baseball or jogging (33). The
mechanisms of exercise-induced airflow limitations
seem to be related to changes in the respiratory
mucosa induced by hyperventilation (9, 29). The
heat loss from the airways during exercise, and
possibly its post-exercise rewarming may contribute
to the exercise-induced bronchoconstriction (EIB)
(27). Additionally, the concomitant dehydration
from the respiratory mucosa during exercise leads to
an increased interstitial osmolarity, which may also
contribute to bronchoconstriction (4, 36). So, the
risk of EIB in asthmatically predisposed subjects
seems to be higher with greater ventilation rates and
the cooler and drier the inspired air is (23). The
incidence of EIA in physically demanding coldweather
sports like competitive figure skating and
ice hockey has been found to occur in up to 30 to
35% of the participants (32). In contrast, swimming
is often recommended to asthmatic individuals,
because it improves the functionality of respiratory
muscles and, moreover, it seems to have a
concomitant beneficial effect on the prevalence of
asthma exacerbations (14, 26), supporting the idea
that the risk of EIB would be smaller in warm and
humid environments. This topic, however, remains
controversial since the chlorified water of
swimming pools has been suspected as a potential
trigger factor for some asthmatic patients (7, 8, 20,
21). In fact, the higher asthma incidence observed in
industrialised countries has recently been linked to
the exposition to chloride (7, 8, 30).
Although clinical and epidemiological data suggest
an influence of humidity and temperature of the
inspired air on the bronchial response of asthmatic
subjects during exercise, some of those studies did
not accurately control the intensity of the exercise
(2, 13), raising speculation of whether the
experienced exercise overload was comparable for
all subjects. Additionally, most of the studies did not
include a control group (2, 10, 19, 39), which may
lead to doubts about whether asthma per se has
conditioned the observed results. Moreover, since
the main targeted age group of these studies has been adults (10, 19, 39), any extrapolation to
childhood/adolescence might be questionable
regarding the different lung maturation. Considering
the higher incidence of asthma in youngsters (30)
and the fact that only the works of Amirav and coworkers
(2, 3) have focused on this age group, a
scarcity of scientific data can be identified.
Additionally, since the main environmental trigger
factors, i.e., temperature and humidity, were tested
separately (10, 28, 39) it would be useful to analyse
these two variables simultaneously because of their
synergic effect on water and heat loss by the airways
(31, 33). It also appears important to estimate the
airway responsiveness to exercise within moderate
environmental ranges of temperature and humidity,
trying to avoid extreme temperatures and humidity
conditions used by others (2, 3).
So, the aim of this study was to analyse the
influence of moderate changes in air temperature
and humidity simultaneously on the acute
ventilatory response to exercise in asthmatic
children. To overcome the above referred to
methodological limitations, we used a 15 minute
progressive exercise trial on a cycle ergometer at 3
different workload intensities, and we collected data
related to heart rate, respiratory quotient, minute
ventilation and oxygen uptake in order to ensure that
physiological exercise repercussions were the same
in both environments. The tests were done in a
“normal” climatic environment (in a gymnasium)
and in a hot and humid environment (swimming
pool); for the latter, direct chloride exposition was
avoided.
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Instituto Politécnico do Porto. Escola Superior de Tecnologia da Saúde do Porto