Exercise-Induced Bronchoconstriction and the Air We Breathe.

An association between airway dysfunction and airborne pollutant inhalation exists. Volatilized airborne fluorocarbons in ski wax rooms, particulate matter, and trichloromines in indoor environments are suspect to high prevalence of exercise-induced bronchoconstriction and new-onset asthma in athletes competing in cross-country skiing, ice rink sports, and swimming. Ozone is implicated in acute decreases in lung function and the development of new-onset asthma from exposure during exercise. Mechanisms and genetic links are proposed for pollution-related new-onset asthma. Oxidative stress from airborne pollutant inhalation is a common thread to progression of airway damage. Key pollutants and mechanisms for each are discussed.

Air quality and temperature effects on exercise-induced bronchoconstriction.

Exercise-induced bronchoconstriction (EIB) is exaggerated constriction of the airways usually soon after cessation of exercise. This is most often a response to airway dehydration in the presence of airway inflammation in a person with a responsive bronchial smooth muscle. Severity is related to water content of inspired air and level of ventilation achieved and sustained. Repetitive hyperpnea of dry air during training is associated with airway inflammatory changes and remodeling. A response during exercise that is related to pollution or allergen is considered EIB. Ozone and particulate matter are the most widespread pollutants of concern for the exercising population; chronic exposure can lead to new-onset asthma and EIB. Freshly generated emissions particulate matter less than 100 nm is most harmful. Evidence for acute and long-term effects from exercise while inhaling high levels of ozone and/or particulate matter exists. Much evidence supports a relationship between development of airway disorders and exercise in the chlorinated pool. Swimmers typically do not respond in the pool; however, a large percentage responds to a dry air exercise challenge. Studies support oxidative stress mediated pathology for pollutants and a more severe acute response occurs in the asthmatic. Winter sport athletes and swimmers have a higher prevalence of EIB, asthma and airway remodeling than other athletes and the general population. Because of fossil fuel powered ice resurfacers in ice rinks, ice rink athletes have shown high rates of EIB and asthma. For the athlete training in the urban environment, training during low traffic hours and in low traffic areas is suggested.

Air quality and exercise-induced bronchoconstriction in elite athletes.

A higher prevalence of airway hyperresponsiveness, airway remodeling, and asthma has been identified among athletes who compete and train in environmental conditions of cold dry air and/or high air pollution. Repeated long-duration exposure to cold/dry air at high minute ventilation rates can cause airway damage. Competition or training at venues close to busy roadways, or in indoor ice arenas or chlorinated swimming pools, harbors a risk for acute and chronic airway disorders from high pollutant exposure. This article discusses the effects of these harsh environments on the airways, and summarizes potential mechanisms and prevalence of airway disorders in elite athletes.

Palliative and end-of-life care training during the surgical clerkship.

BACKGROUND: In 2000, the Liaison Committee on Medical Education required that all medical schools provide experiential training in end-of-life care. To adhere to this mandate and advance the professional development of medical students, experiential training in communication skills at the end-of-life was introduced into the third-year surgical clerkship curriculum at Wright State University Boonshoft School of Medicine. MATERIALS AND METHODS: In the 2007-08 academic year, 97 third-year medical students completed six standardized end-of-life care patient scenarios commonly encountered during the third-year surgical clerkship. Goals and objectives were outlined for each scenario, and attending surgeons graded student performances and provided formative feedback. RESULTS: All 97 students, 57.7% female and average age 25.6 ± 2.04 y, had passing scores on the scenarios: (1) Adult Hospice, (2) Pediatric Hospice, (3) Do Not Resuscitate, (4) Dyspnea Management/Informed Consent, (5) Treatment Goals and Prognosis, and (6) Family Conference. Scenario scores did not differ by gender or age, but students completing the clerkship in the first half of the year scored higher on total score for the six scenarios (92.8% ± 4.8% versus 90.5% ± 5.0%, P = 0.024). CONCLUSIONS: Early training in end-of-life communication is feasible during the surgical clerkship in the third-year of medical school. Of all the scenarios, "Conducting a Family Conference" proved to be the most challenging.

An official American Thoracic Society clinical practice guideline: exercise-induced bronchoconstriction.

BACKGROUND: Exercise-induced bronchoconstriction (EIB) describes acute airway narrowing that occurs as a result of exercise. EIB occurs in a substantial proportion of patients with asthma, but may also occur in individuals without known asthma. METHODS: To provide clinicians with practical guidance, a multidisciplinary panel of stakeholders was convened to review the pathogenesis of EIB and to develop evidence-based guidelines for the diagnosis and treatment of EIB. The evidence was appraised and recommendations were formulated using the Grading of Recommendations, Assessment, Development, and Evaluation approach. RESULTS: Recommendations for the treatment of EIB were developed. The quality of evidence supporting the recommendations was variable, ranging from low to high. A strong recommendation was made for using a short-acting ß(2)-agonist before exercise in all patients with EIB. For patients who continue to have symptoms of EIB despite the administration of a short-acting ß(2)-agonist before exercise, strong recommendations were made for a daily inhaled corticosteroid, a daily leukotriene receptor antagonist, or a mast cell stabilizing agent before exercise. CONCLUSIONS: The recommendations in this Guideline reflect the currently available evidence. New clinical research data will necessitate a revision and update in the future.

Exercise-induced bronchoconstriction and vocal cord dysfunction: two sides of the same coin?

Patients are referred often because of self-reported symptoms of dyspnea and wheeze during exercise. The two common causes of exercise-induced dyspnea are exercise-induced bronchoconstriction (EIB) and vocal cord dysfunction (VCD). It can be extraordinarily difficult to differentiate between the two, especially because they may coexist in the same patient. EIB is caused by bronchial smooth muscle constriction in the lower airways due to the inhalation of dry air or allergens during exercise; it is associated with the release of bronchoconstricting mediators from airway cells. EIB can occur in patients with or without persistent asthma. In contrast, VCD is associated with the paradoxical adduction of the vocal cords, especially during inhalation, which may produce inspiratory stridor. VCD can be solitary or comorbid with asthma and/or EIB. EIB classically is most severe after the cessation of exercise, while VCD typically occurs during exercise and resolves quickly upon exercise cessation. However, history is not adequate to differentiate between EIB and VCD, and appropriate challenge tests and flexible laryngoscopy during exercise are often necessary for diagnosis. This article examines our current understanding of these entities and discusses the mechanism, prevalence, diagnosis, and treatment.

Small things make a big difference: particulate matter and exercise.

The increased risk of morbidity and mortality among adults and children with pre-existing cardiovascular or respiratory illness from emission-derived particulate matter (PM) is well documented. However, the detrimental effects of PM inhalation on the exercising, healthy population is still in question. This review will focus on the acute and chronic responses to PM inhalation during exercise and how PM exposure influences exercise performance. The smaller ultrafine PM (<0.01 µm aerodynamic diameter) appears to have the most severe health consequences compared with the larger coarse PM (2.5 < PM <10 µm aerodynamic diameter). While the response to PM inhalation may affect those with a pre-existing condition, the healthy population is not immune to the effects of PM inhalation, especially during exercise. This population, including the competitive athlete, is susceptible to pulmonary inflammation, decreased lung function (both acute and chronic in nature), the increased risk of asthma, vascular endothelial dysfunction, mild elevations in pulmonary artery pressure and diminished exercise performance. PM exposure is usually associated with vehicular traffic, but other sources of PM, including small engines from lawn and garden equipment, cigarette smoke, wood smoke and cooking, may also impair health and performance. The physiological effects of PM are dependent on the source of PM, various environmental factors, physical attributes and nature of exercise. There are a number of measures an athlete can take to reduce exposure to PM, as well as the deleterious effects that result from the inevitable exposure to PM. Considering the acute and chronic physiological responses to PM inhalation, individuals living and exercising in urban areas in close proximity to major roadways should consider ambient air pollution levels (in particular, PM and ozone) prior to engaging in vigorous exercise, and those exposed to PM through other sources may need to make lifestyle alterations to avoid the deleterious effects of PM inhalation. Although it is clear that PM exposure is detrimental to healthy individuals engaging in exercise, further research is necessary to better understand the role of PM on athlete health and performance, as well as measures that can attenuate the harmful effects of PM.

Inhaled whole exhaust and its effect on exercise performance and vascular function.

CONTEXT: Internal combustion engines are a major source of particulate matter (PM) which has been shown to result in vasoconstriction, yet no present study to our knowledge has investigated the effect of exhaust emissions on both exercise performance and the vasculature. OBJECTIVE: To examine the effect of freshly generated whole exhaust on exercise performance, pulmonary arterial pressure (PP), and flow-mediated vasodilation (FMD) of the brachial artery. MATERIALS AND METHODS: Sixteen male, collegiate athletes (age: 20.8±1.28 years) were randomly assigned to submaximal exercise for 20 min followed by a 6 min maximal work accumulation exercise test in either high PM (HPM) or low PM (LPM) conditions on two consecutive days. After a 7-day washout period, subjects completed identical exercise trials in the alternate condition. HPM conditions were generated from a 4-cycle gasoline engine. The participants' PP and FMD were assessed before and after each exercise trial by tricuspid regurgitant velocity and brachial artery imaging, respectively. RESULTS: Total work (LPM: 108.0±14.8 kJ; HPM: 104.9±15.2 kJ, p=0.019) and FMD (LPM: 8.17±6.41%; HPM: 6.59±2.53%; p=0.034) significantly decreased in HPM while PP was significantly increased (LPM: 16.9±1.13 mmHg; HPM: 17.9±1.70 mmHg; p=0.004). A significant correlation was identified between the change in exercise performance and the change in FMD (r=0.494; p=0.026) after the first HPM trial. CONCLUSION: Exercise performance declined in HPM conditions in part due to impaired vasodilation in the peripheral vasculature.

Exercise-Induced Lung Disease: Too Much of a Good Thing?

Exercise in children has important health benefits. However, in elite endurance athletes, there is an increased prevalence of exercise-induced bronchoconstriction and airway inflammation. Particularly at risk are those who practice in cold weather, ice rinks, swimming pools, and air pollution. The inflammation is caused by repetitive episodes of hyperventilation of cold, dry air, allergens, or toxins such as chlorine or air pollution. Children may be particularly at risk for lung injury under these conditions because of the immaturity and ongoing development of their lung. However, studies in pediatric athletes and exercising young children are sparse. Epithelial injury associated with hyperventilation of cold, dry air has not been described in children. However, exercise in the presence of air pollution and chlorine is associated with airway injury and the development of asthma in children; the effect appears to be modulated by both atopy and genetic polymorphisms. While management of exercise-induced bronchoconstriction and asthma is well established, there is little data to guide treatment or prevention of remodeling in athletes or inhalational lung injury in children. Studies underscore the need to maintain high levels of air quality. More investigations should be undertaken to better define the natural history, pathophysiology, and treatment of exercise-induced pulmonary inflammation in both elite athletes and exercising children.

Asthma in swimmers: a review of the current literature.

Asthma is common in many types of athletes, but its prevalence appears to be particularly high in swimmers. Long-term and acute exposure to swimming pool disinfectants has been shown to increase asthma risk in swimmers through inducing oxidative stress, which results in inflammation of the pulmonary epithelium and subsequent airway remodeling. Individuals with specific genotypes are more likely to develop asthma when exposed to inhaled irritants. Therefore, it is important for physicians to be knowledgeable about the risks associated with asthma in swimmers, as well as the diagnostic techniques and practices to reduce asthma symptoms.

Reproducibility of the airway response to an exercise protocol standardized for intensity, duration, and inspired air conditions, in subjects with symptoms suggestive of asthma.

BACKGROUND: Exercise testing to aid diagnosis of exercise-induced bronchoconstriction (EIB) is commonly performed. Reproducibility of the airway response to a standardized exercise protocol has not been reported in subjects being evaluated with mild symptoms suggestive of asthma but without a definite diagnosis. This study examined reproducibility of % fall in FEV1 and area under the FEV1 time curve for 30 minutes in response to two exercise tests performed with the same intensity and duration of exercise, and inspired air conditions. METHODS: Subjects with mild symptoms of asthma exercised twice within approximately 4 days by running for 8 minutes on a motorized treadmill breathing dry air at an intensity to induce a heart rate between 80-90% predicted maximum; reproducibility of the airway response was expressed as the 95% probability interval. RESULTS: Of 373 subjects challenged twice 161 were positive (≥ 10% fall FEV1 on at least one challenge). The EIB was mild and 77% of subjects had <15% fall on both challenges. Agreement between results was 76.1% with 56.8% (212) negative (< 10% fall FEV1) and 19.3% (72) positive on both challenges. The remaining 23.9% of subjects had only one positive test. The 95% probability interval for reproducibility of the % fall in FEV1 and AUC0-30 min was ± 9.7% and ± 251% for all 278 adults and ± 13.4% and ± 279% for all 95 children. The 95% probability interval for reproducibility of % fall in FEV1 and AUC0-30 min for the 72 subjects with two tests ≥ 10% fall FEV1 was ± 14.6% and ± 373% and for the 34 subjects with two tests ≥ 15% fall FEV1 it was ± 12.2% and ± 411%. Heart rate and estimated ventilation achieved were not significantly different either on the two test days or when one test result was positive and one was negative. CONCLUSIONS: Under standardized, well controlled conditions for exercise challenge, the majority of subjects with mild symptoms of asthma demonstrated agreement in test results. Performing two tests may need to be considered when using exercise to exclude or diagnose EIB, when prescribing prophylactic treatment to prevent EIB and when designing protocols for clinical trials.

Montelukast prevents vascular endothelial dysfunction from internal combustion exhaust inhalation during exercise.

Associations between high particulate matter (PM) pollution and increased morbidity and mortality from coronary heart disease have been identified. This study assessed leukotriene (LT) participation in PM-induced vascular endothelial dysfunction. Ten healthy males exercised 4 times for 30 min in both high PM (550,286 +/- 42,004 particles x cm(-3)) and low PM (4571 +/- 1922 particles x cm(-3)) after ingesting placebo (PL) or 10 mg montelukast (MK; half-life 3-6 h), a leukotriene receptor antagonist. Brachial artery flow-mediated dilation (FMD) was measured pre- and 30 min, 4 h, 24 h post-exercise. No basal brachial artery vascoconstriction was evident from high PM exercise. High PM blunted FMD, whereas high PM MK, low PM PL, and low PM MK demonstrated normal FMD (p < .003). Change in FMD (pre- to post-exercise) for high PM PL was different than for high PM MK, low PM PL, and low PM MK at 30 min post-exercise (p < .007). At 4 h, high PM MK FMD blunting increased (p = .1). At 24 h, high PM FMD blunting persisted (p < .05); no difference was observed between high PM PL or MK treatment, but was different that low PM PL/MK treatments (p < .05). MK blocked high PM post-exercise FMD blunting and maintained normal response, suggesting that leukotrienes are involved in PM-initiated vascular endothelial dysfunction.

Grade influences blood lactate kinetics during cross-country skiing.

The purpose of this study was to examine the effects of level vs. graded skate skiing on capillary blood lactate (B(La)), heart rate (HR), oxygen consumption (V(O2)), and training intensity prescriptions. Eleven Nordic skiers completed 2 submaximal skate roller skiing treadmill protocols during which intensity was increased either by grade (G(inc)) or by speed (S(inc)). The protocols were compared for prethreshold BLa, HR, and V(O2) at lactate threshold (LT) and the HR/V(O2) relationship. Additionally, double-pole (primarily upper body) and skating (arms and legs combined) protocols were used to measure peak V(O2) and peak HR. Heart rate and V(O2) at LT were lower during G(inc) compared with S(inc) (154.9 +/- 6.8 b.min(-1) vs. 162.0 +/- 9.1 b.min(-1) and 46.3 +/- 2.8 ml.kg(-1).min(-1) vs. 49.1 +/- 1.6 ml.kg(-1).min(-1), respectively, both p < 0.01). Pre-threshold B(La) and the HR/V(O2) relationship were not different between the submaximal protocols. V(O2) and HRpeak were higher in skating compared with double poling (64.6 +/- 1.8 ml.kg(-1).min(-1) vs. 60.3 +/- 2.8 ml.kg(-1).min(-1), 192.6 +/- 5.8 b.min(-1) vs. 187.8 +/- 6.7 b.min(-1), respectively, both p < 0.01). Greater reliance on upper-body musculature during graded skiing and its associated lower aerobic capacity increases B(La) when compared with level skiing. The leftward shift in the B(La) vs. intensity curve during uphill skiing should be recognized to properly prescribe training intensity as well as interpret laboratory results.

Peak power during repeated wingate trials: implications for testing.

Maximal power production is of primary importance for many sporting events. Therefore, using a test that has been shown to be both valid and reliable will allow for accurate baseline testing, measurement of progress, and evaluation of performance. This study examined peak power (PP) during repeated Wingate trials after no warm-up (NWU), a steady state warm-up, and an interval warm-up. In a randomized placebo-controlled study, 11 subjects (38 +/- 8.2 years) performed two 10-second Wingate trials with 4 minutes of recovery between efforts. Warm-up protocols were completed before each Wingate trial and were immediately followed by trial I. Peak power was measured during each trial. Results indicate that PP is not significantly (p > 0.05) different from trial I to trial II for either of the warm-up protocols. The NWU trial II was significantly greater than the NWU trial I (855 +/- 230 W > 814 +/- 222 W, p < 0.05) when analyzed with a paired samples t-test. Peak power appears to be greatest after a general self-selected warm-up, but not after a previously intense bike warm-up. When testing for maximal power output via the Wingate anaerobic test, one should allow for a familiarization trial and should ensure full recovery between this trial and the baseline evaluation.

Imitators of exercise-induced bronchoconstriction.

Exercise-induced bronchoconstriction (EIB) is described by transient narrowing of the airways after exercise. It occurs in approximately 10% of the general population, while athletes may show a higher prevalence, especially in cold weather and ice rink athletes. Diagnosis of EIB is often made on the basis of self-reported symptoms without objective lung function tests, however, the presence of EIB can not be accurately determined on the basis of symptoms and may be under-, over-, or misdiagnosed. The goal of this review is to describe other clinical entities that mimic asthma or EIB symptoms and can be confused with EIB.

Exercise and other indirect challenges to demonstrate asthma or exercise-induced bronchoconstriction in athletes.

The prevalence of exercise-induced bronchoconstriction is reported to be high among recreational and elite athletes, yet diagnosis is often symptom-based. Indirect challenges such as the laboratory exercise challenge provide objective criteria for proper diagnosis and treatment. However, a standardized protocol using appropriate exercise intensity, duration, and dry air inhalation is often not implemented, and thus a false-negative test may result. This article reviews and describes the symptom-based diagnosis, the exercise challenge, and other indirect challenges such as eucapnic voluntary hyperpnea, hypertonic saline inhalation, and inhaled powdered mannitol as methods to diagnose and evaluate exercise-induced bronchoconstriction. Advantages and disadvantages of each diagnostic procedure are presented.