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Research Article
Prevalence of Asthma among Norwegian Elite Athletes
Helene Støle Melsom ,
1
,
2
Anders Randa ,
3
Jonny Hisdal ,
1
,
2
Julie Sørbø Stang ,
3
and Trine Stensrud
3
1
Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway
2
Department of Vascular Surgery, Oslo University Hospital, Oslo, Norway
3
Department of Sports Medicine, Norwegian School of Sport Sciences, Oslo, Norway
Correspondence should be addressed to Helene Støle Melsom; h.s.melsom@studmed.uio.no
Received 14 March 2022; Accepted 14 June 2022; Published 6 July 2022
Academic Editor: Jose A. L. Calbet
Copyright ©2022 Helene Støle Melsom et al. is is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
Objective. Asthma is a common problem among elite athletes and represents a health risk interfering with the athlete’s per-
formance status. is study aimed to evaluate the asthma prevalence among Norwegian summer and winter elite athletes and
asthma prevalence across sport categories. We also aimed to examine whether bronchial hyperresponsiveness (BHR), lung
function, fraction of exhaled nitric oxide (FE
NO
), and allergy status differed between asthmatic and non-asthmatic elite athletes.
Methods. Norwegian athletes qualifying for the Beijing Olympic Summer Games 2008 (n�80) and the Vancouver Olympic
Winter Games 2010 (n�55) were included. e athletes underwent clinical respiratory examination including lung function
measurement, methacholine bronchial challenge for assessment of BHR, FE
NO
, and skin prick testing. Asthma was diagnosed
based on respiratory symptoms and clinical examination including objective measurements. Results. Asthma was more prevalent
among winter athletes (50%) than summer athletes (20%). irty-three (52%) endurance athletes, 3 (6%) team sport athletes, and 7
(33%) technical sport athletes had medically diagnosed asthma. Significantly lower lung function (p<0.001) and higher
prevalence of severe BHR (p<0.001) were found in asthmatic athletes compared with non-asthmatic athletes. Conclusion. Asthma
is common among Norwegian elite athletes, with winter and endurance athletes showing the highest prevalence. Asthmatic
athletes were characterized by lower lung function and more severe BHR compared with non-asthmatic counterparts. e high
prevalence among winter and endurance athletes demonstrates a need for increased attention to prevent and reduce the
prevalence of asthma among those athletes.
1. Introduction
A diagnosis of asthma is more frequent among elite en-
durance athletes than both the general population and
athletes within other types of sport [1, 2]. Asthma is char-
acterized by chronic airway inflammation and bronchial
hyperresponsiveness (BHR), which increased sensitivity to a
wide variety of airway narrowing stimuli [1]. e reported
prevalence varies between studies [3–6] and type of sport
[4, 7]. e diagnosis of asthma should be based on objective
measurements, in addition to symptoms and clinical ex-
amination [1]. e reported asthma prevalence among
athletes varies with the criteria used for diagnosis: ques-
tionnaires, anti-doping records, spirometry, or bronchial
provocation challenges [8]. However, asthma is a significant
problem among elite athletes and represents both a health
risk and can interfere with the athlete’s performance status
[9].
Endurance athletes may be at greater risk of developing
asthma, possibly due to higher ventilation rates over pro-
longed periods of time, combined with unfavorable sport-
specific environmental conditions, such as cold and dry air,
indoor swimming pools, and polluted air [1, 10]. Some
investigators also suggest a difference between summer and
winter sports, with the highest asthma prevalence observed
in winter sports [7]. Asthma prevalence in Olympic summer
and winter athletes has been compared in a small number of
questionnaire-based studies [4, 11, 12]. Weiler and Ryan
Hindawi
Translational Sports Medicine
Volume 2022, Article ID 3887471, 10 pages
https://doi.org/10.1155/2022/3887471
found that more winter athletes than summer athletes
suffered from asthma [11, 12]. is contrasts with the study
by Selge et al. [4] of German athletes competing in 2008
Beijing Olympic Summer Games and 2010 Vancouver
Olympic Winter Games. ey found no difference in asthma
prevalence between winter and summer athletes [4].
However, they observed that type of sport was associated
with the asthma prevalence.
Athletes seem to be more affected by the asthma phe-
notype called sports asthma. is asthma phenotype is
characterized by BHR to exercise that usually occurs after the
cessation of a short period of hyperpnea and lasts for about
30–90 minutes when not treated [1, 13]. Characteristics of
sports asthma include late onset (in early adulthood) and
symptoms such as cough, phlegm, and heavy breathing in
response to physical activity [14, 15].
e scientific interest of exercise-induced bronchocon-
striction (EIB) can be dated back to the 1960s, when Jones
and coworkers focused on physiologic responses to exercise
in asthmatic children [16]. Since then, research on asthma
prevalence in athletes has grown, as well as research on the
mechanisms of the development of the phenotype: sports
asthma [8]. Carlsen [17] suggested that the mechanisms of
sports asthma are a combination of respiratory epithelial
damage caused by regularly repeated bouts of increased
ventilation in cold and polluted air and increased para-
sympathetic tone [17]. Together, this may result in bronchial
hyperresponsiveness and asthma symptoms [17].
As asthma is a significant health problem among elite
athletes, the need for greater knowledge about athletes’
respiratory health is warranted. Many studies on asthma
prevalence in athletes are based on questionnaires [1], which
is not in accordance with current guidelines from Global
Initiative of Asthma (GINA) or recommendations from the
International Olympic Committee—Medical Commission
(IOC-MC) on diagnosing asthma [18]. Hence, the primary
aim of this study was to evaluate the prevalence of asthma in
Norwegian summer and winter elite athletes and across
sport categories (endurance, team sport, and technical sport)
using objective measurements in addition to clinical ex-
amination. Secondly, we aimed to assess whether BHR,
fraction of exhaled nitric oxide (FE
NO
), allergy, and lung
function differed between asthmatic and non-asthmatic elite
athletes.
2. Methods
e study was carried out as part of a multicenter study: “e
Asthma and Allergy in Olympians Study.” is was con-
ducted within the framework of the Global Allergy and
Asthma European Network (GA
2
LEN) across nine Euro-
pean countries. is study includes cross-sectional data of
135 Norwegian athletes aiming to qualify for the Beijing
Olympic Summer Games 2008 and the Vancouver Olympic
Winter Games 2010 within different sports. All participants
underwent clinical respiratory examination including lung
function measurement, measurement of FE
NO
, allergy as-
sessment with a skin prick test (SPT), and a methacholine
bronchial challenge (PD
20met
) for the assessment of
bronchial hyperresponsiveness (BHR). e clinical exami-
nation was performed in one day at the respiratory labo-
ratory at the Norwegian School of Sport Sciences by the same
doctor and respiratory physiologist.
Asthma medication was withheld prior to testing
according to current guidelines given by European Respi-
ratory Society (ERS) [19]. Inhaled short-acting beta-2 ago-
nists were withheld for 8 h prior to testing, inhaled long-
acting beta-2 agonists, theophylline, and leukotriene an-
tagonists for the preceding 72 h, antihistamines for 7 days,
and orally administered glucocorticoids for the preceding
3 months. On the test day, inhaled glucocorticoids were
withheld and participants were instructed to refrain from
exercise and food or drinks containing nitrate.
2.1. Definitions. Current asthma was defined as a doctor’s
diagnosis of asthma. e diagnosis was set by the doctor at
the Norwegian School of Sport Sciences. is diagnosis was
based on clinical examination, reported symptoms, lung
function measurements, and bronchial hyperresponsiveness
(BHR) to methacholine (PD
20met
). PD
20met
was defined as
the dose of methacholine causing a 20% reduction in forced
expiratory volume in one second (FEV
1
). Bronchial
hyperresponsiveness was defined as PD
20met
≤8μmol. e
diagnosis could also be verified by demonstration of exer-
cise-induced bronchoconstriction (EIB test) or an increase
in forced expiratory volume in one second (FEV
1
) of ≥12%
after administration of short-acting beta-agonists (SABAs)
or short-acting muscarinergic agonists (SAMAs).
2.2. Design and Subjects. All subjects gave their written
informed consent for participation. e study was approved
by the Regional Committee for Medical and Health Research
Ethics South East Norway (REC; Ref: S-07468a).
In this study, 80 Norwegian summer athletes qualifying
for the 2008 Olympic Summer Games in Beijing and 55
Norwegian winter athletes qualifying for the 2010 Olympic
Winter Games in Vancouver are included. Characteristics
are presented in Table 1. All athletes were categorized into
endurance, technical and team sports, and Summer or
Winter Games. Endurance sports include swimming, cy-
cling, rowing/paddling, long-distance running, cross-
country skiing, biathlon, speed skating, and Nordic com-
bined. Both males and females were included in all en-
durance sports except for Nordic combined where only
males are included. Only 21 athletes are included in the
technical sports group; therefore, types of sports or number
of males/females are not reported to maintain anonymity.
e team sports group consists of summer athletes only.
2.3. Lung Function. Lung function was measured by max-
imal expiratory flow-volume curves (MasterScreen Pneumo
J¨
ager ®, W¨
urzburg, Germany) according to current guide-
lines [20] and recorded as FEV
1
, forced vital capacity (FVC),
and mean expiratory flow between 25 and 75% of FVC
(MEF
25–75
). Predicted values are according to the last
updated reference values from Global Lung Function
2Translational Sports Medicine
Initiative (GLI 2012) published by Quanjer et al. [21]. FEV
1
,
FVC, and MEF
25–75
are reported as percentages predicted
and Z-scores. Z-scores less than −1.645 were considered
below the lower limit of normal (LLN).
2.4. Bronchial Hyperresponsiveness. Bronchial hyper-
responsiveness was performed by methacholine bronchial
provocation. Methacholine was delivered by an inspira-
tory-triggered nebulizer aerosol provocation system (J¨
ager
W¨
urzburg, Germany). It was inhaled in doubling doses
from a starting dose of 0.25 μmol until FEV
1
decreased ≥20% from baseline or if the maximal dose of
methacholine (24.48 μmol or 4.8 mg) was reached, as
measured after inhaled nebulized isotonic saline. e dose
causing 20% reduction in FEV
1
(PD
20met
) was determined
by linear interpolation on the semi-logarithmic dose-re-
sponse curve. A subject was considered to have BHR if their
PD
20met
was ≤8μmol (1.6 mg).
2.5. Expired Nitric Oxide. FE
NO
was measured with a single-
breath technique at a constant expiratory flow rate of 50 mL/
s in accordance with the manufacturer’s instructions (Eco
Medics AG, D¨
urnten, Switzerland) and American oracic
Society (ATS)/ETS Guidelines [22]. Mean values of three
measurements with <10% difference were used in the
analysis.
2.6. Skin Prick Test. Local allergic sensitivity was assessed
according to Nordic guidelines [23] with the following al-
lergens: moulds (Cladosporium herbarum), house dust
mites (Dermatophagoides pteronyssinus), dog dander, cat
dander, birch pollen, grass pollen (Timothy), mug worth
pollen, milk, shrimp, and hen’s egg white (Soluprick, ALK,
Copenhagen, Denmark). A positive response was defined if
the weal was at least ½ of the histamine (10mg·mL
−1
) re-
action or if the average weal exceeded 3 mm.
2.7. Analyses. Continuous data are presented as means with
standard deviation (SD) or 95% confidence intervals (CIs)
after the Shapiro–Wilk test for normality unless otherwise
stated. Categorical variables are presented as counts (n) with
percentages (%). One-way analysis of variance (ANOVA)
with the Bonferroni post hoc tests or, in the case of non-
parametric data, the Kruskal–Wallis tests were used to
compare the three groups. e Mann–Whitney Utest for
independent samples was used to compare two groups of
nonnormally distributed data. Chi-square tests were used to
assess group differences of categorical variables. Sex dif-
ferences for asthma and allergy prevalence, as well as BHR,
were only tested for all included athletes and within the
groups of summer and winter athletes. Due to small sample
size, we could not test sex differences among the athletes in
the sport categories. pvalues below 0.05 were considered
significant. Statistical analyses were performed using IBM
SPSS Statistics version 26 (SPSS Inc., Chicago, IL, USA) and
SigmaPlot 14.5 (Systat Software, San Jose, CA).
3. Results
3.1. Study Population. In total, 135 athletes were included in
the study, 80 (\= 62_= 18) summer athletes and 55
(\= 20_= 35) winter athletes. Characteristics are shown in
Table 1.
3.2. Clinical Measurements. Of the 135 Norwegian athletes,
16 of 80 summer athletes (20%) and 27 of 55 winter athletes
(50%) had medically diagnosed asthma (p<0.001, Table 2).
irty-three (52%) endurance, 3 (6%) team sport, and 7
(33%) technical sport athletes had medically diagnosed
asthma (p<0.001, Table 2). We observed significantly
higher prevalence of asthma (45%) among males compared
with females (23%) (p�0.008) for all included athletes and
among males (39%) compared with females (15%) com-
peting in summer Olympics (p�0.041). However, no sex
difference was seen among the winter athletes, males (49%)
and females (53%), respectively (p�1.000, Figure 1).
Within the endurance group, 20 of 41 males (49%) and 13 of
22 females (59%) had a diagnosed asthma (Figure 1).
Allergy status did not differ between summer and winter
athletes (p�0.166), nor when dividing the athletes into
different sport categories (p�0.403, Table 2). Allergy
prevalence was the same in athletes with asthma (n�18;
41.9%) as in athletes without asthma (n�34; 39.1%,
p�0.761, Table 3). No sex difference was seen for allergy
prevalence for all included athletes (p�0.097), either
among summer athletes (p�0.557) or among winter ath-
letes (p�0.390).
3.3. Lung Function. Summer athletes displayed significantly
better lung function (FEV
1
, FVC, MEF
25–75
, FEV
1
/FVC)
both as percentage of predicted parameters and higher Z-
Table 1: Characteristics of elite athletes, divided into summer and winter athletes and across sport categories. Results are presented as mean
and standard deviation (SD) and sex differences as number and percentage (%).
Variables
Competition season Sport categories
Summer (n�80)
mean (SD)
Winter (n�55)
mean (SD) pvalue Endurance (n�64)
mean (SD)
Team sport (n�50)
mean (SD)
Technical (n�21)
mean (SD)
p
value
Age (years) 27 (4.5) 26 (6.1) 0.564 26 (5.0) 27 (4.3) 30 (6.8) 0.016
Height
(cm) 176 (8.3) 178 (8.2) 0.953 179 (8.2) 175 (7.8) 176 (8.1) 0.014
Weight (kg) 71 (10.7) 74 (11.4) 0.391 74 (10.8) 69 (8.4) 73 (15.8) 0.054
Sex (\), N
(%) 62 (78) 20 (36) <0.001∗23 (36) 48 (96) 11 (52) <0.001
Translational Sports Medicine 3
scores than winter athletes (Table 4). When comparing the
different sport categories, lung function differed significantly
between groups (Figure 2), both in % of predicted and in Z-
scores (p<0.001, Table 3).
Bronchial hyperresponsiveness was less prevalent in
summer athletes than in winter athletes ((n�23; 29%) vs 29;
53%, p�0.005, Table 2). Furthermore, BHR differed
significantly between sport categories (p�0.041), with the
highest prevalence in endurance athletes (n�34; 53%)
compared with team sport (n�9; 18%) and athletes in
technical sports (n�10; 50%; Table 2). We did not observe
sex differences for BHR (PD
20met
≤8μmol) among all in-
cluded athletes (p�0.106), either among summer athletes
(p�0.375) or among winter athletes (p�1.000).
Table 2: Prevalence of medically diagnosed asthma, bronchial hyperresponsiveness (BHR), and allergy defined as one or more positive skin
prick tests (SPT) among elite athletes, divided into summer and winter athletes and across sport categories.
Summer (n�80) Winter (n�55) pvalue Endurance (n�64) Team sport (n�50) Technical (n�21) pvalue
Asthma N(%) 16 (20) 27 (50) <0.001 33 (52) 3 (6) 7 (33) <0.001
#
BHR N(%) 23 (29) 29 (53) 0.005 34 (53) 9 (18) 9 (43) 0.041
∗Allergy N(%) 27 (35) 25 (47) 0.166 26 (41) 16 (33) 10 (50) 0.403
BHR is defined as PD
20met
≤8μmol. PD
20met
: provocation dose of methacholine causing 20% reduction in forced expiratory volume in the first second of
expiration.
#
: for doctor-diagnosed asthma, 54 winter athletes and 63 endurance athletes are included; ∗: for allergy assessment, 77 summer athletes, 53 winter
athletes, 62 endurance athletes, 48 team sport athletes, and 20 technical sport athletes are included.
60
50
40
30
*
*
20
Asthma prevalence (%)
10
0
Total Summer
Males
Females
Winter Endurance Team
sport
Technical
sport
Figure 1: Differences in asthma prevalence between men and women, divided into summer and winter athletes, and by sport category.
Table 3: Bronchial hyperresponsiveness measured as PD20met <8μmol, fractional expired nitric oxide FENO >25 ppb, allergy and lung
function variables presented as Z-score, and lower limit of normal (LLN) among elite athletes with doctor-diagnosed asthma and elite
athletes without asthma.
Variables Current asthma pvalue
Yes (n�43) No (n�90; 87; 91)
#
PD
20met
<8μmol, n(%) 37 (86) 14 (15) <0.001∗
FE
NO
>25 ppb, n(%) 11 (26) 11 (12) 0.079
Allergy, n(%) 18 (42) 34 (39) 0.850
z-FEV
1,
mean (95% CI) −0.50 (−0.78, −0.22) 0.42 (0.25, 0.62) <0.001∗
z-FVC, mean (95% CI) 0.34 (0.04, 0.63) 0.50 (0.35, 0.68) 0.288
z-MEF
25–75,
mean (95% CI) −0.53 (−0.85, −0.20) 0.45 (0.25, 0.64) <0.001∗
z-FEV
1
/FVC, mean (95% CI) −1.24 (−1.50, −0.97) −0.21 (−0.38, −0.03) <0.001∗
LLN FEV
1
n(%) 4 (9) 0 (0) 0.010∗
LLN FVC n(%) 0 (0) 0 (0) ns
LLN MEF
25–75
n(%) 5 (12) 0 (0) 0.003∗
LLN FEV
1
/FVC n(%) 13 (30) 3 (3) <0.001∗
PD
20met
�provocation dose of methacholine causing 20% reduction in forced expiratory volume in the first second of expiration; allergy is defined as one or
more positive skin prick tests; FEV
1
�forced expiratory volume in one second; FVC �forced vital capacity; MEF
25–75
�mean expiratory flow between 25 and
75% of FVC; LLN �lower level of normal defined as Z-score <−1.645.
#
�for the no asthma group; n�89 for FE
NO
,n�87 for allergy, and n�91 for LLN and
lung function values ns �not significant ∗�significant difference between asthmatic and non-asthmatic athletes.
4Translational Sports Medicine
Table 4: Lung function and fractional expired nitric oxide (FE
NO
) among elite athletes, divided into summer and winter athletes and across sport categories.
Summer (n�80) mean
(95% CI)
Winter (n�55) mean
(95% CI) pvalue Endurance (n�64) mean
(95% CI)
Team sport (n�50) mean
(95% CI)
Technical (n�21) mean
(95% CI) pvalue
FEV
1
(% pred) 105 (103, 108) 96 (93, 99) <0.001 99 (96, 101) 107 (104, 110) 96 (90, 102) <0.001
z-FEV
1
0.45 (0.26, 0.65) −0.33 (−0.58, −0.08) <0.001 −0.11 (−0.33, 0.11) 0.63 (0.37, 0.38) −0.33 (−0.80, 0.15) <0.001
LLN (n, %) 0 (0%) 4 (7.4%) 0.026 2 (3.2%) 0 (0%) 2 (9.5%) <0.001
FVC
(% pred) 108 (106, 111) 102 (100, 105) 0.001 106 (103, 108) 108 (106, 111) 99 (95, 103) <0.001
z-FVC 0.66 (0.47, 0.84) 0.19 (−0.0, 0.4) 0.002 0.49 (0.29, 0.70) 0.66 (0.43, 0.89) −0.11 (−0.46, 0.24) <0.001
LLN (n, %) 0 (0%) 0 (0%) ns 0 (0%) 0 (0%) 0 (0%) ns
MEF
25–75
(% pred) 108 (103, 113) 97 (90, 104) 0.005 96 (90, 102) 114 (108, 121) 101 (90, 111) <0.001
z-MEF
25–75
0.35 (0.12, 0.58) −0.17 (−0.46, 0.11) 0.004 −0.21 (−0.45, 0.36) 0.58 (0.30, 0.86) 0.10 (−0.46, 0.67) <0.001
LLN (n, %) 1 (1.3%) 4 (7.4%) 0.158 4 (6.3%) 0 (0%) 1 (4.8%) <0.001
FEV
1
/
FVC
(% pred) 97 (95, 98) 93 (91, 95) 0.007 93 (91, 94) 98 (96, 100) 96 (93, 100) <0.001
z-FEV
1
/
FVC
−0.37 (−0.57, −0.17) −0.81 (−1.07, −0.55) 0,005 −0.89 (−1.12, −0.67) −0.16 (−0.41, 0.09) −0.45 (−0.85, −0.05) <0.001
LLN (n, %) 5 (6.3%) 10 (18.5%) 0.027 11 (17.5%) 2 (4.0%) 2 (9.5%) 0.001
FE
NO
(ppb)∗14.2 (10.5) 13.6 (8.7) 0.933 13.7 (9.6) 14.2 (9.0) 12.8 (12.4) 0.867
∗median (interquartile range); ns �not significant; FEV
1
�forced expiratory volume in one second; FVC �forced vital capacity; MEF
25–75
�mean expiratory flow between 25 and 75% of FVC; LLN �lower limit of
normal; ppb �parts per billion.
Translational Sports Medicine 5
ere was no difference in FE
NO
between summer and
winter athletes (p�0.933), nor between the different sport
categories (p�0.867, Table 3).
4. Discussion
In this study, we assessed the prevalence of asthma among
Norwegian elite winter and summer athletes using stan-
dardized protocols. Our main finding is that asthma is more
prevalent in Norwegian elite winter athletes (50%) than in
summer athletes (20%), which is considerably higher than in
the general population (8–10% in adolescents) [18, 24]. In
addition, the characteristics of asthmatic elite athletes in-
cluded more severe BHR and reduced lung function com-
pared with non-asthmatic elite athletes.
We found asthma to be less prevalent among Norwegian
elite summer athletes than among their winter counterparts.
is is in line with the findings from two studies by Weiler
and Ryan, where they studied asthma prevalence in 699
summer and 196 winter athletes [11, 12]. ey found asthma
to be less prevalent among US summer athletes during the
1996 Olympic summer games than among US winter ath-
letes during the 1998 Olympic Winter Games. In these
studies, the prevalence was found to be 15% among summer
athletes and 22% among winter athletes, lower than that
found in our study (20% and 50%, respectively). Although
the results from our study and the studies by Weiler et al. are
partly in agreement, the studies by Weiler et al. were
questionnaire-based. A strength of our work and possible
reason for this discrepancy may lie in our data that are based
on objective clinical measurements.
In contrast, a study by Selge et al., examining German
Olympic summer (n�283) and winter (n�265) athletes,
examined the prevalence of medically diagnosed asthma [4].
ey found no association between asthma prevalence and
competition season (17.1% vs 12.1%) [4], which conflicts
with our results and the study by Weiler et al. ese findings
might reflect that the studies are based on differing methods
and sample sizes. However, it is remarkable that we found
the asthma prevalence to be as high as 20% in the Norwegian
summer athletes and 50% in the winter athletes, while results
from the other studies show a considerably lower prevalence.
ns
ns
P<0.001*
130
120
110
100
FEV1 (% of predicted)
90
80
0
Endurance Team sport Technical sport
(a)
ns
ns
P<0.001*
130
120
110
100
FVC (% of predicted)
90
80
0
Endurance Team sport Technical sport
(b)
P<0.001*
ns
ns
130
120
110
100
FEV1/FVC (% of predicted)
90
80
0
Endurance Team sport Technical sport
Sport category
(c)
P<0.001*
ns
ns
130
120
110
100
FEV1/FVC (% of predicted)
90
80
0
Endurance Team sport
Sport category
Technical sport
(d)
Figure 2: Lung function, forced expiratory volume in one second (FEV
1
), forced vital capacity (FVC), mean expiratory flow between 25 and
75% of FVC (MEF
25–75
), and FEV
1
/FVC in elite athletes across sport categories. ns �not significant different (p>0.05); FEV1 �forced
expiratory volume in one second; FVC �forced vital capacity; MEF25-75 �mean expiratory flow between 25 and 75% of FVC.
6Translational Sports Medicine
Winter athletes exercise and compete in cold and dry air,
which might be harmful to the airways [25]. However, there
are also studies demonstrating a high asthma prevalence in
summer athletes [2, 12], with swimming, long-distance
running, and road cycling being examples of high-preva-
lence sports [14, 26, 27].
When dividing the sports into different categories
depending on the ventilation rate during competition, we
found that sports with high ventilation rates (endurance
sports) have a higher prevalence of asthma compared with
technical sports and team sports. is is in line with previous
studies [4, 10, 28]. Results from this study show that en-
durance athletes are at increased risk of developing asthma.
Results from previous studies show that asthma is a problem
among swimmers, as well as cyclists, long-distance runners,
and cross-country skiers [3, 5, 6, 27, 29]. Bougault et al.
studied the airways of 32 swimmers and 32 cold air athletes
(11 speed skaters, 16 cross-country skiers, and 5 biathletes)
[26]. Airway hyperresponsiveness was found in 69% of the
swimmers and 28% of the cold air athletes [26]. ese results
indicate that endurance athletes in both summer sports and
winter sports are at increased risk of developing asthma, due
to unfavorable environmental conditions. Winter athletes
are exposed to large amounts of cold air, summer athletes to
allergens, and swimmers to chlorine and its derivatives [30].
us, endurance athletes are exposed to various factors that
affect air quality and contribute to the development of
asthma.
We found a significantly higher prevalence of asthma in
males compared with females competing in the summer
Olympics, but not in the winter Olympics (Figure 2). No
difference was observed for allergy prevalence and BHR
between sexes. Langdeau et al. [31] reported that BHR,
assessed with methacholine challenge, was significantly
higher in female athletes compared with male athletes and
that allergy assessed by one or more positive SPT was more
prevalent among males. However, physician-diagnosed
asthma (self-reported) was similar between sexes [31]. is
is not in accordance with our results and could probably be
explained by the large female ball game group participating
in the summer Olympics. ey were least affected with
asthma, BHR, and allergy (15%, 26%, and 33%, respec-
tively), compared with the males (39%, 39%, and 44%,
respectively). Due to the small sample size in the sport
groups, we cannot test for sex differences and can only
suggest that it seems like asthma prevalence that is similar
between sexes (Figure 1).
During exercise, ventilation increases considerably,
sometimes reaching more than 200 L/min [32]. Ventilation
at these levels in cold, dry, and polluted air exposes athlete’s
airways to frequent unfavorable conditions over time
[27, 30]. Increased ventilation also causes heat and water loss
from the airway epithelium due to insufficient warming and
humidification of the inhaled air. Insufficient warming and
humidification result in heat transfer from the mucosa into
the inspired, cold air, which causes a vasoconstriction of the
microvasculature within the airway. is is followed by a
subsequent rebound hyperemia after exercise when the
airway rewarms, which results in vascular leakage and edema
resulting in airway narrowing [33]. e loss of water leads to
a change in airway osmolarity that initiates epithelial cell and
mast cell activation, leading to release of inflammatory
mediators in the airways that cause bronchoconstriction
[34, 35]. Reduced warming and humidification of inspired
air happen when switching from nasal breathing to mouth
breathing when ventilation levels reach about 30 L/min
[27, 36]. e shift from nasal breathing to mouth breathing
also leads to incomplete filtering of the air reaching the lower
airways [27]. e combination of insufficient air warming
and less air causes airway epithelium damage, and thus
contribute to the development of asthma [37].
Despite the difference in asthma prevalence and lung
function between summer and winter athletes, and between
the sport categories, we did not observe any significant
difference in FE
NO
between those with medically diagnosed
asthma or between the sport categories. FE
NO
is among the
biomarkers used to assess airway inflammation. However,
the evidence is divergent. High levels of FE
NO
do not
necessarily reflect the severity of asthma or asthma control/
lung function parameters [38], especially in relation to sports
asthma [14]. is is in line with results from a meta-analysis
by M¨
aki-Heikkila et al., where no difference was found in
FE
NO
and inflammatory markers in induced sputum be-
tween the asthmatic skiers and healthy controls [39]. Neither
was FE
NO
different between skiers and healthy controls and
was lower in skiers than in asthmatic controls [39]. ese
results suggest that the distribution of inflammatory
endotypes may differ between skiers and nonskiers with
asthma. Furthermore, results indicate that eosinophilic in-
flammation may not be as prevalent in skiers with asthma
and that skiing even in the absence of asthma may trigger
non-eosinophilic inflammation. However, the low levels of
FE
NO
observed in this study support the theory that sports
asthma has a different pathology to atopic asthma. is may
indicate that the gold standard treatment with ICS according
to GINA is not optimal for sports asthma. However, more
research on the relationships between asthma phenotypes,
airway inflammation, and treatment of sport asthma is
needed. Even if FE
NO
is not expected to be elevated in
athletes with asthma, it could be used as a complementary
tool to avoid unnecessary increases in anti-inflammatory
medication. We found no difference in allergy prevalence
across the groups, nor between asthmatic athletes and non-
asthmatic athletes. ese results further support the theory
that sports asthma is driven by other factors than allergy
[14, 17], such as increased parasympathetic activity [40].
When dividing all athletes into asthmatic and non-
asthmatic groups, we found baseline lung function to be
significantly lower in asthmatic athletes compared with non-
asthmatic athletes.
All groups’ mean lung function was within normal
range, with summer athletes and team sport athletes having
the highest lung function. is is in line with previous
studies that have shown high lung volumes and high airflow
rates in swimmers [41, 42]. Our results also suggest that team
sport athletes have higher lung function. In this study, all
team athletes were ball game players and almost all were
female. Rosser-Stanford et al. have similarly suggested better
Translational Sports Medicine 7
than average lung function in this group [42]. Both swim-
mers and team sport players represent summer athletes,
which may partly explain why summer athletes have higher
lung function than winter athletes.
Particular strengths of this study were the use of ob-
jective measures of lung function, BHR, and allergy testing
to diagnose asthma in both summer and winter top-level
athletes aiming to qualify for the Olympic games. Fur-
thermore, all measurements were performed by the same
trained personnel. Nevertheless, the results should be
interpreted with some considerations in mind. All team
sport athletes were ball game players and almost only
women; therefore, our results may be affected with the
inclusion of more male participants. Bronchial hyper-
responsiveness (BHR) was measured using methacholine
provocation test; however, eucapnic voluntary hyperpnea
(EVH) can be considered the gold standard [43]. e cross-
sectional design of this study also limits the possibility to
infer causality. erefore, we emphasize the need for and
importance of prospective studies to examine the devel-
opment of respiratory disorders among athletes. Although
athletes were instructed to avoid inhaled corticosteroids
(ICS) one day prior to testing, the effects of these medica-
tions were potentially still present in those who used them,
which may have influenced our results.
5. Perspectives
is study shows that Norwegian elite athletes have high
asthma prevalence and reduced lung function, particularly
among winter athletes and those involved in endurance
sports. e characteristics of asthmatic elite athletes were
more severe BHR and reduced lung function compared with
non-asthmatic athletes. Allergy prevalence and
FE
NO
>25 ppb did not differ significantly between asthmatic
and non-asthmatic elite athletes. Athletes, medical staff, and
coaches should be aware of the high asthma prevalence
among athletes training in unfavorable environmental
conditions such as cold and dry air, polluted air, and
swimming pools with high concentration of chlorine
combined with poor ventilation. However, it is still unclear
whether asthma, BHR, and reduced lung function are
persistent in elite athletes after retirement from elite sport
and whether respiratory health may be a limitation for
physical activity and exercise after career end. Follow-up
studies are needed to evaluate how athletes’ respiratory
health is over time and whether the asthma diagnosis is
reversible.
Data Availability
e consent given by the participants does not open for
sharing the full data set.
Disclosure
e authors declare that the results are presented clearly,
honestly, and without fabrication, falsification, or inap-
propriate data manipulation.
Conflicts of Interest
e authors have no conflicts of interest or financial ties to
declare.
Acknowledgments
e authors would like to pay a special tribute and thanks to
the late Professor Kai-Haakon Carlsen for initiating and
organizing the multicenter study: “Asthma and Allergy in
Olympians” in 2007. e authors are indeed grateful to all
the athletes who took part in this study and greatly thank
also Md. PhD. Morten Nissen Melsom for input and support
through the whole writing process. e authors greatly
thank Nigel Callender for helping us to improve the written
English of the manuscript. e Olympic study was sup-
ported by the Global Allergy and Asthma European Network
(GA2LEN).
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