The upper and lower airways (above and below the glottis), lung, and chest wall function as an integrated unit to provide for efficient gas exchange during exercise and sports. Dysfunction in any of these components can lead to compromised exercise tolerance. This chapter will consider common conditions that affect the respiratory tract and that can lead to limitation in physical activities. Locating the site of dysfunction through physical examination and laboratory testing, particularly the evaluation of pulmonary function is the first step in solving a sports-related respiratory problem. Consideration of pulmonary function alterations together with signs and symptoms of disease and specific therapies will be the focus of this chapter. Consequently, a general discussion of respiratory exercise physiology and pulmonary function evaluation will form the basis for understanding specific conditions that affect each.

Respiratory Exercise Physiology

There is a significant and interdependent interaction of muscle, cardiovascular output, and ventilation during rest as well as during exercise. Ventilation is dependent on airway caliber, integrity of the central and peripheral nervous system, and respiratory musculature. During quiet breathing, the diaphragm and to some extent the abdominal muscles and inspiratory intercostal muscles are active. With exercise, there is considerable increase in activity of these muscle groups in addition to recruitment of other muscles including the expiratory intercostals and sternocleidomastoids. The sum total is increased ventilation to meet the metabolic demands of more vigorous exercise including increased oxygen consumption and carbon dioxide elimination.

At high levels of exercise, all respiratory muscles are participating and movement of extremities also facilitates breathing.1 Increase in all the body’s muscle activity requires increased oxygen consumption and during strenuous exercise up to 95% of oxygen demands can be accounted for by respiratory and other muscles groups.1 The physiologic adjustments for adequate oxygen consumption to support aerobic metabolism and provide adequate elimination of carbon dioxide are dependent on the linked factors shown in Figure 12-1. These are specifically increased ventilation, increased cardiac output, and redistribution of blood flow to working muscles.1 When oxygen requirements to support aerobic metabolism are exceeded, anaerobic metabolism begins. Increased lactate is the end product. During exercise, the point of transition from aerobic to anaerobic metabolism (the anaerobic threshold) is measured in the laboratory. This will vary with level of conditioning or with disease state (Figure 12-2).2

Conditioning

Physical training has many positive effects on respiratory and circulatory function (Table 12-1).1 In the pulmonary function laboratory, measuring maximal oxygen uptake is a base measure for level of fitness. Increase in maximal cardiac output as a result of increased stroke volume relates directly to increase in maximal O2 uptake. Muscle undergoes a number of changes including increased blood flow above pretraining levels, in increase in density of muscle capillaries, and increased oxygen extraction. Both aerobic and anaerobic work capacity increase with training as measured by increased oxygen consumption and decreased lactate production for a given work load. Maximal ventilation increases with training in some individuals but not all, however at sub maximal levels; ventilation is consistently lower after training.1

Pulmonary Function Testing

Pulmonary function testing (PFT) is important to quantify not only the degree (or lack) of impairment of respiratory function but also the type of dysfunction. It can also be used to monitor response to therapy whether medical, physical, or the effects of training. It is important to note that PFT supports specific diagnoses by determining the type of lung, airway, or chest wall disease but does not give specific pulmonary diagnoses. Clinical correlation is always necessary.

PFTs consist of a measure of airflow (spirometry), lung volumes (static lung volumes), diffusion capacity, and gas exchange (oximetry, blood gases); and specialized tests such as bronchial challenge with chemicals such as methacholine, exercise challenge with serial spirometry, and exercise metabolic testing. In the office setting, spirometry is the most practical measure and most problems associated with sports are supported by spirometric changes; therefore, we will focus on this test. Exercise testing (see section on exercise-induced asthma) or methacholine challenge with serial spirometry done in the hospital PFT laboratory is also useful for determining sports-related respiratory dysfunction. Lung volumes are helpful in evaluating chest wall dysfunction as a cause of reduced exercise capacity and are done in the PFT laboratory.

Figure 12-3 shows a typical expiratory flow volume loop during spirometry. The patient takes as deep a breath as possible and expires as forcibly and completely as possible. For evaluation of upper airway obstruction, (see discussion of vocal cord dysfunction) it is also useful to obtain an inspiratory curve as well. An adequate forced vital capacity (FVC) maneuver is defined by less than 5% variability in three to five FVC attempts. Most children 5 years or older can perform adequate spirometry. Relative changes in FVC and the forced expiratory volume for 1 second (FEV1) determine patterns of dysfunction including obstructive, restrictive, and mixed defects (Figure 12-4 and Table 12-2). Spirometry can suggest restrictive and mixed pulmonary disease but confirmation of this type of dysfunction is made using lung volume measurements in the PFT laboratory. A relatively simple measure of reversible airway obstruction can be done by measuring spirometry before and after 20 minutes of giving an inhaled bronchodilator such as albuterol sulfate. An increase of 12% or greater in FEV1 is diagnostic for reversible airway obstruction. Reference to findings on spirometry with various conditions and need for further testing, if required, will be included with the various sports-related conditions discussed below.

Vocal Cord Dysfunction

Definition and Epidemiology

Vocal cord dysfunction (VCD) (paradoxical vocal cord motion, laryngeal dyskinesia, functional stridor, Munchausen’s stridor, psychosomatic stridor, factitious asthma) often occurs during sports activities and is very common among adolescents, particular females.3 The symptoms are often underrecognized and consequently VCD is under-diagnosed. Thirty to fifty percent of patients with VCD typically also have a history of asthma and may be aggressively over treated with multiple inhaled medications, systemic steroids, and even repeated hospitalizations because of the unrecognized coexisting VCD symptoms.4,5

Clinical Presentation

A typical episode of VCD consists of the sudden onset of inspiratory stridor with accompanying throat tightness, hoarse voice, cough, and occasional wheezing.3 VCD rarely occurs during sleep, but occurs more commonly during activity. Symptoms often remit over minutes with cessation of activity or removal or distraction from a stressful situation. On examination, stridor locates over the glottis and lung evaluation is normal unless coexisting asthma is occurring. Endoscopic examination is typical, with characteristic anterior apposition of the vocal cords with a small, posterior, diamond shape opening (“posterior glottic chink,” Figure 12-5).4,6

Differential Diagnosis

VCD is most often confused with asthma, although a careful history and examination can differentiate the two, eliminating unnecessary treatments (Table 12-3). Throat tightness and upper chest discomfort may also occur with hyperventilation associated with performance anxiety (probable panic attack) but stridor is usually absent.3

Diagnostic Tests

Direct laryngoscopy is definitive but rarely available during an episode. Spirometry may show persistent flattening of the inspiratory portion of the flow volume loop either at rest or during bronchoprovocation with exercise, methacholine, cold air, or histamine in the hospital PFT laboratory (Figure 12-5).4

Treatment

Behavioral treatments, particularly speech therapy for hyperfunctional voice disorders, but also including hypnosis, relaxation, breathing exercises and biofeedback are shown to be helpful in this condition.3,5,7 If there is major underlying anxiety or other psychopathology, more extensive evaluation and therapy for a specific psychological condition is warranted.

Chest Wall Pain

Chest wall pain in sports is common, frequently accompanying local trauma or repetitive strenuous activity and is most often of musculoskeletal origin. Localization of the pain to a specific site and observation of the chest wall for swelling can help differentiate conditions responsible for the discomfort. Most common are costochondritis, Tietze’s syndrome, stress fracture of the rib, and slipping rib syndrome. These conditions are described individually with clinical presentation and pathophysiology where known.

Costochondritis and Tietze’s Syndrome

Definitions and Epidemiology

Up to 30% of patients presenting to the emergency department with chest wall pain have these conditions.8 They occur commonly in youth of either gender, often in those undertaking stressful activity of the upper body such as weight lifting, gymnastics, etc.

Clinical Presentation

The etiology is unknown although there is soft evidence of localized inflammation of the costochondral junction.9 Localized, palpable pain over the costochondral junction without systemic symptoms is typical. If there is a localized, nonsuppurative nodule, usually located at the second or third costochondral junction, the condition is termed Tietze’s syndrome.10 The etiology of this condition is likewise unknown although inflammation is also implicated. Diagnosis of either condition is dependent on history and clinical examination as radiographs are usually normal. Soft tissue swelling and, occasionally partial calcification of the costal cartilage may be evident.11

Differential Diagnosis

Local palpable pain is the key to diagnosis of costochondritis, but always consider other causes of chest pain including that of cardiac, GI, and infectious origin. Spirometric evaluation should not reveal abnormalities unless pain limits the performance of a vital capacity maneuver in which case the evaluation will suggest restrictive disease based on both reduction in VC and FEV1. Dyspnea is not usual and suggests intrinsic pulmonary disease. Chest x-ray is helpful to rule out parenchymal lung disease and rib fracture.

Treatment

These conditions are self-limited and treatment consists of reassurance, mild analgesics, such as oral nonsteroidal anti-inflammatory agents, and discontinuation of any aggravating activity. Severe pain may respond to local injection of corticosteroid, especially with Tietze’s syndrome.10

Stress Fractures of the Ribs

Definitions and Epidemiology

Stress-related rib fracture especially that of the first rib occurs in athletes engaged in strenuous activity, particularly those involving overhead activity such as baseball, basketball, tennis, or weight lifting. Baseball pitching, golf, and surfing have all been associated with traumatic rib fracture. Collegiate rowers appear to be at particular risk with 12% of a national rowing team diagnosed with rib fracture over approximately a 1-year period.12

Clinical Presentation

With first rib fracture, pain occurs in the shoulder, cervical triangle or clavicular region. Fracture may occur in other ribs including the so-called floating ribs (11th and 12th ribs) in cases of extreme chest wall and abdominal muscle contraction. Pain is insidious in onset progressing from ill defined to sharp pain over days to weeks. Pain may be felt in the back as the fracture site is often at the posterolateral rib angle. Examination often reveals local rib tenderness and plain chest x-ray most often is diagnostic.

Differential Diagnosis

Rule out both shoulder injury and clavicular fracture with first rib fracture by careful examination and specific radiographs. Careful palpation of the spine is useful in ruling out local vertebral injury and the possibility of diskitis. The chest x-ray is most useful in diagnosing rib fracture.13

Treatment

Treatment for first rib fracture includes sling immobilization of the shoulder and use of a soft cervical collar. Prognosis is good with return to normal activity within 3 months.

Slipping Rib Syndrome (Painful Rib, Clicking Rib Syndrome)

This occurs in up to 3% of patients presenting with rib pain.14 Sharp pain is often described in the lower chest or upper abdomen along with a tender spot on palpation of the lower costal margin. The etiology is thought to be caused by hyper mobility of the anterior ends of ribs 11 and 12 with a tendency of one rib to slip under the other. The development of this condition may follow chest trauma as might be found in sports activities.10 Pain is likely caused by impingement on the intercostal nerve or strain of the lower costal cartilage.15 The excess rib movement may be accompanied by a snap, click, or pop associated with sharp intermittent pain. The “hooking maneuver” (the examiner hooks his or her fingers under the lower costal margin and pulls anteriorly) will reproduce the pain accompanied by a typical click. There is neither specific radiological diagnostic test nor changes in lung function in this condition. Conservative management consists of rib strapping, avoidance of precipitating activities, and use of mild analgesics. Occasionally local nerve block and injection of corticosteroid may be necessary to relieve severe pain. Excision of the anterior end of the rib and costal cartilages may provide definitive relief in extreme cases.16,17

Pectus Excavatum

Pectus deformities (pectus excavatum and carinatum, Figure 12-6) occur in approximately 1% of the population with boys affected in a 4:1 ratio to girls.18 Pectus excavatum (funnel chest) is the most common with inward indentation of the sternum readily apparent on chest inspection. With adolescent growth acceleration, the defect becomes more severe but stops progressing once one attains adult growth. Dystrophic growth of the costal cartilages appears to be the cause of the sternal depression.18 There is often a familial tendency toward this defect. Although specific symptoms are not routinely associated with pectus excavatum, adolescents may complain of fatigue, decreased exercise tolerance, and chest and back discomfort. Mitral valve prolapse may occur in up to 20% of children with pectus excavatum and resolves about half the time with repair.19–25 Pectus deformities are also seen in connective tissue disorders including Marfan and Ehlers-Danlos syndromes.18 Embarrassment as a result of the cosmetic nature of the deformity most often leads to the patient seeking medical or surgical evaluation of the deformity. Surgery is indicated for primarily cosmetic purposes. Although mild restrictive defects in pulmonary function may accompany severe pectus excavatum deformities, functional improvement in lung function and exercise tolerance is quite variable after surgery.26 The reduced exercise capacity seen in some patients with severe pectus excavatum appears to be primarily caused by impaired cardiovascular performance rather than from ventilation limitation.27 In one large study, FVC, FEV1, and the FEF25–75 (forced expiratory flow rate between 25% and 75% of vital capacity) improved postoperatively in the majority of patients.28 Subjective improvement in exercise tolerance may be noted by patient and family.