Home Educatione-Learning Sports Activities and Lung Health Benefits and Risks
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Sports Activities and Lung Health Benefits and Risks

PCCSU Volume 25, Lesson 10


The American College of Chest Physicians offers this lesson as a review of a previously offered self-study program. The program provides information on pulmonary, critical care, and sleep medicine issues. CME is no longer available for the PCCSU program.


  • Update your knowledge and understanding of pulmonary medicine topics.
  • Update your knowledge and understanding of critical care medicine topics.
  • Update your knowledge and understanding of sleep medicine topics.
  • Learn clinically useful practice procedures.

CME Availability

Effective July 1, 2013, PCCSU Volume 25 is available for review purposes only.

Effective December 31, 2012, PCCSU Volume 24 is available for review purposes only.

Effective December 31, 2011, PCCU Volume 23 is available for review purposes only. CME credit for this volume is no longer being offered

Effective December 31, 2010, PCCU Volume 22 is available for review purposes only. CME credit for this volume is no longer being offered.

Accreditation Statement

The American College of Chest Physicians is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

CME Statement

Credit no longer available as of July 1, 2013.

Disclosure Statement

The American College of Chest Physicians (CHEST) remains strongly committed to providing the best available evidence-based clinical information to participants of this educational activity and requires an open disclosure of any potential conflict of interest identified by our faculty members. It is not the intent of CHEST to eliminate all situations of potential conflict of interest, but rather to enable those who are working with CHEST to recognize situations that may be subject to question by others. All disclosed conflicts of interest are reviewed by the educational activity course director/chair, the Education Committee, or the Conflict of Interest Review Committee to ensure that such situations are properly evaluated and, if necessary, resolved. The CHEST educational standards pertaining to conflict of interest are intended to maintain the professional autonomy of the clinical experts inherent in promoting a balanced presentation of science. Through our review process, all CHEST CME activities are ensured of independent, objective, scientifically balanced presentations of information. Disclosure of any or no relationships will be made available for all educational activities.

CME Availability

Volume 25 Through June 30, 2013
Volume 24 Through December 31, 2012
Volume 23 Through December 31, 2011
Volume 22 Through December 31, 2010

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PCCSU Volume 25 Editorial Board

Steven A. Sahn, MD, FCCP

Director, Division of Pulmonary and Critical Care Medicine, Allergy, and Clinical Immunology
Medical University of South Carolina
Charleston, SC

Dr. Sahn has disclosed no significant relationships with the companies/organizations whose products or services may be discussed within Volume 25.

Deputy Editor
Richard A. Matthay, MD, FCCP

Professor of Medicine
Section of Pulmonary and Critical Care Medicine
Yale University School of Medicine
New Haven, CT

Dr. Matthay has disclosed no significant relationships with the companies/organizations whose products or services may be discussed within Volume 25.

Alejandro C. Arroliga, MD, FCCP
Professor of Medicine
Texas A&M Health Science Center
College of Medicine
Temple, TX

Dr. Arroliga has disclosed no significant relationships with the companies/organizations whose products or services may be discussed within Volume 25.

Paul D. Blanc, MD, FCCP
Professor of Medicine
University of California, San Francisco
San Francisco, CA

Dr. Blanc has disclosed significant relationships with the following companies/organizations whose products or services may be discussed within Volume 25:

National Institutes of Health, Flight Attendants Medical Research Institute – university grant monies
University of California San Francisco, US Environmental Protection Agency, California Environmental Protection Agency Air Resources Board – consultant fee
Habonim-Dror Foundation Board of Trustees – fiduciary position

Guillermo A. do Pico, MD, FCCP
Professor of Medicine
University of Wisconsin Medical School
Madison, WI

Dr. do Pico has disclosed no significant relationships with the companies/organizations whose products or services may be discussed within Volume 25.

Ware G. Kuschner, MD, FCCP
Associate Professor of Medicine
Stanford University School of Medicine
Palo Alto, CA

Dr. Kuschner has disclosed no significant relationships with the companies/organizations whose products or services may be discussed within Volume 25.

Teofilo Lee-Chiong, MD, FCCP
Associate Professor of Medicine
National Jewish Medical Center
Denver, CO

Dr. Lee-Chiong has disclosed significant relationships with the following companies/organizations whose products or services may be discussed within Volume 25:

National Institutes of Health – grant monies (from sources other than industry)
Covidien, Respironics, Inc. – grant monies (from industry-related sources)
Elsevier – consultant fee

Margaret Pisani, MD, MPH, FCCP
Assistant Professor of Medicine
Yale University School of Medicine
New Haven, CT

Dr. Pisani has disclosed no significant relationships with the companies/organizations whose products or services may be discussed within Volume 25.

Stephen I. Rennard, MD, FCCP
Professor of Medicine
University of Nebraska Medical Center
Omaha, NE

Dr. Rennard has disclosed significant relationships with the following companies/organizations whose products or services may be discussed within Volume 25:

AstraZeneca, Biomark, Centocor, Novartis – grant monies (from industry-related sources)

Almirall, Aradigm, AstraZeneca, Boehringer Ingelheim, Defined Health, Dey Pharma, Eaton Associates, GlaxoSmithKline, Medacrop, Mpex, Novartis, Nycomed, Otsuka, Pfizer, Pulmatrix, Theravance, United Biosource, Uptake Medical, VantagePoint – consultant fee/advisory committee

AstraZeneca, Network for Continuing Medical Education, Novartis, Pfizer, SOMA – speaker bureau

Ex Officio
Gary R. Epler, MD, FCCP

Clinical Associate Professor of Medicine
Harvard Medical School
Brigham & Women's Hospital
Boston, MA

Dr. Epler has disclosed no significant relationships with the companies/organizations whose products or services may be discussed within Volume 25.

Lilly Rodriguez
ACCP Staff Liaison

By Robert R. Kempainen, MD

Dr. Kempainen is Associate Professor of Medicine, University of Minnesota School of Medicine, Minneapolis, Minnesota.

Dr. Kempainen has disclosed no significant relationships with the companies/organizations whose products or services may be discussed within this chapter.


  1. Describe the physiologic adaptation of the respiratory system to regular exercise.
  2. Compare and contrast the presentation of patients with exercise-induced bronchoconstriction vs those with paradoxical vocal cord motion.
  3. Compare and contrast the pathophysiologic basis of high-altitude pulmonary edema to that of diving-related barotrauma.
  4. List environmental factors that lead to respiratory disease in swimmers and ice skaters.
  5. Highlight uncommon causes of respiratory symptoms associated with sporting activities, including stress fractures of the rib, swimming-induced pulmonary edema, pneumothorax, and thoracic outlet syndrome.

Key words: athletic injuries; diving; exercise tolerance; mountaineering; sports medicine

Abbreviations: AMS = acute mountain sickness; EIB = exercise-induced bronchoconstriction; HACE = high-altitude cerebral edema; HAPE = high-altitude pulmonary edema; PVCM = paradoxical vocal cord motion

Regular exercise is recommended for the prevention and treatment of a variety of diseases, but the effect of physical activity on lung health has received less attention. Health-care providers need additional knowledge to optimally counsel patients on the respiratory risks and benefits of exercise, as well as recognize and treat respiratory complications of various sports activities. The notion that exercise improves one’s health is widely accepted and a substantial body of research indicates that this belief is well placed. The salutary effect of exercise on cardiovascular risk is especially well characterized, but individuals with cerebrovascular disease, depression, and even some forms of cancer also may benefit from regular exercise.1 Furthermore, exercise can play a role in maintaining the health of patients with established lung disease. For instance, pulmonary rehabilitation increases exercise tolerance and quality of life in patients with COPD2 and exercise augments airway clearance in cystic fibrosis patients.3 For individuals without respiratory disease, however, it is much less clear whether faithfully heading to the gym is in any way lung-protective. In fact, given the wrong combination of individual characteristics, environmental factors, and the nature of the activity, sports activities can pose a threat to respiratory health. This lesson summarizes what is known about the positive and negative effects of exercise on the respiratory system of healthy individuals.

Exercise and Measures of Pulmonary Function

To begin, it is worth reviewing how the respiratory system adapts to a sustained exercise regimen. Endurance training in athletes improves cardiac output and the capacity of the peripheral musculature to extract and utilize oxygen. In contrast, there is little to suggest the lung parenchyma adapts to regular exercise. With training, athletes can sustain higher peak respiratory rates at maximal exertion and perform better on tests of ventilatory endurance when compared with nonathletes. These differences exist in cross-sectional studies comparing athletes and nonathletes, but prospective studies have also documented gains in ventilatory endurance in individuals initiating an exercise program.4,5 Similarly, inspiratory muscle training has been shown to improve inspiratory muscle strength in elite rowers, although this did not necessarily translate into improved rowing performance.6

Studies of the effect of regular aerobic exercise on spirometry and lung volumes have produced mixed results. For instance, a small cross-sectional study found spirometry and lung volumes did not differ in young trained vs untrained individuals, but older endurance athletes had higher pulmonary function test values than their sedentary older counterparts.7 Other studies indicate competitive swimmers have larger lung volumes than land-based athletes and sedentary control individuals, apparently independent of inspiratory muscle strength.8,9 Of note, the cross-sectional design and frequent inclusion of elite athletes in these studies raises the possibility of selection bias. At least one prospective study found that endurance training did not improve spirometric performance in a group of 11 adults,4 while another involving 10 competitive endurance runners documented gains in FEV1, but not FVC, as training intensity escalated.10

Another important consideration is that respiratory system adaptations to training are relevant to athletic performance, but have unclear implications for lung health. Normally there is a slow, steady decline in lung function as healthy adults age, but this does not limit survival. Theoretically, having increased respiratory fitness might improve the chances that a patient survives a critical illness, but certainly there is no robust evidence indicating improving lung function translates into improved health.

Exercise and Lower Respiratory Tract Infections

Potential adverse respiratory effects of exercise and sports activities are summarized in Table 1. The relationship between exercise and immune function is an active area of research that was recently reviewed.11 Some studies suggest exercise bolsters the immune system; this perception is shared by many recreational athletes in the general population. However, there is also the belief among elite athletes that they are more vulnerable to upper respiratory tract infections during periods of intense training. Studies indicate vigorous exercise reduces secretory IgA levels, impairs neutrophil function, and produces transient reductions in T-cell function.11,12 In contradistinction to these observations, other studies have found that intense training enhances natural killer cell function and moderate exercise increases IgA production. Of note, aside from one study that linked lower IgA levels to an increased incidence of upper respiratory infections in American football players,12 the clinical implications of such immunologic findings have not been assessed. At this juncture, there is insufficient evidence to recommend for or against exercise for the purpose of modulating the risk of respiratory infections.

Table 1Adverse Respiratory Effects of Exercise and Sporting Activities

Context Diagnosis Examples Comments
Endurance athletics Exercise-induced bronchoconstriction Cross-country skiing, long-distance running Cold, dry air increases risk
  Paradoxical vocal cord motion Endurance sports Asthma mimicker

Diagnosis by pulmonary function testing or laryngoscopy
  Lower respiratory tract infection Exercise regimen of any kind Unclear risk

High intensity may increase risk, moderate intensity may decrease risk
Extremes in barometric pressure Pneumothorax and pneumomediastinum Scuba diving Associated with rapid ascent, obstructive lung disease
  Air embolism Scuba diving Via barotrauma or severe decompression illness
  High-altitude pulmonary edema Mountaineering, extreme skiing Consider pharmacologic and nonpharmacologic prophylaxis
Poor air quality NO2, CO poisoning Ice skating, ice hockey Owing to faulty ice resurfacers
  Chlorine and trinitrochlorine toxicity Swimming Acute lung injury; asthma, rhinitis in elite swimmers
  Outdoor CO, particulate matter, ozone Endurance athletics Can impair athletic performance; unclear long- term risk
Valsalva maneuver Pneumothorax and pneumomediastinum Weightlifting, javelin throw, wrestling  
Musculoskeletal overuse injury Stress fracture of first rib Baseball, basketball, tennis, weightlifting Presents with chest pain without trauma
  Stress fracture of other ribs Golf, rowing Presents with chest pain without trauma
Paget-Schroetter syndrome Axillosubclavian venous thrombosis Weightlifting, tennis, baseball pitching Associated with repetitive overhead activity; often associated with thoracic outlet syndrome
Miscellaneous water-related Swimming-induced pulmonary edema Vigorous swimming Also described in water aerobics
  Near-drowning Swimming or lack thereof Risk of pneumonia and acute lung injury
  Infection Triathlon competition Leptospirosis is a particularly notable pathogen


Risks of Exercise: Asthma and Vocal Cord Dysfunction

Exercise can be the sole cause of bronchoconstriction in some patients and can exacerbate symptoms in others with underlying asthma. This phenomenon is termed exercise-induced bronchoconstriction (EIB). Our understanding of the pathogenesis is evolving, but elevated minute ventilation associated with endurance exercise is thought to dry the airways, thereby inducing osmotic changes in the epithelium that lead to bronchoconstriction.13 As would be expected, EIB is particularly common in athletes exercising in cold, dry air conditions. For instance, studies indicate a third of winter Olympic athletes have EIB and that the incidence approaches 50% among elite cross-country skiers.14 Confirmation of EIB can be challenging, as patient-reported symptoms lack sensitivity and specificity. Stationary cycle and treadmill tests are often used, but may be falsely negative for EIB if bronchoconstriction is triggered by a combination of increased ventilation and environmental factors such as ambient air temperature and humidity.14 Eucapnic voluntary hyperventilation, inhalation of dry-powder mannitol, hypertonic saline challenge, and pharmacologic challenge with methacholine are other bronchoprovocation tests used to support the diagnosis of EIB.13,14 First-line treatment of EIB entails inhaled short-acting β2-agonists and/or cromolyn sodium prior to exercise, but a number of other asthma medications can also be used if adequate control is not achieved.13

Paradoxical vocal cord motion (PVCM), also known as vocal cord dysfunction, is an important alternative to EIB to consider in patients poorly tolerating exercise owing to excessive dyspnea. PVCM is well described in athletes, and is most commonly encountered in women between the ages of 20 and 40 years.15,16 EIB and PVCM can both yield normal flow-volume loops between episodes, and both disorders can be present concomitantly.15 PVCM is characterized by adduction of the true vocal cords during inspiration or, less commonly, excessive adduction of the cords during expiration. The underlying trigger for PVCM is unclear, but laryngeal irritants (such as gastroesophageal reflux disease) and psychogenic factors are believed to play important roles.16 Besides dyspnea, patients can experience throat tightness, a choking sensation, dysphonia, and cough. The presence of upper airway stridor on examination is an important clue, but additional evaluation is generally recommended. Truncation or flattening of the inspiratory limb of a flow-volume loop following an exercise challenge or during a methacholine challenge further supports the diagnosis. Laryngoscopy is typically used to confirm or elicit a new diagnosis and simultaneously allows assessment for anatomical abnormalities and stigmata of laryngeal irritation that could underlie PVCM.16 Aside from treating causes of laryngeal irritation, speech therapy, sometimes accompanied by psychological counseling, is the mainstay of long-term management.16 Although PVCM is rarely life-threatening and does not directly involve the lung, it has implications for lung health when misdiagnosed as asthma, given the morbidity of long-term asthma treatments.

Exercise at Barometric Extremes

The location of exercise can have important implications for lung health independent of the actual activity in which the individual is engaging. This is particularly true of sports taking place at extremes of barometric pressure, such as mountaineering or scuba diving. The primary threat to lung health posed by scuba diving is barotrauma, which most often occurs with rapid ascent from a dive.17 As the diver ascends, ambient pressure falls, and unventilated gas will therefore expand according to Boyle’s law. This in turn causes alveolar rupture with consequent pneumothorax and/or pneumomediastinum. Barotrauma can subsequently cause arterial air embolism and fatal obstruction of the central vasculature. Barotrauma can largely be prevented if the diver avoids breath holding, but individuals with air trapping from obstructive lung disease, such as asthma and COPD, are particularly vulnerable. Guidelines exist for determining whether individuals with obstructive disease should be cleared for diving.18 Obstruction of the pulmonary vasculature can also occur during severe decompression sickness (the bends).18 Treatment of arterial gas embolism and severe decompression sickness involves use of 100% supplemental oxygen and hyperbaric oxygen therapy when available. Although the mechanism is poorly understood, divers also appear to be at risk of accelerated decline in lung function, including FEV1, FVC, and diffusing capacity of the lung for carbon monoxide.19

At the other end of the barometric spectrum, exercise at elevations greater than 2,500 m places individuals at risk of acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). The cardinal feature of AMS is headache, which is typically accompanied by variable degrees of malaise, anorexia, nausea, vomiting, and poor sleep.20 AMS is a common, self-limited illness, assuming there are no further rapid gains in elevation. HACE is believed to be a more severe manifestation of AMS and is associated with neurologic deficits caused, at least in part, by cerebral edema.20 In contrast to AMS, HACE is life threatening and can manifest with ataxia, upper motor neuron signs, intractable vomiting, stupor, and coma. Allowing time for acclimatization is the best approach to preventing these illnesses. However, pharmacologic prevention and treatment of AMS with acetazolamide or dexamethasone is often indicated. Dexamethasone is the drug of choice to prevent HACE and is coupled with descent to manage individuals with HACE.20

HAPE is a cause of potentially lethal noncardiogenic pulmonary edema and is typically seen at elevations greater than 3,000 m. The risk increases with increasing elevation, faster rate of ascent, and vigorous exertion. Individuals with a previous history of HAPE are at increased risk of recurrence.20 HAPE appears to be caused by severe, nonuniform pulmonary arterial vasoconstriction in a vulnerable subset of persons with an inadequate ventilatory response to hypoxia. This in turn results in excessive perfusion of, and injury to, portions of the pulmonary capillary bed, with subsequent hypoxemia from leakage of cells, proteins, and fluid into the interstitium and alveolar spaces.20 In severe cases, patients rapidly progress from exertional dyspnea to dyspnea at rest and may develop a cough productive of pink, frothy secretions or even frank hemoptysis. As with AMS and HACE, allowing sufficient time for acclimatization, with gradual, step-wise exposure to increasing altitude, is the mainstay of prevention.20 Pharmacologic prophylaxis, including phosphodiesterase inhibitors and the calcium channel blocker nifedipine, are appropriate for individuals with a prior history of HAPE.21 The mainstay of treating HAPE is supplemental oxygen, limiting physical activity, and/or descent to lower altitude. Nifedipine may offer additional benefit, particularly if the patient is unable to descend.

Exercise and Other Environmental Factors

Indoor environmental conditions can also affect the risk of exercise. For instance, there are numerous reports of respiratory illness attributed to release of nitrogen dioxide and carbon monoxide from malfunctioning ice-resurfacers at indoor ice arenas.22,23 Ski waxing with fluoropolymer treatments has been associated with acute lung injury.24 Indoor pools, particularly those with water sprays, can cause granulomatous pneumonitis, but such outbreaks have been observed in lifeguards rather than pool users with less sustained exposure.25 Furthermore, exposure to chlorine from swimming pool water treatment system malfunction or misadventure is associated with acute lung injury. Lower-level chronic exposure to chlorine byproducts (trinitrochlorine) in swimming pools is associated with increased prevalence of atopy, rhinitis, asthma, and airway hyperresponsiveness in elite swimmers (and there is growing concern that children and recreational swimmers may also be affected).26,27

A number of landmark studies have established a link between air pollution exposure and increased morbidity and mortality. For instance, greater exposure to road traffic is associated with greater decrements in lung function among asthmatic individuals,28 while exposure to fine particulate matter is associated with increased risk of lung cancer and cardiopulmonary mortality.29 It follows that exercising in environments with poor air quality could place the individual at even greater risk, but few studies have explored this specific issue. Carbon monoxide levels are known to increase with heavy exercise in urban environments, which can transiently reduce exercise capacity.30 Furthermore, outdoor exercise increases ozone exposure, which can cause acute decrements in lung function accompanied by cough, wheeze, dyspnea, chest tightness, and substernal chest pain. Of note, ozone poses a risk in both rural and urban environments.30

In the Southern California Children’s Health Study, which explored longer-term effects of exercise in communities with high levels of air pollution, children participating in team sports in areas with high ozone concentrations had >3 times the risk of developing asthma than children not participating in sports; in contrast, exposure to nitrogen dioxide, particulate matter, and inorganic-acid vapor was not associated with new-onset asthma.31 Hence, it appears that outdoor exercise in environments with poor air quality not only causes a transient adverse effect on athletic performance, but may also increase the long-term risk of developing asthma. Given the known benefits of regular physical activity, it is reasonable to advise patients to continue to exercise, but to avoid heavy traffic areas and midday exercise, when ozone levels peak.

Exercise and Specific Activities

A host of sporting activities are capable of causing injury to the lung or chest wall via overt trauma. For instance, lung contusion, rib fractures, and pneumothoraces are not out of the ordinary and generally do not present a diagnostic conundrum when the clinician is evaluating an injured alpine skier, rock climber, or rodeo bull rider. The cause of chest pain or dyspnea, however, can be more subtle. For instance, pneumomediastinum can occur in sports that prompt athletes to perform the Valsalva maneuver, such as weight lifting, javelin throwing, and wrestling.32,33 Weight lifting, baseball pitching, playing tennis, swimming, and other sports that require repetitive overhead activity can also cause spontaneous axillosubclavian vein thrombosis (Paget-Schroetter syndrome). Typically this is associated with narrowing of the thoracic outlet as a result of scalene muscle hypertrophy, but thrombosis also occurs in the absence of narrowing.34 Patients typically present with unilateral shoulder or axillary pain along with upper-extremity edema. The risk of pulmonary embolization is approximately 20%. Treatment entails anticoagulation, often combined with thrombolytics and/or surgery depending on anatomy and clinical course.34

Exercise-induced musculoskeletal injury in the absence of recognized discrete trauma can also prompt individuals to seek medical attention for respiratory complaints. Stress fracture of the first rib is a well-described complication of pitching baseballs, hitting baseballs, lifting weights, and playing basketball or tennis.35 Other activities that place repetitive, high-stress loads on the remaining ribs, such as golf and rowing, can cause stress fractures.

Swimming, aside from the aforementioned risks specific to diving and chlorine exposure, can adversely affect the lungs. The negative effects of drowning obviously extend beyond lung health, but patients who have been victims of near-drowning are at risk of pneumonia and acute lung injury. Prophylactic glucocorticoids and antibiotics do not appear to reduce the risk of lung injury or pneumonia, respectively, in patients with submersion injury.36 The mainstay of managing near-drowning victims with acute lung injury is low tidal volume ventilation. A variety of uncommon causes of pneumonia have been identified in patients who have experienced near-drowning, including the fungus Scedosporium apiospermum.37 Furthermore, leptospirosis and fulminant Aeromonas hydrophila pneumonia have been reported in swimmers even in the absence of frank aspiration.38,39 Leptospirosis is particularly associated with triathletes who swim in fresh water. In addition, vigorous swimming can cause transient pulmonary edema in otherwise healthy young adults.40 Swimming-induced pulmonary edema is thought to result from increased capillary pressures that develop in conjunction with heavy exertion. Of note, pulmonary edema has also been reported with aqua-jogging,41 which suggests water-based exercise in general poses a greater risk than land-based activities. One possible explanation for this difference is that cold water immersion causes central pooling of blood, which could thereby excessively increase left-sided filling pressures during vigorous exercise.


Participation in essentially any sporting activity can adversely affect the respiratory system of a healthy individual in a variety of ways. Furthermore, for the general population, exercise does not appear to offer substantial benefits specific to the lung. However, given the known important benefits of exercise on other organ systems, these considerations are by no means a reason for individuals to maintain a sedentary lifestyle. Rather, clinicians should be familiar with the risks associated with various activities to ensure prompt diagnosis and appropriate management of exercise-induced pulmonary and chest wall disorders. Provider recognition of the precipitating factors—including individual patient characteristics, type of activity, intensity of activity, and environmental factors—is important for formulating a treatment plan that will optimize patients’ ability to maintain healthy, active lives.


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