Seasonal Allergy and Seasonal Decrements in Athletic Performance
2005; Elsevier BV; Volume: 24; Issue: 2 Linguagem: Inglês
10.1016/j.csm.2004.12.006
ISSN1556-228X
AutoresHirsh D. Komarow, Teodor T. Postolache,
Tópico(s)Food Allergy and Anaphylaxis Research
ResumoAllergic diseases are among the most common chronic diseases and have been increasing worldwide over the past several decades for reasons that are still not clearly understood [1Annesi-Maesano I. Epidemiological evidence of the occurrence of rhinitis and sinusitis in asthmatics.Allergy. 1999; 54: S7-S13Crossref PubMed Google Scholar, 2Dykewicz M.S. Fineman S. Skoner D.P. et al.Diagnosis and management of rhinitis: complete guidelines of the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology. American Academy of Allergy, Asthma, and Immunology.Ann Allergy Asthma Immunol. 1998; 81: 478-518Abstract Full Text PDF PubMed Google Scholar, 3International Consensus Report on the diagnosis and management of rhinitis. International Rhinitis Management Working Group.Allergy. 1994; 49: S1-S34Google Scholar, 4Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee.Lancet. 1998; 351: 1225-1232Abstract Full Text Full Text PDF PubMed Scopus (3342) Google Scholar, 5Casale T.B. Amin B.V. Allergic rhinitis/asthma interrelationships.Clin Rev Allergy Immunol. 2001; 21: 27-49Crossref PubMed Scopus (26) Google Scholar, 6Rosenwasser L.J. Treatment of allergic rhinitis.Am J Med. 2002; 113: S17-S24Abstract Full Text Full Text PDF PubMed Google Scholar]. There has been considerable research elucidating the impact that allergic disease has on athletic performance. Athletes who have allergic disease can benefit from the tremendous progress that has been made in understanding the pathophysiologic basis of their disease. Accessing the host of international climatic and seasonal pollen reports available can enable athletes to be better prepared for training and performance. Additionally, athletes can benefit from an evolving repertoire of therapeutic modalities for allergic diseases that conform to current antidoping codes (www.wada-ama.org). Atopic diseases such as asthma, allergic rhinitis, urticaria, and anaphylaxis are characterized by hypersensitivity to a particular allergen, resulting in secretion of specific immunoglobulin E (IgE) antibodies and acute, recurrent, or chronic inflammation. Certain individuals with an atopic predisposition synthesize IgE antibodies on initial exposure to allergen. IgE binding to mast cells and basophils sets the stage for the allergic response. On re-exposure, allergen cross-links IgE on cell surfaces, which causes the release of a host of inflammatory mediators. Early response mediators include granule mediators (eg, histamine, tryptase) and lipid mediators (eg, leukotrienes, prostaglandins). Cytokines such as tumor necrosis factor-alpha (TNF-α), interleukins, and chemokines (IL-8, MCP-1 and MIP-1α) are produced minutes to hours later (Fig. 1) [7Boyce J.A. Mast cells: beyond IgE.J Allergy Clin Immunol. 2003; 111 ([Quiz Review 33]): 24-32Abstract Full Text Full Text PDF PubMed Scopus (145) Google Scholar, 8Schwartz L.B. Effector cells of anaphylaxis: mast cells and basophils.Novartis Found Symp. 2004; 257: 65-74Crossref PubMed Google Scholar]. The type of allergen, the degree and length of exposure, and the atopic tendency of the individual determine the manifestation of symptoms. Sources of allergens include the environment (eg, tree, grass and weed pollen, dust, mold), foods, drugs, and stinging insects. Aeroallergens are further subdivided into seasonal aeroallergens, like tree, grass and weed pollen, and nonseasonal aeroallergens like mold and dust [[9]Solomon W.R. Airborne pollen: a brief life.J Allergy Clin Immunol. 2002; 109: 895-900Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar]. The concentration of pollen in the atmosphere, which correlates with allergic manifestations, is reported and disseminated at multiple centers internationally. In the United States and Canada, a useful resource is The National Allergy Bureau, which provides pollen and mold counts from approximately 75 counting stations (www.aaaai.org/nab/). Physical manifestation of allergy is often debilitating. In the lung there may be bronchoconstriction or asthma; in the nose, rhinitis; in the skin, urticaria; in the eyes, conjunctivitis. Systemic manifestations of allergy characterize anaphylaxis, which may be life threatening and require immediate medical attention. Anaphylaxis that occurs in conjunction with exercise, termed exercise-induced anaphylaxis, has been reported in certain individuals [[10]Castells M.C. Horan R.F. Sheffer A.L. Exercise-induced anaphylaxis.Curr Allergy Asthma Rep. 2003; 3: 15-21Crossref PubMed Scopus (55) Google Scholar]. In addition to the inflammatory response, allergic disease manifestations have been associated with fatigue [[11]Marshall P.S. O'Hara C. Steinberg P. Effects of seasonal allergic rhinitis on fatigue levels and mood.Psychosom Med. 2002; 64: 684-691PubMed Google Scholar], depression [[12]Timonen M. Jokelainen J. Herva A. et al.Presence of atopy in first-degree relatives as a predictor of a female proband's depression: results from the Northern Finland 1966 Birth Cohort.J Allergy Clin Immunol. 2003; 111: 1249-1254Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar], and decrements in cognition [[13]Wilken J.A. Berkowitz R. Kane R. Decrements in vigilance and cognitive functioning associated with ragweed-induced allergic rhinitis.Ann Allergy Asthma Immunol. 2002; 89: 372-380Abstract Full Text PDF PubMed Scopus (92) Google Scholar]. In fact, epidemiologic evidence suggests that seasonality of even extreme behavioral manifestation, such as suicide, may be associated with allergy [[14]Timonen M. Viilo K. Hakko H. et al.Is seasonality of suicides stronger in victims with hospital-treated atopic disorders?.Psychiatry Res. 2004; 126: 167-175Abstract Full Text Full Text PDF PubMed Scopus (43) Google Scholar] or with exposure to seasonal allergens, specifically tree pollen [[15]Postolache T.T., Stiller J.W., Herrell R., et al. Tree pollen peaks are associated with increased nonviolent suicide in women. Mol Psychiatry, in pressGoogle Scholar]. In addition to the clinical manifestations of an allergic disorder, in vivo and laboratory-based testing for allergen sensitivity is used to strengthen the diagnosis of allergic disease. Skin-prick and intradermal testing provide a rapid and functional measure of IgE-mediated hypersensitivity in the skin with a resultant wheal and flare response that occurs within 15 minutes of allergen contact. In situations of decreased skin response from treatment with antihistamines, increased skin sensitivity from dermatographism, or logistical constrains, athletes may opt for the radioallergosorbent test (RAST), which detects specific IgE antibodies in serum with comparable sensitivity and specificity to skin-prick testing [[16]Hamilton R.G. Adkinson Jr, N.F. 23. Clinical laboratory assessment of IgE-dependent hypersensitivity.J Allergy Clin Immunol. 2003; 111: S687-S701Abstract Full Text Full Text PDF PubMed Scopus (129) Google Scholar]. Athletes are particularly vulnerable to the effects of the environment, as many athletic activities—whether they are for leisure, training, or competition—occur outdoors. When athletes train and compete, often for long durations of time, they make intimate contact with the outdoor elements that are comprised of a host of topographical, seasonal, and climatic components. Exposure to the various elements is magnified by increased ventilation (up to 200 L/min during exercise), which intensifies the contact between the respiratory system and environment, and by inhalation of poor quality and cold air, which often affects those who train year-round in temperate climates [17Helenius I.J. Tikkanen H.O. Haahtela T. Occurrence of exercise induced bronchospasm in elite runners: dependence on atopy and exposure to cold air and pollen.Br J Sports Med. 1998; 32: 125-129Crossref PubMed Scopus (148) Google Scholar, 18Katelaris C.H. Carrozzi F.M. Burke T.V. Allergic rhinoconjunctivitis in elite athletes: optimal management for quality of life and performance.Sports Med. 2003; 33: 401-406Crossref PubMed Scopus (37) Google Scholar]. During the winter months, cold air inhalation during exercise exacerbates exercise-induced asthma in people with asthma [[19]McFadden Jr, E.R. Gilbert I.A. Exercise-induced asthma.N Engl J Med. 1994; 330: 1362-1367Crossref PubMed Scopus (372) Google Scholar]. Track and field athletes have extensive exposure to various seasonal pollen allergens during the spring (trees), summer (grass), and early fall (ragweed) [[20]Helenius I. Haahtela T. Allergy and asthma in elite summer sport athletes.J Allergy Clin Immunol. 2000; 106: 444-452Abstract Full Text Full Text PDF PubMed Scopus (187) Google Scholar]. Susceptible athletes may develop conjunctival inflammation, rhinitis, or bronchial inflammation as a consequence of these environmental conditions. Based on a 15-year database of aeroallergen records, an in-depth study reported the predicted aeroallergen counts that would be observed in association with the 2004 Olympic games in Athens, Greece. The study predicted that peak pollen concentrations would be observed during training in March and May, and high levels of goosefoot, mugwort, Alternaria, and Cladisporum spores would be observed in August and September during the Olympic games [[21]Gioulekas D. Damialis A. Papakosta D. et al.15-year aeroallergen records. Their usefulness in Athens Olympics, 2004.Allergy. 2003; 58: 933-938Crossref PubMed Scopus (21) Google Scholar], thus highlighting the need for preparation, testing, and therapy. An earlier survey of allergic disease in elite athletes reported that 20% of the 1984 Australian Olympic team had allergic disorders based on clinical evaluation (not including skin testing or RAST) [[22]Fitch K.D. Management of allergic Olympic athletes.J Allergy Clin Immunol. 1984; 73: 722-727Abstract Full Text PDF PubMed Scopus (51) Google Scholar]. Of 214 Australian Olympic athletes studied during the 2000 Sydney Olympics, which took place during the period of high tree pollen (over 5000 grains per CμM), a high prevalence of perennial and seasonal allergic disease was reported. Within that group, 56% reported a history of allergic rhinoconjunctivitis, 41% were symptomatic with a positive skin test to a potential allergen, 29% were diagnosed with seasonal allergic rhinoconjunctivitis based on history and skin testing, and 21% suffered from asthma [[23]Katelaris C.H. Carrozzi F.M. Burke T.V. Fitch K.D. A springtime Olympics demands special consideration for allergic athletes.J Allergy Clin Immunol. 2000; 106: 260-266Abstract Full Text Full Text PDF PubMed Scopus (101) Google Scholar]. Before the 2004 Olympics in Athens, Greece, information regarding circulating aeroallergens in neighboring cities was published to attempt to minimize the allergy symptoms and help athletes achieve peak performance. Understandably, the incidence of adverse responses to seasonal allergens is common amongst athletes. Although athletes with allergic diseases have successfully won many Olympic medals, the detrimental contribution of pollutants, allergens, or other environmental factors has occasionally produced severe exacerbations of allergic conditions, warranting medical attention and causing suboptimal performance. Seasonal exposures to infectious agents may also induce seasonal decrements in athletic performance. Viral infections reviewed in Nelson et al [[24]Nelson R.J. Demas G.E. Klein S.L. Seasonal patterns of stress, immune function, and disease. 1st edition. Cambridge University Press, Cambridge, MA2002Crossref Google Scholar], such as influenza, reovirus, and respiratory syncytial virus, manifest a seasonal peak in winter and early, cause significant morbidity, may trigger bronchial hyper-reactivity, and may result in secondary bacterial infections such as sinus or bronchial infections (Table 1).Table 1Seasonality of infectious diseasesInfectionPeak prevalenceMalariaWinter–early springLeishmaniasisWinter–early springInfluenzaWinter–early springHuman reovirusWinterCoronavirusWinter–early springRespiratory syncytial virusWinter–early spring, summerAdapted from Nelson RJ, Demas GE, Klein SL, et al. Seasonal patterns of stress, immune function, and disease. 1st edition. Cambridge, MA: Cambridge University Press; 2002. Open table in a new tab Adapted from Nelson RJ, Demas GE, Klein SL, et al. Seasonal patterns of stress, immune function, and disease. 1st edition. Cambridge, MA: Cambridge University Press; 2002. Several studies have characterized the relationship between viral infection, which is primarily a T-helper type 1 (Th1) response, and enhancement of allergic disease, which is a T-helper type 2 (Th2) response. Viral infections like influenza A may trigger allergic asthma by interfering with tolerance to aeroallergens [[25]Tsitoura D.C. Kim S. Dabbagh K. et al.Respiratory infection with influenza A virus interferes with the induction of tolerance to aeroallergens.J Immunol. 2000; 165: 3484-3491Crossref PubMed Scopus (61) Google Scholar], inducing a concomitant Th1 response [[26]Dahl M.E. Dabbagh K. Liggitt D. et al.Viral-induced T helper type 1 responses enhance allergic disease by effects on lung dendritic cells.Nat Immunol. 2004; 5: 337-343Crossref PubMed Scopus (191) Google Scholar], and causing recruitment of Th2 cells into the lung [[27]Stephens R. Randolph D.A. Huang G. et al.Antigen-nonspecific recruitment of Th2 cells to the lung as a mechanism for viral infection-induced allergic asthma.J Immunol. 2002; 169: 5458-5467Crossref PubMed Scopus (69) Google Scholar]. In some people, seasonal allergy and mood vulnerability to inflammation may interact, and people with allergies may experience more post-flu mood worsening than those without allergies [[28]Bell I.R. Jasnoski M.L. Kagan J. et al.Depression and allergies: survey of a nonclinical population.Psychother Psychosom. 1991; 55: 24-31Crossref PubMed Scopus (104) Google Scholar]. Often the initial contact of pollen and other airborne components is with nasal mucosal and eyes. Studies have shown that allergic rhinoconjunctivitis is under-recognized and certainly undertreated in elite athletes [[18]Katelaris C.H. Carrozzi F.M. Burke T.V. Allergic rhinoconjunctivitis in elite athletes: optimal management for quality of life and performance.Sports Med. 2003; 33: 401-406Crossref PubMed Scopus (37) Google Scholar]. Helenius et al [[29]Helenius I.J. Tikkanen H.O. Sarna S. et al.Asthma and increased bronchial responsiveness in elite athletes: atopy and sport event as risk factors.J Allergy Clin Immunol. 1998; 101: 646-652Abstract Full Text Full Text PDF PubMed Scopus (230) Google Scholar] reported the results of a survey of 49 athletes competing in summer events. The diagnosis of allergic rhinoconjunctivitis was more common among athletes than in a control group of nonathletes (P = .037). Helbling et al [[30]Helbling A. Jenoure P. Muller U. [The incidence of hay fever in leading Swiss athletes].Schweiz Med Wochenschr. 1990; 120 ([German]): 231-236PubMed Google Scholar] surveyed 2961 Swiss athletes who participated in 68 sports. Of the 79% who responded to the questionnaire, 16.8% indicated they suffered from hay fever and 59% reported that they needed medication during the pollen season. Individuals who have allergic rhinitis also often have increased bronchial hyperresponsiveness [31Prieto L. Gutierrez V. Linana J. et al.Bronchoconstriction induced by inhaled adenosine 5′-monophosphate in subjects with allergic rhinitis.Eur Respir J. 2001; 17: 64-70Crossref PubMed Scopus (36) Google Scholar, 32Ramsdale E.H. Morris M.M. Roberts R.S. et al.Asymptomatic bronchial hyperresponsiveness in rhinitis.J Allergy Clin Immunol. 1985; 75: 573-577Abstract Full Text PDF PubMed Scopus (182) Google Scholar]. Allergic rhinitis (AR) is characterized by nasal mucosa edema as a result of IgE-mediated release of early- and late-phase mediators and Th2 cytokines, which promotes the infiltration of mucosa with inflammatory cells such as eosinophils, neutrophils, basophils, T cells, and macrophages [2Dykewicz M.S. Fineman S. Skoner D.P. et al.Diagnosis and management of rhinitis: complete guidelines of the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology. American Academy of Allergy, Asthma, and Immunology.Ann Allergy Asthma Immunol. 1998; 81: 478-518Abstract Full Text PDF PubMed Google Scholar, 33Berger W.E. Treatment update: allergic rhinitis.Allergy Asthma Proc. 2001; 22: 191-198PubMed Google Scholar, 34Borish L. Allergic rhinitis: systemic inflammation and implications for management.J Allergy Clin Immunol. 2003; 112: 1021-1031Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar]. AR is characterized by nasal congestion, rhinorrhea, sneezing, itching of the nose, or postnasal drainage and is often associated with allergic conjunctivitis manifested by ocular itch, tearing, redness, and sometimes swelling and photophobia. These and other signs and symptoms of AR are listed in Box 1. Allergic, irritant, infectious, hormonal, occupational, and other factors are causative agents in nasal mucosal edema [[35]Dykewicz M.S. 7. Rhinitis and sinusitis.J Allergy Clin Immunol. 2003; 111: S520-S529Abstract Full Text Full Text PDF PubMed Scopus (117) Google Scholar]. Peak presentations of allergic rhinoconjunctivitis occur between 10 to 25 years, which includes the age range of most elite athletes [[3]International Consensus Report on the diagnosis and management of rhinitis. International Rhinitis Management Working Group.Allergy. 1994; 49: S1-S34Google Scholar].Box 1Signs and symptoms of allergic rhinitisItching of the nose, ears, palate, throatSneezing spellsClear and watery rhinorrheaCongestionSinus headacheMouth breathingPost-nasal dripSleep disturbanceCoughFatigue Itching of the nose, ears, palate, throatSneezing spellsClear and watery rhinorrheaCongestionSinus headacheMouth breathingPost-nasal dripSleep disturbanceCoughFatigue Although exercise may increase nasal airway patency, likely by way of increased sympathetic nerve discharge [[36]Richerson H.B. Seebohm P.M. Nasal airway response to exercise.J Allergy. 1968; 41: 269-284Abstract Full Text PDF PubMed Scopus (96) Google Scholar], there are several reasons why AR may interfere with athletic performance. Rhinitis often causes changes in sleep patterns because of nasal obstruction, rhinorrhea, and sinus pressure that add to tiredness and fatigue and impair athletic performance [[18]Katelaris C.H. Carrozzi F.M. Burke T.V. Allergic rhinoconjunctivitis in elite athletes: optimal management for quality of life and performance.Sports Med. 2003; 33: 401-406Crossref PubMed Scopus (37) Google Scholar]. Additionally, short bursts of sprinting require nasal breathing for optimal performance [[36]Richerson H.B. Seebohm P.M. Nasal airway response to exercise.J Allergy. 1968; 41: 269-284Abstract Full Text PDF PubMed Scopus (96) Google Scholar], implicating nasal obstruction as a deleterious factor in performance. AR has been associated with alteration in central nervous system (CNS) function, which may significantly affect the athlete's ability to perform. Using a standardized computer-based battery of cognitive processing tests, subjects who have AR experienced decrements in reaction time, attention, and vigilance when exposed to pollen [[13]Wilken J.A. Berkowitz R. Kane R. Decrements in vigilance and cognitive functioning associated with ragweed-induced allergic rhinitis.Ann Allergy Asthma Immunol. 2002; 89: 372-380Abstract Full Text PDF PubMed Scopus (92) Google Scholar]. Others associated AR with increased fatigue [[11]Marshall P.S. O'Hara C. Steinberg P. Effects of seasonal allergic rhinitis on fatigue levels and mood.Psychosom Med. 2002; 64: 684-691PubMed Google Scholar], depression [11Marshall P.S. O'Hara C. Steinberg P. Effects of seasonal allergic rhinitis on fatigue levels and mood.Psychosom Med. 2002; 64: 684-691PubMed Google Scholar, 37Hurwitz E.L. Morgenstern H. Cross-sectional associations of asthma, hay fever, and other allergies with major depression and low-back pain among adults aged 20–39 years in the United States.Am J Epidemiol. 1999; 150: 1107-1116Crossref PubMed Scopus (100) Google Scholar], and anxiety in women [[38]Addolorato G. Ancona C. Capristo E. et al.State and trait anxiety in women affected by allergic and vasomotor rhinitis.J Psychosom Res. 1999; 46: 283-289Abstract Full Text Full Text PDF PubMed Scopus (136) Google Scholar], which all pose a potential hindrance to performance. The mechanism by which seasonal environmental exposures may affect these cognitive and emotional parameters has not been elucidated. Reichenberg et al [[39]Reichenberg A. Yirmiya R. Schuld A. et al.Cytokine-associated emotional and cognitive disturbances in humans.Arch Gen Psychiatry. 2001; 58: 445-452Crossref PubMed Scopus (1124) Google Scholar] has shown activation of the innate immune response in humans by low-dose endotoxin exposure and subsequent release of pro-inflammatory cytokines (eg, IL-1, IL-6, TNF-α), some of which are also released by IgE-mediated responses in the nasal mucosa (see Fig. 1) [40Schwartz L.B. Mediators of human mast cells and human mast cell subsets.Ann Allergy. 1987; 58: 226-235PubMed Google Scholar, 41Schwartz L.B. Bradford T.R. Irani A.M. et al.The major enzymes of human mast cell secretory granules.Am Rev Respir Dis. 1987; 135: 1186-1189PubMed Google Scholar]. The exposure to endotoxins and secretion of cytokines induced depressive symptoms, anxiety, and cognitive impairment in the absence of constitutional symptoms (eg, decreased energy, anorexia, drowsiness) [39Reichenberg A. Yirmiya R. Schuld A. et al.Cytokine-associated emotional and cognitive disturbances in humans.Arch Gen Psychiatry. 2001; 58: 445-452Crossref PubMed Scopus (1124) Google Scholar, 42Pollmacher T. Haack M. Schuld A. et al.Low levels of circulating inflammatory cytokines–do they affect human brain functions?.Brain Behav Immun. 2002; 16: 525-532Crossref PubMed Scopus (179) Google Scholar]. Circulating cytokines may also induce activation of the HPA-axis [[43]Turnbull A.V. Rivier C. Regulation of the HPA axis by cytokines.Brain Behav Immun. 1995; 9: 253-275Crossref PubMed Scopus (239) Google Scholar], and elevation of corticotrophin-releasing factor (CRF) and cortisol have been shown to contribute to major affective illness [[44]Gold P.W. Chrousos G.P. Organization of the stress system and its dysregulation in melancholic and atypical depression: high vs low CRH/NE states.Mol Psychiatry. 2002; 7: 254-275Crossref PubMed Scopus (1076) Google Scholar]. Furthermore, cytokines in the respiratory tract may stimulate specific receptors present in the vagus nerve and affect brain function through this pathway [[45]Goehler L.E. Gaykema R.P. Hansen M.K. et al.Vagal immune-to-brain communication: a visceral chemosensory pathway.Auton Neurosci. 2000; 85: 49-59Abstract Full Text Full Text PDF PubMed Scopus (428) Google Scholar]. As such, cytokine release could contribute to decrements in cognition and to the onset or exacerbation of depression or anxiety, thus having detrimental effects on athletic performance. Athletes must prepare themselves for the various climatic conditions they will encounter in their training locale and the competition destinations. Knowledge of the temperature, humidity, sunlight, altitude, season, and type and concentration of pollen they will be exposed to can help athletes achieve peak performance through the use of prophylactic measures [[21]Gioulekas D. Damialis A. Papakosta D. et al.15-year aeroallergen records. Their usefulness in Athens Olympics, 2004.Allergy. 2003; 58: 933-938Crossref PubMed Scopus (21) Google Scholar]. Various nonpharmacologic therapies have been effective under certain conditions. For the treatment of AR, saline nasal irrigation is a safe and effective method of cleansing the nasal mucosa of allergens, and improving nasosinus disease [[46]Tomooka L.T. Murphy C. Davidson T.M. Clinical study and literature review of nasal irrigation.Laryngoscope. 2000; 110: 1189-1193Crossref PubMed Scopus (241) Google Scholar]. External nasal dilators have been used by athletes [[47]Griffin J.W. Hunter G. Ferguson D. et al.Physiologic effects of an external nasal dilator.Laryngoscope. 1997; 107: 1235-1238Crossref PubMed Scopus (85) Google Scholar] to increase nasal valve area, which is the narrowest area in the nasal canal [46Tomooka L.T. Murphy C. Davidson T.M. Clinical study and literature review of nasal irrigation.Laryngoscope. 2000; 110: 1189-1193Crossref PubMed Scopus (241) Google Scholar, 48Portugal L.G. Mehta R.H. Smith B.E. et al.Objective assessment of the breathe-right device during exercise in adult males.Am J Rhinol. 1997; 11: 393-397Crossref PubMed Scopus (40) Google Scholar], and to significantly decrease submaximal exercise-perceived exertion, heart rate, ventilation, and volume of oxygen use [[47]Griffin J.W. Hunter G. Ferguson D. et al.Physiologic effects of an external nasal dilator.Laryngoscope. 1997; 107: 1235-1238Crossref PubMed Scopus (85) Google Scholar]. Beginning with the earliest Olympic games, athletes have enhanced athletic performance through the use of foreign substances. In 1967, the International Olympic Commission developed a list of prohibited methods and substances to protect the health of, and foster equality for, all competing athletes [[49]Fraser A.D. Doping control from a global and national perspective.Ther Drug Monit. 2004; 26: 171-174Crossref PubMed Scopus (39) Google Scholar]. In the realm of allergic diseases, these restrictions have generated significant challenges. For example, the overall Olympic champion in women's gymnastics at the 2000 Olympics was disqualified and her gold medal withdrawn because she used a medication for AR which contained pseudoephedrine, allegedly without the intent of doping. Pseudoephedrine is no longer on the Prohibited List (Table 2). In 1972, the winner of the 400-meter men's Freestyle was disqualified because significant levels of the banned drug ephedrine were detected in his post-race urinalysis. The swimmer had used a combination ephedrine/theophylline preparation for the prerace treatment of his asthma [[22]Fitch K.D. Management of allergic Olympic athletes.J Allergy Clin Immunol. 1984; 73: 722-727Abstract Full Text PDF PubMed Scopus (51) Google Scholar]. These examples highlight the importance for athletes, coaches, and team physicians to understand the potential that a particular medication, apparently innocuous, may contain or be contaminated by a particular banned substance. To establish a universal internationally standardized Olympic antidoping code, the World Anti-Doping Agency (WADA) was established in 1999. The WADA disseminates current information on substances prohibited for use by competitive athletes. WADA maintains and updates the World Anti-Doping Code Prohibited List, which includes substances that are prohibited only during competition, others that are always prohibited, and others that are on the monitoring list (see Table 2). More and current updated information regarding antidoping rules, regulations, and prohibited substance listings can be found at www.wada-ama.org.Table 2Medical treatment of seasonal allergic diseases related to athletesDrugMode of actionUseCommentsWADA statusaBased on the WADA 2005 Prohibited List International Standard, see www.wada.com for current updated information.AntihistaminesHistamine antagonist at H1 receptor siteAllergic rhinitis and conjunctivitis, urticaria, allergic asthmaFirst-line therapy for mild to moderate symptomsNot prohibited Oral first-generationOften combined with oral decongestant Oral second-generationVery effective for symptoms of rhinorrhea, sneezing, and nasal and ocular itch IntranasalFirst-generation formulations have significant CNS adverse effects, second-generation preferred Topical (optical)CorticosteroidsAntiinflammatoryTreatment of many allergic diseases: allergic rhinitis and conjunctivitis, asthma, urticaria, and atopic dermatitisPotent antiinflammatorySystemicbOrally, rectally, IV, or IM. uses are prohibitedcIn competition only. Any substance or method that is on the Prohibited List must be granted a Therapeutic Use Exemption (TUE) for use.; inhaled and intranasal only require abbreviated TUEdnonsystemic routes require the completion of an abbreviated TUE application. Dermatological preparations are not prohibited.; topical are not prohibited Oralintranasal — first-line therapy for moderate to severe symptoms of rhinitis Inhaledoral — severe exacerbations of asthma, urticaria Intranasal Topical (skin)Decongestantsα-adrenergic agonistRhinitisReduces nasal congestionEphedrine is prohibitedeProhibited when its concentration in urine is >5 mcg/mL., phenylephrine, phenylpropanolamine, pseudoephedrine, and synephrine are on monitoring listfThese stimulants are no longer on the Prohibited List, but are on the 2005 monitoring program "in order to detect patterns of misuse in sports." OralCauses nasal vasoconstrictionMay cause insomnia, loss of appetite, and nervousness IntranasalIntranasal may cause rebound nasal congestion (rhinitis medicamentosa)Cromolyn/nedocromil sodiumMast cell stabilizerAsthma, allergic rhinitisNonsteroidal antiinflammatoryNot prohibited OralInhibits degranulationMinimal adverse effects InhaledRequires multiple daily dosing IntranasalAnticholinergicMuscarinic receptor antagonistAsthma, rhinitisEffectively reduce rhinorrheaNot prohibited InhaledRole in acute bronchospasm IntranasalLeukotriene inhibitorsInhibit phospholipid metabolismAsthmaNonsteroidal antiinflammatoryNot prohibited OralVery effective in preventing EIASteroid sparing controllerAllergen immunothera
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