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Nasal Issues in Athletes

Navarro, Rodolfo R. MD, CAQSM1,2; Romero, Leigh MD, CAQSM3; Williams, Kwani MD1

doi: 10.1249/JSR.0b013e31827dc22c
Head, Neck, and Spine: Section Articles

Nasal problems in athletes can have detrimental impacts on athletic performance. Increasingly strenuous physical exercise requires the nasal respiratory system to function efficiently in order to meet the increasing oxygen demand. Generally, nasal issues can be grouped into traumatic and nontraumatic categories. Rhinitis is the most common nasal issue in athletes and can have numerous effects on athletes. Recent studies demonstrate the “J curve” and “open window” theories of upper respiratory infection incidence in athletes yet are unable to link immunoglobulin or serum immune markers to incidence of symptoms or infection. Acute nasal trauma can be misleading; thus, a detailed examination is appropriate. Trauma also can be a cause of chronic nasal issues in athletes, as demonstrated by subsequent decreased olfaction in boxers.

1Department of Family and Community Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX; 2Department of Orthopedic Surgery, University of Texas Health Science Center at San Antonio, San Antonio, TX ; and 3MedSpring Urgent Care, Austin, TX

Address for correspondence: Rodolfo R. Navarro, MD, CAQSM, Department of Family and Community Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, MS 7795, San Antonio, TX 78229; E-mail:

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The nasal structure plays an obviously important role in athletic performance. Infectious, chronic, or traumatic nasal issues can adversely affect athletes and are very common. Increasingly strenuous physical exercise requires the nasal respiratory system to function efficiently in order to meet the increasing oxygen demand (24,28). Athletes have reported substantial decrements in athletic performance and quality of life due to upper respiratory symptoms (22,31,32). Upper respiratory infection (URI) has been the most common infectious illness reported by elite athletes, including Olympians (34,44). Additionally, nasal fractures account for almost 40% of acute bony injuries, which mostly are due to the prominent position of the nose on the face (24,25). Generally, nasal issues can be grouped into either traumatic or nontraumatic categories. Traumatic issues are more visible, have the possibility of a residual facial defect, and often cause psychological trauma (37). Despite this, many nasal fractures go undiagnosed because patients do not recognize the injury (25). Nontraumatic nasal issues include URI, rhinitis, sinusitis, and polyposis (8). This review will synthesize recent investigations regarding nasal issues in athletes.

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Anatomy and Function

The bones of the nose include the nasal bones, the vomer, the ethmoid, the frontal process of the maxilla, and the nasal process of the frontal bone. The cartilaginous structures of the nose include the septum, the two lower lateral cartilages, and the two upper lateral cartilages. Overlying this framework of bones and cartilage are soft tissues, mucous glands, muscles, and nerves responsible for sensation and function of the nose (25). The blood supply to the nose is extensive, and epistaxis typically arises from Kiesselbach’s plexus. Epistaxis also is encountered frequently in acute nasal injuries. The anterior ethmoid artery and the sphenopalatine artery can be sources of anterior and posterior epistaxis, respectively, in cases of trauma.

Functionally, the nasal passages are important in conditioning inspired air as it courses to the lungs. This same mechanism also serves an important immunologic role. The highly vascularized epithelial tissue of the nasal passageways warms air to ideal temperatures. The nasal hair and mucociliary elevator system function to filter and remove foreign air particles. The turbulent airflow can cause air particles to become entrapped within the nasal hair and mucous. Finally, the epithelial skin layer and acellular basement membrane of the upper respiratory tract serve as a hard physical barrier to entry of pathogens. Thus, the entire complex forms a natural barrier to infection and provides the first system of defense against potentially infectious pathogens (19,24).

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Rhinitis, allergic and nonallergic, is the most common nasal condition in athletes, affecting as many as one half of all athletes, and atopy is also common in this same cohort (5,6,15,23). Endurance athletes, including swimmers, more often report symptoms of rhinitis (1,5,15,23). There also is growing evidence that asthma and allergic rhinitis are linked, given their common comorbidity and growing pathophysiologic proof of a unified upper and lower airway (6,9,12,18).

Most athletes typically will experience exposure to one or more symptom triggers of rhinitis, including seasonal allergens, cold air, pollutants, chemicals, and even exercise itself. Typical rhinitis symptoms include nasal congestion, increased mucous expression, nasal itching, sneezing, rhinorrhea, and postnasal drainage (5,6,22,24). The nasal, sinus, and airway obstruction and decreased mucociliary clearance can lead to sinus pain or infection (sinusitis), headache, cough, fever, and epistaxis. As well, rhinitis has been linked to difficulties with sleep from nasal congestion and from the direct influence of inflammatory mediators. This can result in daytime somnolence, fatigue, irritability, difficulty learning, decreased physical performance, and productivity (1,5,10). Missed school days, as well as poor school performance, have been noted in patients with allergic rhinitis, and overall quality of life in patients with perennial allergic rhinitis has been reported to be as poor as in patients with asthma (18).

Treatment for rhinitis is multifactorial and includes numerous medications. Intranasal corticosteroids are considered first-line therapy for treatment of rhinitis, whether perennial or seasonal (18,19,22,40). Intranasal corticosteroids have been shown also to improve asthma symptoms. Treatment of comorbid allergic rhinitis is recommended in known asthmatic patients (13). Usual treatment also includes nasal saline flushes, systemic or topical decongestants, oral or topical antihistamines, cromolyn, leukotriene receptor antagonists, avoidance of known triggers, corticosteroids, and immunotherapy (12,18). Table 1 summarizes treatment options for allergic and nonallergic rhinitis. Considerations that should be accounted for when prescribing such medications include route of administration, individual response, effectiveness for a specific symptom, cost, and status regarding prohibition of use (4,12). For example, despite a low cost and powerful efficacy in relieving severe symptoms, systemic glucocorticosteroids are prohibited by the World Anti-Doping Agency (WADA) for athletes in competition.

Table 1

Table 1

Classically, sympathomimetic agents have been considered performance enhancing and thus are prohibited by many competitive governing bodies, including WADA (6,24). These medications have been replaced largely by the intranasal medications discussed previously. Few sympathomimetic agents are still widely used in the treatment of rhinitis, but only pseudoephedrine is prohibited while in competition, with a urine threshold of 150 μg·mL−1 (46). Individual variability of pseudoephedrine excretion makes a single threshold difficult to establish. However, a recent investigation funded by WADA found that maximum therapeutic doses of oral pseudoephedrine (240 mg·d−1) do not cause urine concentrations above the 150 μg·mL−1 threshold if the medication is stopped at least 24 h before a urine test (3). Phenylephrine, phenylpropanolamine, and synephrine are not considered prohibited substances but remain on the WADA 2013 Monitoring Program (46).

Many upper airway symptoms often can be relieved by exercise (the “neck check”), but some athletes complain of increased rhinitis symptoms in the postexercise period (6,15,24,). There is proof of an increased risk for an exercise-induced rhinitis, which especially is noted in swimming athletes, even if only temporary (1,15,23). Gelardi et al. (15) recently showed the presence of an inducible neutrophilic rhinitis in 74 competitive teenage swimmers, suggestive of an irritant exposure cause. At baseline, the athletes most commonly reported nasal obstruction, rhinorrhea, and nasal burning that occurred within 1 h of swimming and lasted at least 12 h. Otolaryngology evaluation, nasal cytology by smear, and skin prick allergy testing revealed that in symptomatic patients, 35% expressed a neutrophilic rhinitis without identification of infectious agents. After use of the nasal clip, the same group showed a significant reduction in the nasal cellular infiltration and decreased (improved) nasal resistance.

This correlates with multiple previous studies. In competitive swimmers at a local Italian swimming pool, almost one third reported new temporary rhinosinusitis symptoms after swimming. They also reported no chronic negative effects on nasal patency or frequency of rhinosinusitis (28). Competitive swimmers in an intense training period have been shown to have increased rhinitis symptoms that normalized with 2 wk of rest (5). Conversely, a team of adolescent Scottish competitive swimmers showed no increase in tidal or nasal nitric oxide following a high-intensity training session, suggesting no association between upper or lower respiratory tract inflammation and high-intensity training (7).

Given the burden of rhinitis in athletes, and the potential for performance decrement, athletes should be encouraged to seek treatment for rhinitis symptoms. Additionally, those with routine or chronic rhinitis should be screened for comorbid asthma and atopy.

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Acute upper respiratory tract infection is quite common in athletes, despite common thought that competitive athletes are “healthier.” As mentioned, URI has been reported to be the most common reason for presenting to a sports medicine clinic and can account for at least one third of such visits (8,14). Data from the Sydney 2000 Olympic Games show that 33% of all consultations with the medical team were categorized as respiratory tract illnesses (35). One half of Australian Olympic athletes self-reported experiencing allergic rhinoconjunctivitis (23). Within athletes as a group, the incidence of URI is highest in swimmers (as high as 74%) (5).

Because of the potential to affect performance, rapid diagnosis and resolution of symptoms are the primary goal. Common symptoms include nasal congestion, rhinorrhea, sore throat, cough, fatigue, and headache. Given that most URIs are caused by viral pathogens, the symptoms are typically transient in nature. Upper respiratory symptoms can be misleading to both athletes and physicians, and objective confirmation of a viral or bacterial pathogen is not found in almost one third of cases (8). The “J curve” is a model for demonstrating the relationship between exercise intensity and immune response. It proposes that individuals who partake in moderate physical activity are at lower risk of illness versus those who engage in excessive amounts of strenuous physical exercise, such as endurance athletes. While moderate amounts of exercise have been shown to decrease the incidence of URI, the proposed immune impairment that has been observed in endurance athletes has not been related consistently to incidence of infection (17,26).

A growing concept in URI incidence in athletes is the “open window” theory, which purports that temporary immune system suppression following high-volume or intensity training leaves these athletes susceptible to infection. This has been theorized to be due to temporary suppression of cellular and humoral components of the innate and acquired immune systems. Kakanis et al. (21) investigated male cyclists’ immunologic status after a single bout of high-intensity endurance exercise. Neutrophil phagocytic function, lymphocyte concentration, and natural killer cell concentration remained suppressed up to 24 h after the single bout of exercise. Neutrophil concentration and neutrophil phagocytic function showed an initial increase up to 2 h postexercise but a subsequent decrease to or below baseline levels afterward. The authors propose that circulating stress hormones incite a release in stored neutrophils. Despite this initial surge, the decrease in phagocytic function, lymphocyte concentration, and NK cell concentration certainly has implications on potential illness in athletes in the postexercise period.

Additionally, multiple studies have utilized salivary immunoglobulin levels as objective markers for decreased immunologic function. Peters et al. (30) demonstrated a drop in the 2-h postcompetition salivary IgA levels of ultramarathon runners during a 6-wk investigation. The salivary IgA levels required 24 h to return to precompetition levels. There was no demonstrable association of self-reported URI symptoms and salivary IgM or IgA levels. Moreira et al. (27) also demonstrated a decline in absolute salivary IgA and secretion rates in professional Brazilian Futsal (indoor soccer) athletes when measured immediately before and immediately after a competitive match. Two thirds of the athletes subjectively rated their exertion levels for the matches as “strong” and “extremely strong.” Yamauchi et al. (47) found a significant relationship between decreased salivary IgA levels 1 d before the increased salivary expression of Epstein-Barr DNA in 32 collegiate rugby players during a 1-month study. The Epstein-Barr virus expression also correlated with the appearance of self-reported URI symptoms.

Conversely, some data demonstrate poor association between salivary markers and URI incidence. Vardiman et al. (42) reported incidence rates of URI symptoms similar to controls and without significant association to absolute salivary IgA levels in female collegiate soccer athletes across a single division I level competitive season. Despite correction for dehydration, no significant differences in expression rates were found between the test subjects and controls. The authors propose that the level of intensity or the timing of intensity (i.e., most intense training at the beginning of season) was not sufficient to affect the salivary IgA levels. Cunniffe et al. (11) followed professional European rugby players across a 48-wk season, showing that salivary flow rates, salivary IgA levels, salivary lysozyme, and cortisol levels did not correlate with URI incidence. Overall, 92% of the athletes self-reported at least one URI in the season or a mean of nearly four URIs per athlete per season.

While the data presented here supports the notion that salivary IgA expression has no direct relation to URI incidence, the evidence suggests a complex threshold for URI incidence in athletes. A 30% decrease in salivary IgA concentrations may increase the risk of URI, and evidence suggests a noninfectious inflammatory response or viral reactivation causing upper respiratory symptoms (11,30). Additionally, upper respiratory symptoms have shown a trend toward an inverse relationship between salivary Epstein-Barr DNA expression and salivary IgA expression (47). There is a suggestion that the “open window” reflects an IgA threshold that must be attained in conjunction with a noninfectious response or a reactivation of latent Epstein-Barr infection (47). This also would help explain the difficulty in diagnosing an infectious pathogen in many patients, a known limitation found in many of the studies discussed here (8,27,30,39,42,47). Most of the investigations reviewed here relied on athletes’ self-reporting of symptoms. Two studies attempted to quantify the URI but showed no particular association except between their reported immune system markers and URI incidence (11,15).

Finally, treatment of URIs in athletes is the same as the typical management in the outpatient setting for nonathletic populations. Given that most symptoms are of noninfectious etiologies or viral in nature, standard treatment involves use of conservative measures without need for antibiotics. These conservative measures include adequate fluid intake, humidified air, nasal saline flushes, antipyretic medication, analgesic medication, antitussive medication, and rest (45). Rising prevalence of antibiotic resistance has led to recommendations to utilize conservative measures prior to initiation of antibiotic therapy, which are mostly indicated for identified bacterial complications, including otitis media and sinusitis (45).

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The nose is the most commonly fractured bone in the adult face (33). Nasal fractures account for 40% of facial bone injuries and up to 84.7% in combative sports (25,38). Although most of the nasal structures are cartilaginous, the nasal bones are fractured usually in an injury (25). Nasal injuries can occur in isolation or in association with other facial injuries. However, the most common injury to the nose is a fracture (41). Almost half of all facial fractures have been reported to be sports related, and more than 60% of all facial fractures included a nasal fracture. Additionally, almost half of these cases involved patients aged 17 years and younger (29). An international study in 2009 demonstrated the highest incidence of sports-related facial bone fracture was 40.3% in the 11- to 20-year-old age group with a significant male predominance (20). The two sports most likely to result in nasal fracture in the high school population in the United States are softball (22.8%) and basketball (19.7% boys and 19.3% girls). This is followed distantly by baseball (11.5%), soccer (9.4% boys and 8.6% girls), volleyball (4.2%), wresting (3.9%), and football (1.4%) (41).

The assessment of a nasal injury should be thorough to rule out any other head and neck injury. The initial assessment should begin with fundamental trauma management principles: ensure the athlete has a patent airway, is ventilating well, and has uncompromised circulatory status (36). Once overall stability is ensured, other associated fractures and injuries should be ruled out. All bony structures of the face and neck should be inspected meticulously and palpated systematically. The eye should be examined for symmetry and mobility of gaze (25). Palpation of the nasal structures may reveal edema, epistaxis, or deformity and may elicit crepitus and tenderness. If epistaxis is noted, hemostasis usually can be achieved by applying direct pressure by pinching the nasal septum or applying ice to the nasal septum for up to 10 to 15 min. Ice also can be applied to the back of the neck to cause reflex vasoconstriction. Sometimes nasal packing and decongestant spray are necessary for hemostasis (33). Nasal packing rarely is associated with toxic shock syndrome (25). If packing fails to control the epistaxis, arterial ligation or interventional arterial embolization may be needed (33). It is imperative to rule out a nasal septal hematoma, which is a blood-filled cavity between the cartilage and the supporting perichondrium and usually can be visualized directly within hours of the initial injury. Any septal hematoma should be aspirated or incised immediately using local anesthesia. Failure to identify a septal hematoma (or if left untreated) can lead to infection, followed by necrosis, and finally may result in a permanent saddle nose deformity, which requires surgical repair.

Nondisplaced nasal fractures typically require no treatment, whereas displaced or acutely angulated fractures can be reduced by digital pressure (37). The goal of closed reduction is to realign cartilaginous and bony structures to their locations before the injury to decrease discomfort and maximize airway patency. The indications for closed reduction are unilateral or bilateral fracture of the nasal bone and fracture of the nasal-septal complex with nasal deviation less than one half the width of the nasal bridge (2). However, the indications for open reduction are extensive fracture-dislocation of the nasal bones and septum, nasal–septal complex with nasal deviation exceeding one half the width of the nasal bridge, fracture-dislocation of the caudal septum, open septal fractures, and persistent deformity after closed reduction (2). No clinical evidence exists to mandate early fracture reduction; however, reduction should be done within the first 10 d after the injury, before the nasal bones begin to fixate (25). However, after closed reduction, the incidence of nasal deformities requiring subsequent rhinoplasty can be as high as 50% (25). Need for rhinoplasty after closed reduction has been reported as high as 36% in high school students in the United States (41).

Although intervention should occur as soon as possible, even a nasal fracture does not require immediate removal from sports. Romeo et al. (36) described conditions under which athletes with a nasal fracture may return to play. These conditions are summarized in Table 2. If the athlete does return to play after an acute nasal fracture, protective headgear/face mask is recommended. A follow-up examination should be scheduled within 3 to 5 d if edema, epistaxis, or ecchymosis limits the examination. Other findings that should prompt immediate subspecialty referral are cerebrospinal fluid leakage, subcutaneous emphysema, mental status changes, new malocclusion, or limited extraocular movement. Although plain radiography is indicated rarely for uncomplicated nasal fractures and will not allow identification of cartilaginous disruptions, computed tomography imaging is necessary to assess for facial and mandibular fractures when findings such as cerebrospinal fluid (CSF) rhinorrhea, extra-ocular movement abnormalities, or malocclusion are noted (25).

Table 2

Table 2

A recent study investigated the impact of recurrent head trauma on olfactory function in boxers. It concluded that boxing and chronic nasal trauma reduces olfactory performance, particularly olfactory threshold and odor identification. The study enrolled 50 men who trained and competed regularly. Subjective olfactometry was tested for threshold, discrimination, and identification. Odor threshold and identification were found to be reduced significantly in the boxers. The authors propose that the olfactory loss appears to be explained best by anatomical changes due to recurrent nasal trauma reducing the airflow toward the olfactory cleft (conductive smell loss) and partial disruption of the olfactory fila at the cribriform plate (peripheral neuronal damage). The olfactory threshold is a sign for conductive olfactory loss, as well as the most sensitive measure of general olfactory impairment. Protective equipment showed associations with reduced olfactory losses. Interestingly, associations also were made between glove cushioning and better odor identification, as well as the use of head protection in fights and odor threshold. The study highlights that use of protective equipment should be more valued, even in competitive fights (43).

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Review of recent investigations on the topic of nasal problems in athletes confirms previous findings. Rhinitis is common in athletes and occurs slightly more frequently in swimming athletes, though this appears to be an inducible and temporary issue (15). There exists a prevalence of upper respiratory symptoms or infections at similar rates to the general population. Cytological evidence points to an immunosuppressed “open window” for infection, especially following prolonged high-intensity bouts of physical exercise. Markers of immunity, especially salivary IgA, do not correlate with incidence of upper respiratory symptoms or infection (21,27,30,42,47). Training levels are related variably to incidence of URI (11,30,42). Nasal trauma needs to be evaluated and managed systematically to limit untoward outcomes. Recurrent head trauma in boxers appears to be associated with decreased long-term olfactory sensation due to anatomic or neuronal changes (43).

With nasal issues being common and affecting athletes’ quality of life and performance, sports medicine physicians need to recognize and manage appropriately such issues. Because of the potential for use of a prohibited medication, physicians and athletes should have open discussions about appropriate use of medications. Should an athlete require use of a prohibited medication, they are advised to submit a Therapeutic Use Exemption via their International Federation or National Anti-Doping Agency. More information about Therapeutic Use Exemptions, WADA-prohibited substances, and drug testing can be found at the WADA Web site ( For convenience, the WADA Prohibited List also is available via a mobile Web site ( and a downloadable smartphone application.

Drs. Navarro, Romero, and Williams have no conflicts of interest or funding disclosures to report with regard to the work of this manuscript.

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1. Alves A, Martins C, Delgado L, et al.. Exercise-induced rhinitis in competitive swimmers. Am. J. Rhinol. Allergy . 2010; 24: e114–7.
2. Bailey BJ. Nasal fractures. In: Bailey BJ, editor. Head and Neck Surgery — Otolaryngology Volume 1 . Philadelphia: J. B. Lippincott Company; 1993.
3. Barroso O, Goudreault D, Carbó Banús ML, et al.. Determination of urinary concentrations of pseudoephedrine and cathine after therapeutic administration of pseudoephedrine-containing medications to healthy subjects: implications for doping control analysis of these stimulants banned in sport. Drug Test Anal . 2012; 4: 320–9. doi: 10.1002/dta.291.
4. Berry C, Wagner DR. Effect of pseudoephedrine on 800 m run times of female collegiate track athletes. Int. J. Sports Physiol. Perform . 2012; 7: 237–41.
5. Bougault V, Turmel J, Boulet LP. Effect of intense swimming training on rhinitis in high-level competitive swimmers. Clin. Exp. Allergy . 2010; 40: 1238–46. Epub 2010 Jun 7.
6. Boulet LP. Cough and upper airway disorders in elite athletes: a critical review. Br. J. Sports Med . 2012; 46: 417–21.
7. Clearie KL, Vaidyanathan S, Williamson PA, et al.. Effects of chlorine and exercise on the unified airway in adolescent elite Scottish swimmers. Allergy . 2010; 65: 269–73.
8. Cox AJ, Gleeson M, Pyne DB, et al.. Clinical and laboratory evaluation of upper respiratory symptoms in elite athletes. Clin. J. Sport Med . 2008; 18: 438–45.
9. Ciprando G, Cirillo I. The lower airway pathology of rhinitis. J. Allergy Clin. Immunol . 2006; 118: 1105–9.
10. Craig TJ, McCann JL, Gurevich F, Davies MJ. The correlation between allergic rhinitis and sleep disturbance. J. Allergy Clin. Immunol . 2004; 114: S139–45.
11. Cunniffe B, Griffiths H, Proctor W, et al.. Mucosal immunity and illness incidence in elite rugby union players across a season. Med. Sci. Sports Exerc . 2011; 43: 388–97.
12. Dykewicz MS, Hamilos DL. Rhinitis and sinusitis. J. Allergy Clin. Immunol . 2010; 125: S103–15.
13. Feng CH, Miller MD, Simon RA. The united allergic airway: connections between allergic rhinitis, asthma, and chronic sinusitis. Am. J. Rhinol. Allergy . 2012; 26: 187–90.
14. Fricker PA. Infectious problems in athletes: an overview. In: Fields KB, Fricker PA, editors. Medical Problems in Athletes . Malden (MA): Blackwell Science; 1997. pp. 3–5.
15. Gelardi M, Ventura MT, Fiorella R, et al.. Allergic and non-allergic rhinitis in swimmers: clinical and cytological aspects. Br. J. Sports Med . 2012; 46: 54–8.
16. Gillies H, Derman WE, Noakes TD, et al.. Pseudoephedrine is without ergogenic effects during prolonged exercise. J. Appl. Physiol . 1996; 81: 2611–7.
    17. Gleeson M. Immune function in sport and exercise. J. Appl. Physiol . 2007; 103: 693–9.
    18. Greiner AN, Hellings PW, Rotiroti G, Scadding GK. Allergic rhinitis. Lancet . 2011; 378: 2112–22.
    19. Harris MD. Infectious disease in athletes. Curr. Sports Med. Rep . 2011; 10: 84–9.
    20. Hwang K, You SH, Lee HS. Outcome analysis of sports-related multiple facial fractures. J. Craniofac. Surg . 2009; 20: 825–9.
    21. Kakanis MW, Peake J, Brenu EW, et al.. The open window of susceptibility to infection after acute exercise in healthy young male elite athletes. Exerc. Immunol. Rev . 2010; 16: 119–37.
    22. Katelaris CH, Carrozzi FM, Burke TV, Byth K. Effects of intranasal budesonide on symptoms, quality of life, and performance in elite athletes with allergic rhinoconjunctivitis. Clin. J. Sport Med . 2002; 12: 296–300.
    23. Katelaris CH, Carrozzi FM, Burke TV, Byth K. Patterns of allergic reactivity and disease in Olympic athletes. Clin. J. Sport Med . 2006; 16: 401–5.
    24. Katz RM. Rhinitis in the athlete. J. Allergy Clin. Immunol . 1984; 73: 708–11.
    25. Kucik CJ, Clenney T, Phelan J. Management of acute nasal fractures. Am. Fam. Physician . 2004; 70: 1315–20.
    26. Matthews CE, Ockene IS, Freedson PS, et al.. Moderate to vigorous physical activity and risk of upper-respiratory tract infection. Med. Sci. Sports Exerc . 2002; 34: 1242–8.
    27. Moreira A, Arsati F, de Oliveira Lima-Arsati YB, et al.. Salivary immunoglobulin A responses in professional top-level Futsal players. J. Strength Cond. Res . 2011; 25: 1932–6.
    28. Ondolo C, Aversa S, Passali F, et al.. Nasal and lung function in competitive swimmers. Acta Otorhinolaryngol. Ital . 2009; 29: 137–43.
    29. Perkins SW, Dayan SH, Sklarew EC, et al.. The incidence of sports-related facial trauma in children. Ear Nose Throat J . 2000; 79: 632–4, 636, 638.
    30. Peters EM, Shaik J, Kleinveldt N. Upper respiratory tract infection symptoms in ultramarathon runners not related to immunoglobulin status. Clin. J. Sport Med . 2010; 20: 39–46.
    31. Pyne DB, Hopkins WG, Batterham AM, et al.. Characterising the individual performance responses to mild illness in international swimmers. Br. J. Sports Med . 2005; 39: 752–6.
    32. Pyne DB, McDonald WA, Gleeson M, et al.. Mucosal immunity, respiratory illness, and competitive performance in elite swimmers. Med. Sci. Sports Exerc . 2001; 33: 348–53.
    33. Reehal P. Facial injury in sport. Curr. Sports Med. Rep . 2010; 9: 27–34.
    34. Reeser JC, Willick S, Elstad M. Medical services provided at the Olympic Village polyclinic during the 2002 Salt Lake City Winter Games. WMJ . 2003; 102: 20–5.
    35. Robinson D, Milne C. Medicine at the 2000 Sydney Olympic Games: the New Zealand health team. Br. J. Sports Med . 2002; 36: 229.
    36. Romeo SJ, Hawley CJ, Romeo MW, et al.. Sideline management of facial injuries. Curr. Sports Med. Rep . 2007; 6: 155–61.
    37. Schultz RC, de Camara DL. Athletic facial injuries. JAMA . 1984; 252: 3395–8.
    38. Shirani G, Kalantar Motamedi MH, Ashuri A, et al.. Prevalence and patterns of combat sport related maxillofacial injuries. J. Emerg. Trauma Shock . 2010; 3: 314–7.
    39. Spence L, Brown WJ, Pyne DB, et al.. Incidence, etiology, and symptomatology of upper respiratory illness in elite athletes. Med. Sci. Sports Exerc . 2007; 39: 577–86.
    40. Sur DK, Scandale S. Treatment of allergic rhinitis. Am. Fam. Physician . 2010; 81: 1440–6.
    41. Swenson DM, Yard EE, Collins CL, et al.. Epidemiology of US high school sports-related fractures, 2005–2009. Clin. J. Sport Med . 2010; 20: 293–9.
    42. Vardiman JP, Riggs CE, Galloway DL, et al.. Salivary IgA is not a reliable indicator of upper respiratory infection in collegiate female soccer athletes. J. Strength Cond. Res . 2011; 25: 1937–42.
    43. Vent J, Koenig J, Hellmich M, et al.. Impact of recurrent head trauma on olfactory function in boxers: a matched pairs analysis. Brain Res . 2010; 1320: 1–6.
    44. Weidner TG, Anderson BN, Kaminsky LA, et al.. Effect of a rhinovirus-caused upper respiratory illness on pulmonary function test and exercise responses. Med. Sci. Sports Exerc . 1997; 29: 604–9.
    45. Wong DM, Blumberg DA, Lowe LG. Guidelines for the use of antibiotics in acute upper respiratory tract infections. Am. Fam. Physician . 2006; 74: 956–66.
    47. Yamauchi R, Shimizu K, Kimura F, et al.. Virus activation and immune function during intense training in rugby football players. Int. J. Sports Med . 2011; 32: 393–8. doi: 10.1055/s-0031-1271674.
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