A rise in FEV1 to bronchodilator ≥12 % of the baseline or predicted FEV1 and exceeds 200 ml
A fall in FEV1 ≥10 % from the baseline in response to exercise or eucapnic voluntary hyperpnea
A fall in FEV1 ≥15 % from the baseline after inhaling 22.5 ml of 4.5 g% NaCl or ≤635 mg of mannitol
A fall in FEV1 ≥20 % from the baseline in response to methacholine
PC20 ≤4 mg/ml or PD20 ≤ 400 μg (cumulative dose) or ≤200 μg (noncumulative dose) in those not taking inhaled corticosteroids (ICS) and PC20 ≤16 mg/ml or PD20 ≤1600 μg (cumulative dose) or ≤800 μg (noncumulative dose) in those taking ICS for at least 1 month
48.1.2 Treatment of Exercise-Induced Asthma
Drugs effective in the treatment of asthma are likely to be effective in the treatment of EI-asthma or EI-bronchoconstriction. Inhaled β2-adrenoceptor agonists are most effective in reversing EI-asthma/bronchoconstriction and are also used for prevention [6]. The effectiveness of inhaled short-acting β-agonists such as salbutamol or terbutaline against EI-asthma/bronchoconstriction is optimal 20 min after inhalation and wanes within a few hours. Long-acting β2-agonists, such as formoterol and salmeterol, protect for up to 12 h after a single inhalation. However, only formoterol acts as fast as quick-acting beta-agonists; therefore, formoterol but not salmeterol should be chosen to reverse EI-asthma/bronchoconstriction [13]. Inhaled β2-agonists may mask worsening airway inflammation and should never be used regularly without an inhaled glucocorticoid.
Regular treatments with inhaled glucocorticoids and/or leukotriene pathway antagonists control underlying asthma and reduce EI-asthma/bronchoconstriction. Montelukast and zafirlukast are cysLT receptor-1 antagonists. H1-antihistamines have minimal effects on EI-asthma/bronchoconstriction, whereas cromones administered before exercise mildly reduce EI-bronchoconstriction. In difficult-to-control EI-asthma/bronchoconstriction, combining inhaled glucocorticoids, oral leukotriene antagonists, and/or inhaled β2-agonists may be beneficial [13].
Optimal control of underlying asthma minimizes airway narrowing during exercise. Worsening EI-asthma may be a sign of inadequate control of underlying asthma, and “step-up” therapy should be considered. On the other hand, allergic rhinitis is also a very common disease among athletes and may negatively impact athletic performance; its early recognition, diagnosis, and treatment are crucial for improving nasal function and reduce the risk of asthma during exercise and competition. Certain medications for athletes with asthma and rhinitis who participate in regulated competitions are not allowed, and physician, athletes, and coaches should be aware of the updated regulatory aspects of asthma treatment (Table 48.2).
Table 48.2
Drugs regulated for asthma treatment during training and competition by the World Anti-Doping Agency (WADA) in 2016
Beta-agonists | ||
All oral (taken by mouth and swallowed) or injected beta-2 agonists are prohibited | ||
Inhaled beta-2 agonists are prohibited and require a Therapeutic Use Exemption (TUE), except for albuterol (also called salbutamol) dosages under 1600 μg in any 24 h period, formoterol dosages less than 54 μg in any 24 h period, and salmeterol when taken according to manufacturer’s instructions. If you use more than the amounts listed in the table below, you are required to submit a TUE for use. The presence of salbutamol in urine in excess of 1000 ng/mL is presumed not to be an intended therapeutic use of the substance and will be considered as an adverse analytical finding unless the athlete proves, through a controlled pharmacokinetic study, that the abnormal result was the consequence of the use of a therapeutic dose (maximum 1600 μg over 24 h) of inhaled salbutamol | ||
Inhaler brands and strengths | Recommended dosing by manufacturer | WADA maximum doses per 24 h |
Advair Diskus 100/50, 250/50, or 500/50 Each has salmeterol 50mcg per puff | 1 puff twice each day (100 mcg salmeterol) | Take as directed by the drug manufacturer |
Advair HFA 45/21, 115/21, or 230/21Each has salmeterol 21 mcg per puff | 2 puffs twice each day (84 mcg salmeterol) | Take as directed by the drug manufacturer |
Albuterol 108 mcg per puffProAir, Proventil, Ventolin | 1–2 puffs every 4 h as needed for wheezing | Salbutamol 108 mcg per puff: 14 puffs a day (<1600 mcg) |
Dulera 100 mcg/5 mcg per puff or 200mcg/5mcg per puff | 2 Puffs twice each day (20 mcg formoterol) | Formoterol 5 mcg per puff: 10 puffs a day (<54 mcg) |
Foradil Aerolizer 12 mcg per puff | 1 Capsule inhaled every 12 h (24 mcg formoterol) | Formoterol 12 mcg per cap: 4 puffs a day (<54 mcg) |
Serevent Diskus 50 mcg per puff | 1 puff twice each day (100 mcg) | Take as directed by the drug manufacturer |
Symbicort 80 mcg/4.5 mcg per puff or 160 mcg/4.5 mcg per puff | 2 puffs twice each day (formoterol 18 mcg) | Formoterol 4.5 mcg per puff: 12 puffs a day (<54 mcg) |
Advisory | ||
The use of oral beta-2 agonists is prohibited even if the athlete has a TUE for the same inhaled beta-2 agonist. If the athlete’s doctor prescribes an oral beta-2 agonist, the athlete should submit an application for a TUE | ||
Use the table above as a guide to determine the dosage of albuterol or formoterol that may be used in sport without a TUE. However, an athlete should examine his/her inhaler closely to determine the exact dose delivered | ||
Some dietary supplements claim to contain ingredients that have beta-2 agonist activity such as norcoclaurine. It is not known whether such products actually contain these ingredients, but USADA considers such products to be high risk | ||
Albuterol (urine amount over 1000 ng/mL) and formoterol (urine amount over 40 ng/mL) are “threshold substances,” which means they may be used in sport without a TUE as long as they are used under a certain threshold. However, if an athlete also takes a substance that falls into the category of diuretics and masking agents, a TUE is required for albuterol or formoterol even if the athlete already has a TUE on file for the diuretic or masking agent | ||
The presence of albuterol in urine in excess of 1000 ng/mL is presumed not to be an intended therapeutic use and may be considered as an adverse analytical finding, possibly leading to a sanction | ||
Some inhalers have more than one active ingredient. Make sure to check all active ingredients on GlobalDRO.com | ||
Glucocorticosteroid | ||
Inhalation of glucocorticoids (e.g., for asthma) is permitted. All glucocorticosteroids are prohibited when administered by oral, intravenous, intramuscular, or rectal routes | ||
A few notes should be taken on the effects of exercise as a non-pharmacological to asthmatic patients. At the current knowledge, evidence-based prescription of physical activity in asthma seems to be restricted to improvements in the physical fitness of the subjects. It is recommended that children and adolescents participate in at least 60 min of moderate-intensity physical activity most days of the week and preferably daily. Engagement in physical activity promotes the normal psychosocial development, neuromuscular coordination, and self-esteem. Changing from sedentary behaviors such as television viewing and computer games to moderate-intensity physical activity has been associated with enhanced overall health and prevention of chronic diseases. In asthmatics, exercise training may reduce the perception of breathlessness through strengthening of respiratory muscle and decrease the likelihood of exercise-induced symptoms by lowering the ventilation rate during exercise.
Currently, the GINA Guidelines do not include recommendations for exercise as part of the treatment for patients with asthma. Exercise is a powerful trigger for asthma symptoms. For this reason, caretakers may be reluctant to allow their asthmatic children to engage in sports practice, fearing an exacerbation of the disease. Every subject with asthma should be questioned about exercise performance, tolerance, and symptoms, but there is no reason to discourage asthmatic with a controlled disease to exercise [14].
48.2 Allergic Rhinitis
Rhinitis is defined as an inflammation of the nasal mucosa, characterized by two or more of the following symptoms: nasal congestion, anterior and posterior rhinorrhea, sneezing, and itching [15, 16]. Asthma and allergic rhinitis frequently coexist [15]. The prevalence of asthma in patients with rhinitis varies between 10 and 40%, and rhinitis seems to be an independent factor in the risk of asthma [4]. It is not still clear whether allergic rhinitis is an earlier clinical manifestation of allergic disease in atopic patients who will develop asthma or the nasal disease itself is a causative for asthma [15]. Rhinitis is classified etiologically in three main types [17]: allergic rhinitis (AR) (IgE mediated), nonallergic noninfectious rhinitis (non-IgE-mediated inflammation), and infectious rhinitis (Table 48.3) [15, 16]. Despite 30–50% of patients with rhinitis have nonallergic triggers, 44–87 % might have a mixed phenotype combining both allergic and nonallergic rhinitis mechanisms [18].
Table 48.3
Rhinitis classification
I Allergic rhinitis |
II Nonallergic noninfectious rhinitis A. Vasomotor rhinitis (triggered by irritant, cold air, exercise, undetermined trigger) B. Gustatory rhinitis |
III Infectious rhinitis (acute infectious rhinitis, chronic rhinosinusitis) |
III Occupational rhinitis A. IgE mediated (protein or chemical allergens) B. Uncertain immune mechanism (chemical respiratory sensitizers) C. Work-aggravated rhinitis |
IV Rhinitis syndromes A. Hormonal induced (pregnancy or menstrual cycle induced) B. Drug induced 1. Rhinitis medicamentosa 2. Nonsteroidal anti-inflammatory drugs 3. Oral contraceptives 4. Antihypertensive and cardiovascular agents C. Atrophic rhinitis D. Rhinitis associated with inflammatory-immunologic disorders 1. Granulomatous infection 2. Wegener granulomatosis 3. Sarcoidosis 4. Midline granuloma 5. Churg-Strauss syndrome 6. Relapsing polychondritis 7. Amyloidosis 8. Nonallergic rhinitis with eosinophilia syndrome (NARES) |
V Rhinitis by structural causes |
The upper airways, including the nasal cavity and its tissues, lie in a bony structure that, unlike the lower airway structure, cannot change shape [20]. Upper airways comprise an epithelium with a basement membrane and a submucosal layer, which contains venous sinusoids [20]. These vessels and mucosa glands are responsible for filtration, humidification, and warming of inhaled air, and they are regulated by autonomic nervous system reflexes [21]. Swelling of the venous sinusoids can lead to upper airway obstruction, and activation of local nerve reflexes causes sneezing, watery discharge, and vasodilation, symptoms associated with rhinitis [20].
During exercise, autonomic reflexes improve nasal efficiency [4]. In dynamic exercise training due to an increase of nasal sympathetic activity, venous sinusoids constrict. A watery discharge can also be produced, because cold air induces glandular hypersecretion [4, 20].
During training athletes are repeatedly exposed to risk factors, like allergens, but also cold air and pollutants, therefore increasing rhinitis symptoms in susceptible individuals [21]. Some experience improvement with exercise, mediated by nasal sympathetic tone, and others may have their symptoms worsen [22]. Weather conditions, like cold or dry air, and inhalation of irritants in outdoor exercise exposure can explain the worsening symptoms in some athletes [7].
Rhinitis is the most common cause of nasal symptoms in athletes [23]. Associated risk factors, such as atopy, family history of allergy, and exposure to allergens and pollution, might explain why AR prevalence has increased in all population, including athletes [15, 24]. AR is a multifactorial disease influenced by genetic and environmental interaction [25].
The World Health Organization (WHO) through the working group Allergic Rhinitis and its Impact on Asthma (ARIA) changed the classification from the time of exposure (seasonal, perennial, and occupational) to a symptomatic definition and severity characterization (Fig. 48.1). The seasonal and perennial rhinitis classification is still useful for diagnosis and immunotherapy (IT) treatment decision and can be used alongside with ARIA classification [15].
The most frequent allergic triggers are inhalant allergens, namely, mites, pollens, animals, and fungi. According to the triggers, they can cause perennial or seasonal symptoms. Preexisting rhinitis can be exacerbated by workplace irritants like smoke, cold air, and pollutants [24].
Rhinitis is largely underdiagnosed and self-managed in athletes [26]. However, it has debilitating consequences, significantly interfering with patient’s quality of life and activity, namely, in sports practice [27]. Previous studies support its negative impact on cognitive functions, school performance, sleep, quality of life, and even behavior, which can significantly affect athletic performance [27]. This is particularly important, as a higher prevalence of rhinitis has been reported in athletes than in general population [21]. Excluding exercised-induced rhinitis, idiopathic rhinitis, and nasal symptoms related to physical, cold air, and chemical contact factors, allergic rhinitis can account for prevalence up to 30% in an athlete population.
48.2.1 Epidemiology and Risk Factors
Allergic rhinitis has a prevalence of 10–20% in the general population, which is higher in elite competitive athletes [15, 28]. In the last two decades, a prevalence range between 13.3 and 48.6% was found (Table 48.4) [21].
Table 48.4
Prevalence of rhinitis or seasonal allergic rhinoconjunctivitis (SARC) in athletes
Reference | Design and methods | Year of study, subjects (n) | Rhinitis/SARC* prevalence |
|---|---|---|---|
Fitch [29] | Retrospective; medical records analysis | 1976, Australian Olympics (185) | 8.6 |
1980, Australian Olympics (106) | 7.5 | ||
Helbling [30] | Cross-sectional; questionnaire | 1986, Swiss athletes (2,060) | 16.8* |
Kaelin [31] | Cross-sectional; questionnaire | 1990, Swiss athletes (1530) | 19.7%* |
Potts [32] | Cross-sectional; questionnaire | 1995, Canadian swimmers (738) | 19.0* |
Helenius [33] | Cross-sectional; skin prick tests with medical diagnosis | 1996, Finnish summer athletes (162) | 29.6* |
Weiler [34] | Cross-sectional, questionnaire (USOC-MHQ) | 1996, US Summer Olympics (699) | 16.9 |
Weiler [35] | Cross-sectional, questionnaire (USOC-MHQ) | 1998, US Winter Olympics (699) | 13.3 |
Katelaris [36] | Cross-sectional; skin prick tests with medical diagnosis | 1997/8, Australian Summer Olympics (214) | 41.0/29.0* |
Katelaris [28] | Cross-sectional; skin prick tests with medical diagnosis | 1999, Australian Olympics/Paralympics (977) | 37.0/24.0* |
Lapucci [37] | Cross-sectional; skin prick tests with medical diagnosis | 2000, Italian Summer Olympics (265) | 25.3* |
Bonadonna [38] | Cross-sectional, questionnaire on cold-induced rhinitis | 2001, Italian skiers (144) | 48.6 |
Alaranta [39] | Cross-sectional; self-reported medical diagnosis | 2002, Finnish Olympic athletes (446); | 26.5 |
Subgroup of endurance athletes (108) | 36.1 | ||
Randolph [40] | Cross-sectional; questionnaire (USOC-MHQ) | 2003/4, US recreational runners (484) | 34.7 |
Moreira [41] | Cross-sectional; self-reported medical diagnosis | 2003, Finnish marathon runners (141) | 17.3 |
Bonini [42] | Cross-sectional; medical diagnosis | 2006, Italian preOlympics (98) | 34.7 |
Macucci [43] | Cross-sectional; medical diagnosis | 2006, Italian young athletes (352) | 22.2 |
Salonen [44] | Cross-sectional; self-reported medical diagnosis | 2007, Finnish young hockey players (793) | 18.3 |
Thomas [45] | Cross-sectional; questionnaire | 2008, German athletes candidates for Summer Olympic Games (291) | 25* |
Bonini [46] | Cross-sectional surveys from 2000 to 2012 | 2000–2012, Italian Olympic Delegation at Summer and Winter Olympic Games (659 | 26.2 |
Kurowski [47] | Cross-sectional; self-reported medical diagnosis | 2008, Polish athletes Olympic (222) | 27.0 |
The allergic response causes nasal and conjunctival congestion, tearing, breathing difficulties, pruritus, fatigue, and mood changes, which might affect athletic performance [48]. Kateralis showed over spring season a negative effect of allergic rhinoconjunctivitis on performance scores (ability to train and compete). Also a resolution of those symptoms, namely, eye symptoms, and improvement on quality of life and performance scores were seen after treatment with intranasal corticosteroids [49].
During exercise, ventilation increases for a short period of time in power athletes and for longer periods in resistance athletes [4]. Most of this exercise is practiced in outdoor environments; therefore, athletes are strongly and repeatedly exposed to large amounts of aeroallergens and pollutants. This contact in training or in competition periods may increase the likelihood of exercise-induced respiratory symptoms [21]. The climate conditions, namely, the inhaled air, temperature, and humidity, also affect these patients [4, 50].
Athletes involved in outdoor sports are frequently exposed during peak allergen seasons. Indeed, major sports events frequently occur at the end of the spring and beginning of the summer [21]. Aerobiological records of pollens are used to monitor the pollen levels, and it is important for athletes to prepare themselves, particularly if they are symptomatic to some allergen. An example was the setup of an aerobiological network for the Athens Summer Olympic Games [51].
Indoor allergens, namely, mites, are not usually studied, due to the decreased frequency of contact and the specific association of more severe symptoms with endurance to outdoor exercise. However, in some more indoor sports, persistent rhinitis symptoms can occur, and it may be relevant to control this environmental exposure.
Urban-type pollution interacts with allergens and induces sensitization and triggers symptoms in allergic patients [4]. There are several studies pointing to adverse effects of outdoor air pollution, caused by carbon monoxide, nitric oxide, and ozone [21]. The two agents that most frequently affect upper respiratory airways and rhinitis are particulate matter, namely, diesel exhaust particles (DEPs) [15] and volatile organic compounds. Their peak production is from April to September in the Northern Hemisphere, and a large percentage (40%) is completely absorbed by the nasal mucosa [15]. They enhance the production of oxygen’s derivatives increasing the permeability of epithelial cells [38]. Ozone increases the late-phase response to nasal allergens, increasing the eosinophilic influx after exposure, and, in the nasal mucosa, the histamine and inflammatory cells are increased in number [21].
In several studies, it has been shown that patients living in traffic-congested areas have more severe rhinitis and conjunctivitis symptoms [52]. A study in Beijing, using questionnaires in 31,829 individuals and monitoring PM10, SO2, and NO2 air levels, found a significant association between outpatient visits for allergic rhinitis and increasing air pollutant levels [53]. This finding is particularly relevant for athletes who train or compete in outdoor urban environments. So, at the Olympic Games in China, air quality was monitored in order that athletes could perform their sports safely [54]. In fact, elite athletes practice sport around the world under different conditions and should be informed to what environment exposure they will be submitted, to adapt themselves and have appropriate preventive measures, namely, their allergic symptoms fully controlled.
Tobacco smoke is not advised in all populations, and especially in sports practice. Despite this, some athletes smoke or are exposed to passive smoke. Nasal symptoms, rhinorrhea, and nasal obstruction can occur under tobacco exposure, but these are not always consistent with increased total and specific IgEs [15].
The exposure to different environmental conditions that are specific to a particular sport also contributes to rhinitis symptoms. Rhinorrhea and nasal congestion after exposure to cold air, known as “skier’s nose,” can occur in normal individuals [55]. In high-performance athletes, namely, skiers, long-distance runners, and swimmers with long-term exposure to cold, the repeated cooling and drying of the mucosa results in an inflammatory infiltration of the airway mucosa, and these effects are reversed after stopping the high-performance exercise [56].
In runners, an initial decongestion of the mucosa occurs, and it is maintained nearly 30 min after stopping exercise. This reduction of nasal resistance can lead to mucosa dehydration and a rebound increase in nasal secretion to compensate it. This “runner’s nose” is also integrated in differential diagnosis of allergic rhinitis [4].
Swimmers are also a specific population of athletes. Their long-term and high exposure to chlorine derivatives during regular trainings and competition at increased ventilation can induce mucosal inflammation which facilitates the responsiveness to airborne allergens and induces bronchial hyperresponsiveness. Kateralis found in a group of swimmers that they were more likely to have rhinitis symptoms and allergic sensitization than those active in other sports [36]. These results were similar when compared with healthy controls [57]. When swimmers stopped training for 2 weeks, they showed an improvement in nasal symptoms [57]. In a study comparing competitive swimmers with runners, the first experienced worsening of nasal function after training independently of being atopic [50].
48.2.2 Effects of Allergic Rhinitis on Exercise Performance
Allergic rhinitis has a negative impact on quality of life in the general population. Cognitive functions, school performance, sleep, and behavioral effects have been described, namely, in children with attention-deficit hyperactivity disorders [58]. In a questionnaire of quality of life performed during spring time, Kateralis showed poorer results in the allergic group [27]. In another study with 145 athletes with allergic rhinitis who agreed to be treated had a significant improvement of their quality of life scores under budesonide therapy [49]. In a high-level competitive swimmers population, stopping training for 2 weeks improved rhinitis-related QoL. It was not possible yet to confirm a direct association of poorly treated rhinitis and a bad exercise performance [59]; however, an indirect one can be inferred. However, it seems likely that altered airflow dynamics and ventilation and nasal obstruction can potentially have a negative effect, mainly in high-intensity activities [59]. Any factors that affect sleep, decrease ability to concentrate, or reduce physical fitness have an easy understandable impact on sports performance.
The cognitive impact (learning ability and memory) of rhinitis has been particularly studied in children [58]. Learning disability is caused as a consequence of the frequent sleep disturbances and resulting daytime sleepiness. Impaired sleep is secondary to nasal congestion which causes micro-arousal and irregular breathing, with snoring and apnea. An associated effect is school and work absenteeism and training capacity disability [58]. Correct diagnosis and management of allergic rhinitis can reduce the disease impact.
48.2.3 Diagnosis
Diagnosis of allergic rhinitis in athletes is based in the concordance of a suggestive history of allergic symptoms and physical examination and supported by diagnostic tests [15, 60].
A complete allergic history is the best diagnostic tool for rhinitis diagnosis, allowing to assess severity and guide treatment [16, 60]. The patient, namely, the athlete, may present several symptoms, namely, sneezing; anterior rhinorrhea; bilateral nasal obstruction; postnasal drip cough; itchy nose, ears, and throat; loss of smell (hyposmia or anosmia); or snoring [15, 59]. Frequently, ocular symptoms are concomitant with tearing, burning, and itching. In athletes, clinical presentation is frequently more subtle and might include poor-quality sleep, fatigue, reduced exercise performance, and difficulty to recover after more demanding exercise sessions [59]. Patient evaluation should include symptom’s pattern characterization, chronicity, seasonality and triggers of nasal and related symptoms, response to treatment, presence of coexisting conditions, and the relation with training practice. It is also very important to include assessment of quality of life [16].
Physical examination of all organ systems potentially affected by allergies should be performed. Further attention should be given for the upper respiratory tract system, namely, nasal and oropharyngeal examination. In some patients, nasal examination can show bluish-gray discoloration and edema or erythema of the mucosa with clear watery rhinorrhea [60]. Infectious complications of rhinitis to which athletes seems to be more prone, like otitis and sinusitis, should be discarded during this examination [61], as well as structural causes of symptoms. It is important to explore during clinical investigations differential diagnosis for similar symptoms, like nonallergic ones.
In an athlete, when an allergic etiology is suspected, skin prick testing (SPT) with standardized allergens and/or measurement of allergen-specific IgE in serum should be used. Skin prick tests are relevant markers of the IgE-mediated allergic reaction [15, 24]. The result can depend on several variables, quality of the allergen extracts, age, and medications and is dependent on operator interpretation [15, 60]. Serum total IgE and serum-specific IgE are measured by radioimmunoassay or enzyme immunoassay and can be requested when skin tests are not possible or when SPT in association with the clinical exam is not concordant [15, 16, 24]. The sensitivity of serum-specific IgE measurements compared with SPT can vary with the immunoassay technique used [16].
Nasal and conjunctival challenge tests can be used to assess if any discrepancy occurs between history and results of skin prick test or IgE measurement and to define clinically relevant allergens in cases of multiple sensitizations [15, 24, 62].
Imaging of the nose and sino-nasal cavity is used to corroborate diagnosis and differentiate the source of sino-nasal symptoms, the relation of sino-nasal problem with surrounding structures, and the extent of the disease [60]. Plain sinus radiographs are not indicated in allergic rhinitis or rhinosinusitis diagnosis [15, 63]. Computerized tomography scanning is used to evaluate paranasal sinuses due to optimal display of air bone and soft tissue. It is indicated for differential diagnosis purposes, to exclude chronic rhinosinusitis, to eliminate rhinitis complication, and to evaluate nonresponders to treatment [15, 60]. It can be particularly useful in athletes, to exclude traumatic lesions, which occur frequently in close-contact sports, like boxing or football.
To evaluate rhinitis severity measurements of nasal obstruction and smell can be used [15]. These tests are not made in routine clinical practice but can be useful when allergen challenges are undertaken or septal surgery is contemplated [24]. Nasal patency can be monitored objectively using nasal peak inspiratory and expiratory flow, acoustic rhinometry, that measures the nasal cavity volume and rhinomanometry that measures nasal airflow and pressure [60]. In clinical practice the most frequently used is peak nasal inspiratory flow because it is simple, cheap, fast, and available and it can be used for disease home monitoring [16]. Nasal nitric oxide measurement may be a useful tool in diagnosis and management and to alert for possible mucociliary defects, but its utility in allergic rhinitis needs to be further evaluated [15, 60].
Rhinitis control is frequently monitored with control questionnaires and visual analogue scales [15]. The Rhinitis Control Assessment Test, a 6-item patient completed instrument, and Control of Allergic Rhinitis and Asthma Test (CARAT) are such examples [64, 65]. Specific questionnaires for athletes are the Allergy Questionnaire for Athletes (AQUA) that was developed by Bonini [66].
48.2.4 Management of Allergic Rhinitis in Athletes
Management of allergic rhinitis encompasses patient education, environmental control, pharmacotherapy, and allergen-specific immunotherapy. Surgical options might be used in highly selected cases [15]. Appropriate management requires an “evidence-based medicine” approach [15, 67]. For the elite athlete, it is also important to minimize the potential detrimental effects of allergic symptoms and treatment on performance [27]. Treatment requires careful planning to comply to the “anti-doping” regulations and avoid detrimental influences of treatment adverse effects [27]. Specific aims for the athlete population are the following: avoid exposure to peak levels of clinically relevant allergens and pollutants; reduce symptoms and improve nasal functions to minimize potential negative effects on sports performance; and use therapies complying with the WADA rules that do not affect performance.
Reducing allergen exposure can improve disease control and decrease the need for treatment [68]. In most cases and specifically in athletes, complete avoidance is difficult to achieve [41]. Nevertheless, measures aiming to reduce relevant allergens should be promoted. Removing carpets from the bedroom, careful and daily cleaning, and regular change of bed linen can be useful for reducing house dust mite exposure. For pollen exposure avoidance, following pollen forecasts and adapting training venues and training schedule and using appropriate face equipment may minimize exposure, at least to peak pollen levels [16, 59]. Irritants reported to cause nasal symptoms, including pollution, chlorine, and cold air, should also be minimized [16]. In order to prevent high-level exposure to these agents, training environment should be more controlled by improving ventilation systems of swimming pools and ice arenas [21] and taking measures to reduce global pollution [53].
48.2.4.1 Pharmacologic Therapy of Rhinitis in Athletes
The selection of treatment for a patient depends on multiple factors: type of rhinitis, symptom severity, age, and job [16]. In elite athletes, management of allergic rhinitis should be adapted to accommodate factors that may hazard the athletic performance, and the balance between efficacy and safety should be addressed before prescribing. In elite athletes the drug must be accepted by the most recent World Anti-Doping Agency (WADA) rules.
Antihistamines
H1-receptor antagonists block histamine at H1-receptor level (neutral antagonists or inverse agonists). They are effective in symptoms mediated by histamine, namely, rhinorrhea, sneezing, and nasal and eye itching [15]. Antihistamines can be divided accordingly into their chemical class in alkylamines, piperazine, piperidines, ethanolamines, ethylenediamines, and phenothiazines [69]. However, the most used classification is functional as first generation, which is sedating, and second generation which is relatively nonsedating [69]. Second-generation oral H1-antihistamines (e.g., rupatadine, ebastine, azelastine, levocetirizine, desloratadine, or bilastine) are recommended in the most updated guidelines as they do not have anticholinergic and sedative, cognitive, and psychomotor effects [67]. Athletes benefit the most with these recommendations, since first-generation H1-antihistamines may reduce psychomotor skills by their sedative effect and, by their anticholinergic activity, cause mucosal drying and reduce sweating and temperature regulation [21, 59]. Some authors even propose a cautious approach in the prescription of any antihistamines 24–48 h before a major competition [59].
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