Journal Logo


Exercise and Asthma

A Review

Laslovich, Steven M. PT, DPT, CPed; Laslovich, Joanne M. PT, MA, DPT

Author Information
Strength and Conditioning Journal: August 2013 - Volume 35 - Issue 4 - p 38-48
doi: 10.1519/SSC.0b013e31829d232f



Asthma is a complex and frequently occurring chronic inflammatory disorder of the airways generally thought to involve hypersensitivities to various types of stimuli (8). Although it often begins in childhood, asthma can affect individuals of all ages (16). The typical presentation of intermittent respiratory distress, wheezing, breathlessness, or chest tightness that can occur in the asthmatic individual results directly from narrowing of the lower airways (bronchoconstriction) caused by a combination of inflammatory processes, excessive mucus production, and smooth muscle dysfunction within the lower airways (27). In the asthmatic individual, inflammation of the airways appears to facilitate exaggerated airway narrowing responses from various stimuli (triggering substances or physical mechanisms), which can be described as airway hyperresponsiveness (AHR). The various triggers associated with acute and chronic asthmatic lower airway narrowing appear to be remarkably diverse, ranging from exposure(s) to lower air temperatures, aspirin, viral respiratory infection, stress, tobacco smoke, respiratory allergens, and as a result of exercise (11,25,32,33).

As a trigger of AHR, exercise in asthmatic individuals can result in increases of airway resistance leading to unwanted exercise-induced bronchoconstriction (EIB). However, although exercise may result in EIB, regular physical conditioning and activity are recognized as beneficial in the overall management of asthma and helping to improve cardiorespiratory conditioning, muscular fitness, and overall quality of life. It is now recognized that AHR and EIB during or after exercise are not strictly limited to those clinically diagnosed with asthma. EIB has also been shown to be present in a significant number of exercising individuals, including recreational and elite athletes previously undiagnosed with asthma (45,46). Interestingly, although many of the common symptoms of asthma (coughing, wheezing, shortness of breath, excessive mucus production, and chest tightness pain) are also seen in the nonasthmatic with EIB, it is presently unclear if the pathogenesis of EIB is the same across both nonasthmatic and asthmatic individuals. Exercise-induced asthma (EIA) and EIB are terms often used synonymously in the literature, but for the purposes of this review, in agreement with the Joint Task Force on the Pathogenesis, Prevalence, Diagnosis, and Management of EIB, we define EIB as “the airway obstruction that occurs in association with exercise in the presence or absence of clinically recognized asthma” (58).

For the exercise professional, it is important to understand the basic physiology of asthma and asthmatic AHR when involved with asthmatic individuals who may wish to initiate a formal exercise or physical activity program, are currently involved with physical training programs, or participating in recreational or competitive athletics. The purpose of this review is to examine the current literature surrounding the roles of physical exercise and physical activity in individuals with asthma and specifically highlight the prevalence, pathogenesis, diagnosis, and current pharmacological and nonpharmacological management of the asthmatic individual.


Asthma is an increasingly (up to approximately 12% in the last decade) common condition affecting 1 in 7 children and 1 in 15 adults in the United States; approximately 26 million (18.7 million adults and 7.0 million children) in the United States are living with clinically recognized asthma (Figure). The prevalence of asthma is higher among females, children, non-Hispanic black persons, and in individuals with family income below the national poverty level (16).

Asthma prevalence percentages by age, sex, and race, United States, 2011. Source: CDC Fast Stats, Summary Health Statistics for U.S. Adults and Children (14).

Development of asthma can occur at any stage of life; however, the majority of cases appear to begin in early childhood. EIB is reported to occur in 60–90% of asthmatic individuals of all ages and appears to be seen more frequently and with greater severity in those with poor or inadequate asthma control (13,29,57,58). An estimated 5–20% of the general population (currently not diagnosed with asthma) and up to 50% of various elite athletes may experience EIB (46,49,51,52,60).


It is important to understand that asthma is a complex syndrome thought to be associated with physiological dysfunction of nearly all components of the airway system. Within the airways, epithelial damage occurs, mucus gland hyperplasia is present resulting in mucus hypersecretion, remodeling and hypertrophy of bronchial smooth muscle takes place, and activation of multiple inflammatory cells occurs.

An increasing body of evidence suggests that several different molecular and cellular pathways may be involved, which can negatively affect the airways in the asthmatic individual (38). The increasing evidence of overlapping and complex cellular and molecular changes associated with asthmatic airway dysfunction begins to challenge the universally accepted definition of asthma as a single chronic disease. The appearance of asthma in many individuals occurs when the immune system develops an exaggerated response to specific foreign substances or allergens. After initial exposure to an allergen, an immunologic cascade of events involving various immune cells occurs resulting in the initiation of a series of inflammatory processes within the airway tissues. This immunologic cascade has long been hypothesized to involve the binding of immunoglobulin E (IgE) (an antibody) to an exposed allergen (dust mite, pollen, dander, etc.) (25,38). Allergens appear to induce specific white blood cells (T cells) to activate other white blood cells (B cells) to develop into plasma cells; plasma cells produce and release IgE antibodies. Typically, in individuals not genetically predisposed toward hypersensitivity, IgE is produced and binds to the allergen but no significant response occurs. In individuals with a genetic predisposition toward allergic sensitivity, T cells appear to be easily activated to produce and release antibodies in response to allergens. In allergic prone individuals, when sufficient numbers of allergen–IgE complexes are formed and bound to airway mast cells, mast cells are triggered to release histamine and cytokines, which act as proinflammatory mediators initiating airway inflammation and bronchoconstriction. Chronic and repeated allergen exposure and inflammation are thought to result in damage to various lower airway cells making them additionally susceptible to allergens (32,33).

A significant body of evidence suggests that not only T cells, B cells, and mast cells are involved but dendritic cells, macrophages, and eosinophils also appear to play important and crucial roles in the initiation and progression of the inflammatory processes associated with asthma (8). Dendritic cells and macrophages offer up allergens to the T cells, which subsequently induce B lymphocytes to produce allergen-specific IgE (61). Increased production and release of molecules such as histamine is associated with an initial (early) inflammatory response causing AHR, acute bronchoconstriction, bronchial swelling, and increased mucus secretion. Eosinophils attracted to the bronchial walls by cytokines and other molecules from the immune cells activated early on appear to induce an additional inflammatory response and bronchoconstriction that may occur hours later.

Because historically allergen-induced inflammation in asthma has been hypothesized to be driven primarily by T-cell responses, basic research on the pathogenesis of asthma has been focused on understanding the complex roles of T-cell cytokines as central regulators of allergic inflammation. Although allergen sensitization contributes to asthma in the majority of asthmatic individuals, inflammation and airway remodeling can also develop outside of cell-mediated IgE-dependent immune responses to allergens (31,32,48,61).

Asthma can occur without atopy (described as the genetic predisposition for production of specific IgE in response to common environmental allergens), but atopy is currently recognized as the single most significant risk factor associated with the incidence of asthma. However, the long held view that airway inflammation and changes in the structure of the lower airways in asthma is primarily because of the effects caused by repeat or prolonged sensitization to common environmental allergens is repeatedly being questioned (3,23,30,59). Multiple cellular and molecular pathways beyond allergic IgE-mediated responses appear to contribute to the development of asthma as well. The identification of multiple pathogenic processes occurring in asthmatic individuals has given rise to the recognition and assignment of specific asthmatic phenotypes (combined characteristics that define particular types of asthma) (9,10,31,37,38,42).

Independent of the genetic predisposition for asthma, there is evidence to suggest that an initial exposure and subsequent sensitization to an environmental allergen, repeated exposures to rhinoviruses, tobacco smoke, and other environmental pollutants during early childhood may interact to initiate asthma in early life and promote adult onset asthma (33). Evidence is emerging that suggests dysfunctional airway epithelium may be partly at the root of the clinically observed responses to environmental allergen, viral, or pollutant exposures (33). Airway epithelial cells function to act as a complex physical barrier against exposure from potentially harmful inhaled substances or pathogens and function as a regulator of airway immune and defense mechanisms. In nonasthmatic individuals, bronchial epithelium functions adequately as a barrier to limit allergens from reaching the subepithelial immune cells and initiating an immune response. In allergic asthma, defective functions of the airway epithelium permit allergens greater access into the subepithelium and promote immune responses. Although not yet fully understood, it has been suggested that a damaged (through viral or environmental exposure) or a genetically susceptible airway epithelium in early life could facilitate allergic sensitization and predispose the airways to repeated bouts of airway inflammation (32,33).

Nonallergic types of asthma (individuals without a genetic predisposition for allergen hypersensitivity) have also been linked not only to chronic or recurrent bacterial or viral infections and environmental pollutants but also to anxiety, stress, exercise, cold air, and hyperventilation. Although the molecular pathways are different and may overlap across the various asthma phenotypes, nearly all types appear to be characterized by similar clinical manifestations of airway inflammation, AHR, and transient airway obstruction (8). It is hoped that the increasing recognition of asthma as not a single disease but one with differing phenotypes (Table 1) and different pathological processes beyond IgE-based responses will help provide even better and more effective treatment strategies in the future.

Table 1
Table 1:
Commonly described asthma phenotypes


Inflammation in allergic asthma can be characterized into early and late responses after allergen exposure. Initial inhalation of allergens by individuals with allergic asthma results in an early asthmatic response characterized by acute airway obstruction because of abnormal airway smooth muscle (ASM) contraction induced by local inflammatory mediators. This early asthma response is associated with mast cell activation and results in abnormal bronchoconstriction occurring within minutes of allergen exposure, often reaching its peak within 2–3 hours after the initial exposure (39).

A late response is also recognized in approximately 60% of asthmatic individuals, which can occur 3–7 hours after initial allergen exposure. The late response is associated with other cells of the immune system (eosinophils and neutrophils) recruited by chemical mediators released from mast cell activation in the early phase. This late immune response phase can last up to 24 hours and involves prolonged airway inflammation leading to progressive and lingering bronchoconstriction (19,56). For the exercise professional, it becomes important to recognize the consequences of these early and late phase responses and institute careful monitoring of these in the actively exercising asthmatic individual.


There is increasing interest in understanding the specific mechanisms behind ASM contraction as a cause of airway narrowing seen in AHR. Muscular contraction of the ASM contributes in part to asthmatic bronchoconstriction, but it is presently not known whether AHR in asthmatic individuals arises from fundamental chronic alterations to ASM cells as a result of inflammation, as an adaptive response to changes in the mechanical microenvironment (higher airway resistance), or both (6). The role of ASM hyperplasia, hypertrophy, and the mechanical properties of the ASM including its shortening and relaxation characteristics in AHR have been investigated; however, no clear relationship between ASM characteristics and AHR has so far emerged (35,47).

In asthmatic individuals, the postexercise bronchoconstrictor response has been attributed to the inhalation of larger volumes of inadequately conditioned air as the triggering mechanism. Inhalation of high volumes of unconditioned air (because of increased mouth versus nasal breathing) leads to loss of both heat and water from the mucosa lining the lower airways (37). During heavy physical activity or exercise, high ventilation rates cause a drying effect across the airway mucosa resulting in a hyperosmolar environment as water is evaporated from the airway surface liquid. The increase of airway surface osmolarity is thought to induce mast cells to release prostaglandins, leukotrienes, and histamine leading to ASM contraction, inflammation, and subsequent bronchoconstriction (58). Hyperosmolarity, currently as the leading theory on the pathophysiology behind EIB, suggests that the most significant mediators of bronchoconstriction associated with exercise are likely the levels of work achieved and sustained during the exercise activity and the environment (water content of the inhaled air) (14). In individuals with EIB, the first 3–5 minutes of vigorous physical activity appear to have minimal effects after which rapid declines in pulmonary function and increases in symptoms are seen. Although individual response varies, acute bronchoconstriction associated with EIB typically peaks very rapidly (3–15 minutes) after cessation of exercise and often resolves spontaneously within 20–60 minutes (28).

After recovery from an episode of EIB, a refractory period between 40 minutes and 3 hours occurs during which repeat exercise may cause less bronchorestriction in roughly half of the individuals with EIB (54). The specific mechanism resulting in this refractory period is presently unclear but may be related to the depletion of mast cell mediators after the initial episode of EIB (4). A recent systematic review provides some evidence that the manipulation of this refractory interval through preexercise warm-up routines (close to peak oxygen consumption or maximal heart rate) can partially reduce the severity EIB in asthmatic individuals for short periods of time during the refractory period (5,53). With proper guidance, the use of preexercise warm ups; increasing stepwise to higher intensity exercises that induce controllable levels of bronchospasm (i.e., inducing a mild asthma attack) can temporarily allow for increased exercise workloads during the subsequent refractory periods. Use of the refractory period as a strategy for improving tolerance for high levels of exercise in training or sports competition while effective in individuals with controllable asthma should be thoroughly evaluated by the individual's medical provider before being attempted.

It is also important to recognize that in a limited number of individuals demonstrating EIB, a later return of symptoms (late response) can occur 4–12 hours after cessation of the physical activity. In contrast to the more severe and prevalent early phase reaction related to allergen exposure and asthma attack, the late phase response associated with EIB symptoms is typically described as less severe but more prolonged, lasting up to 24 hours (7).

In summary, both the clinical presentation and the pathogenesis of asthma are diverse and complex involving allergic and nonallergic processes associated with AHR and structural changes to the bronchial airway. The responses associated with these processes in the asthmatic exercising individual, while variable, are directly linked to the pathomechanics of the bronchial airways.


Because medical history and physical examination alone are not reliable means of excluding other pulmonary diagnoses or determining the degree of airflow restriction in asthma, spirometry is often used to assess pulmonary function when asthma is suspected. Spirometry is a commonly performed lung function test used to measure the maximal volume of air forcibly exhaled from the point of maximal inhalation, defined as forced vital capacity (FVC) and the volume of air exhaled during the first second of this maneuver (FEV1). In the presence of acute or chronically narrowed bronchi, FEV1 and the ratio between FEV1 and FVC are reduced (42). Spirometry may also be performed before and 10–15 minutes after treating with medications that produce rapid and short-term bronchodilation. Increases in FEV1 of 12% or more after use of bronchodilators are suggestive of the presence of asthma. Additional testing may include bronchoprovocation through use of the inhalation of irritative substances, such as methacholine or histamine (known asthma triggers) that can cause excessive bronchoconstriction in asthmatic individuals. Significant decreases in FEV1 with methacholine or histamine challenge testing are considered indicative of AHR (21).

Classification of asthma severity is often done and is based on frequency of nighttime awakenings, response to inhaled short-acting bronchodilators (short-acting bronchodilator agonists, SABA), frequency of asthma symptoms, physical activity limitations, and lung function tests (Table 2). Although asthma is classified based on severity, at the moment, there is no clear method for classifying the different subgroups of asthma discussed above (40,43).

Table 2
Table 2:
Classification of asthma symptoms


Currently, there is no accepted gold standard test to confirm a diagnosis of EIB. In current practice, the standardized exercise challenge test adopted by the American Thoracic Society is performed using a treadmill or bicycle ergometer and is generally considered the best currently available standardized method for evaluating EIB (21) (Table 3). Although healthy individuals will usually have an increase in FEV1 after exercise, a decrease of >10% in serial FEV1 values after the standardized challenge test is currently the recommended diagnostic threshold for diagnosis of EIB (21).

Table 3
Table 3:
Exercise testing protocol


In general, asthma medications are characterized as either bronchodilators or anti-inflammatory in nature. Their effects may be short acting and used for quick therapeutic relief of asthma symptoms or may have long-term effects (controllers) aimed at long-term maintenance and prophylaxis. Table 4 provides the most common pharmacological interventions and their mechanisms of action. It is important to recognize that although the use of asthma controlling drugs can be very effective in controlling asthma symptoms, a significant portion of asthmatic individuals do not regularly use the prescribed medications as directed. The proper use of both short-acting and long-acting medications is often paramount not only to the control of asthma symptoms but also to the quality of life including the ability to consistently perform physical, work, and recreational activities (27). It is important to realize that asthmatic individuals may be using both short- and long-acting bronchodilators as part of their asthma management. Inhaled asthma medications such as bronchodilators and corticosteroids are commonly delivered through handheld metered-dose inhalers (MDI) or dry-powdered inhalers (DPI). MDIs are designed to provide short bursts of aerosolized medications through pressurized canisters that fit into boot-shaped mouthpieces. They deliver medication when the device is activated (pumping action on the canister) by the individual either manually or automatically on inhalation. For effective use of manually activated MDIs, the individual must learn to coordinate inhaling at the same time as pushing on the actuator mechanism. Spacers can be used to increase the ease of use and effectiveness of MDIs and spacers consist of clear plastic tubes or chambers placed between the MDI device and the individual's mouth. Aerosolized medicine from the MDI is propelled into the spacer allowing the individual to inhale the medication more slowly and deeply (5–10 slow deep breaths). DPIs are another method for self-delivery of inhaled asthma medications. A DPI provides medication in the form of a fine dry powder, which is breath-activated, requiring the individual to actively breathe (deep and fast) in through the inhaler for release of the medicine from the device. A DPI is somewhat simpler to learn to use compared with the MDI but may be less efficient in times when the individual may not be able to breathe in deep and fast. Although it is beyond the scope of practice of exercise professionals to instruct or train asthmatic individuals in the proper use of MDIs or DPIs, observation and recognition of improper inhaler technique demonstrated by the asthmatic individual warrant referral back to the individual's medical care provider for adequate reassessment and training in the proper and efficient use of the inhaler.

Table 4
Table 4:
Commonly used asthma medications: type, brand names, delivery method, and mechanism of action

Additionally, although it is also clearly out of the scope of practice of the exercise profession to prescribe or manage the uses of medication and other substances for asthma or EIB, it is important to recognize that use of these in some cases by the competing athletes may be considered performance-enhancing drugs by regulating bodies associated with competitive sports. Performance-enhancing drugs (prescribed or over the counter) are subject to prohibition or restrictions in the United States by the National Collegiate Athletic Association (NCAA), United States Anti-Doping Agency, and the International Olympic Committee World Anti-Doping Agency. For example, albuterol, a commonly prescribed SABA used as a short-acting bronchodilator, is considered a banned substance by the NCAA; however, it is permitted by inhalation with a medical prescription. Regulatory organizations involving competitive athletics publish their current lists of banned or restricted substances and the exercise professional can, if needed, help to direct the individual and their medical provider to these important resources (34,41,55).


For the exercising asthmatic individual, AHR causing bronchoconstriction becomes one of the primary pathomechanical factors affecting exercise tolerance, exercise performance, and physical activity both subjectively and physiologically. Individuals with asthma may often demonstrate lower tolerances for exercise because of a combination of factors related to decreased pulmonary function, EIB, muscular deconditioning, or as a result of decreased cardiorespiratory fitness because of lower physical activity levels. Although EIB can be prevented or reduced through pretreatment with various medications, anxiety from potential EIB and the feelings of breathlessness have been shown to be associated with lower participation levels in sports, overall lower physical activity levels, and lower quality of life (36). Not surprisingly, asthmatic individuals with low physical activity levels also demonstrate lower physical fitness levels (26). Cardiorespiratory and muscular deconditioning may negatively impact subjective sensations of breathlessness during normal physical or exercise activities because of heightened muscular fatigue and increased ventilation rates. Additionally, lower levels of physical activity appear to be significantly associated to the severity and prevalence of asthma (20,39).

The important role of regular physical activity and exercise to the overall health of the asthmatic is well established. The results from a recent Cochrane review support previous evidence suggesting that exercise training, including aerobic and resistance training, is generally well tolerated among most stable asthma patients (17). Additionally, the authors report evidence of clinically significant increases in maximal oxygen uptake with physical training in asthmatic individuals (mean difference, 5.57 ml/kg/min; 95% confidence interval [CI], 4.36–6.78). Physical training programs involving cycling, group exercises, or swimming, 30–60 minutes, 2–3 times per week, improved maximal expiratory ventilation (6.0 L/min; 95% CI, 1.57–10.43), but these and other similar physical training programs failed to significantly alter the results of resting pulmonary function tests. These findings of improved aerobic fitness (V[Combining Dot Above]O2 max) with physical training and no significant effects on resting lung function are similar to the results of previous studies and reviews (50). Although exercise and increased activity do not appear to improve FEV1 or FEVC, there is some limited evidence to suggest aerobic exercise training may help to improve overall asthma control (22,39). Improved levels of ventilation after successful completion of aerobic conditioning programs in some asthmatic individuals can help to decrease frequency and severity of EIB and therefore may indirectly promote overall improved asthma control.

Physical inactivity is increasingly recognized as an important risk factor for chronic disease and because it is potentially modifiable will provide an opportunity for overall health improvements in the asthmatic individual. With proper management, individuals with stable asthma and EIB can often participate safely in physical activity and training programs. In the majority of controlled asthmatic individuals, use of proper medications as directed by medical personnel, including short-acting bronchodilators and proper individualized and tailored warm-up and cooldown to control AHR can enhance successful long-term adherence and tolerance to more vigorous physical training and conditioning programs (1,53).

To date, there has been limited research on the cellular and molecular mechanisms of improved aerobic fitness in regard to the various asthmatic phenotypes (12,32). Although the physiological basis for the observed improvements in aerobic capacity experienced by many asthmatics from regular exercise programs is not yet fully understood, the American College of Sports Medicine and the American Thoracic Society support the implementation of low to moderate intensity aerobic exercise (large muscle activities such as walking, cycling, swimming, light jogging) for well-controlled mild and moderate severity asthmatic patients ranging from 2 to 5 days per week at 50–75% of maximal workload (24,44). Based on the current evidence, the incorporation of aerobic training into the overall exercise programs can be done to help facilitate improvements in ventilation threshold (lowering the minute ventilation during mild and moderate exercise), cardiorespiratory fitness (V[Combining Dot Above]O2 max), and lowering breathlessness. Use of the Borg CR-10 dyspnea scale (Table 5) for assessment of breathlessness in asthmatic individuals during exercise activities is a valid and reliable method to regulate and monitor targeted exercise levels and reduce anxiety associated with breathing difficulties (18,24). Exercise professionals working with individuals with asthma should consider use of a dyspnea scale early on and throughout their exercise programming and while the exercise program should be specifically tailored to the specific individual, in general, exercising at a Borg CR-10 dyspnea scale in the range of 3–4 is a reasonable target goal for improving cardiorespiratory fitness.

Table 5
Table 5:
Modified Borg scale for perceived dyspnea (shortness of breath) (16)

It is also extremely important that individuals with asthma should be taught to consistently perform a minimum of 10–15 minutes low-intensity aerobic warm-up and cool-down (such as slow walking or slow jogging) to reduce the risk for developing EIB during the performance of higher level exercise activities and after the exercise program has ended. Warm-up and cool-down activities should also involve low-intensity activities for both the upper and the lower extremities and flexibility exercises. Use of activities that allow a proper cool-down in contrast to stopping an exercise or physical activity program suddenly can allow a more gradual airway rewarming and help to reduce the severity of EIB responses after exercise. Importantly, for the exercise professional, careful monitoring of postexercise responses related to acute bronchoconstriction should be a standard practice followed in all asthmatic individuals engaging in exercise programs.

Most individuals with asthma can safely perform resistance training to improve muscular fitness with lower risk for provocation of EIB when incorporating low-resistance high-repetition exercises. The benefits of a well-designed resistance training program (2–3 d/wk) for increasing strength, endurance, and neuromuscular coordination are similar to nonasthmatic individuals. Specific to asthmatic individuals, lower resistance (5–6 on the Borg 10-point rating of perceived exertion scale), higher repetition (2–4 sets of 10–15 repetition per set) exercises focusing on major muscle groups, and more extended rest intervals (3–4 minutes between sets) may be more easily tolerated with lowered risk of provoking EIB. As with aerobic training, resistance training should always consistently include extended warm-up and cooldown activities to reduce the risk for developing EIB. Additionally, musculoskeletal flexibility exercises as part of the required warm-up and cooldown before a resistance exercise program should be included in any comprehensive exercise program for individuals with asthma.

For the exercise professional, having a formal plan that includes careful monitoring of current and past asthma symptoms, severity, exposures to triggering mechanisms (temperature, humidity, and allergens) and knowing the time course of peak EIB as a result of training can help mediate the decision processes related to exercise prescription. Although athletes and asthmatic individuals can successfully manage many aspects of their asthma condition, it is extremely unwise for an individual with asthma or EIB to independently self-manage his or her asthma condition when exercising without proper and ongoing medical advice and guidance. It is strongly advised that each individual has a specific “asthma action plan” that has been developed directly through their current health care provider. As recommended by the American Lung Association and Centers for Disease Control and Prevention, an asthma action plan is a written individualized worksheet that identifies the processes and actions that will help prevent worsening of asthma symptoms and importantly it provides guidance to when it becomes necessary to directly contact the health care provider or when to seek emergency care (2,15). Those working and developing physical activity and training programs with asthmatic individuals should review the individual's specific medically directed asthmatic action plan or if one has not yet been developed encourage one to be developed directly through the individual's current health care provider. A basic action plan should include emergency contact information, contact information of the individual's health care provider, asthma classification (intermittent, mild, moderate, and severe), current medications and their individualized uses, and identified triggers of asthma. Individuals with asthma can be encouraged to use personal flow meters to assess the expiratory flow rates on a daily basis. Peak flow meters are low cost, simple to use over-the-counter devices that measure peak expiratory flow rate. The results (rate of peak expiratory flow) from a peak flow meter, when used properly, can provide indications as to the current levels of bronchial constriction. The individual's action plan should include a list of peak flow meter readings based on established personal bests from which to gauge current measurements. The use of personal flow meters can often help guide current exercise programming and importantly provide guidance in when to seek immediate medical attention. The action plan can be organized into zones based on a traffic light system (green—safe, yellow—caution, and red—danger) as seen in Table 6. Use of the peak flow measurements can help categorize the individual into 1 of the 3 zones and provide further guidance to the asthmatic individual and their exercise professional on the current status of their asthma control (2,15).

Table 6
Table 6:
Asthma action plan zones


Asthma is a diverse and complex disease resulting in AHR and transient bronchoconstriction. Emerging evidence of multiple asthma phenotypes, whether distinct or overlapping, suggests the need for continued research to improve current control and management strategies based on both the pathophysiology and the pathomechanics of a disease, which is increasing in frequency and presently incurable. Although the evidence remains still somewhat underdeveloped to unequivocally define exercise as the best practice across all asthmatic phenotypes, there appears to be sufficient evidence to suggest a valuable role for physical training in the overall management of the asthmatic individual's health. Exercise professionals working with the asthmatic individual exhibiting EIB need to consider the implications of AHR, the important roles of preventative and controlling medications, the negative effects of environmental pollutants and humidity in the prescription, and management of physical training programs. Careful monitoring of asthmatic symptoms and understanding the various levels of severity can help to produce a safer and efficient result from exercise training.


1. Ali Z, Norsk P, Ulrik CS. Mechanisms and management of exercise-induced asthma in elite athletes. J Asthma 49: 480–486, 2012.
2. American Lung Association. Asthma action plan. Available at: Accessed: March 3, 2013.
3. Anderson GP. Endotyping asthma: New insights into key pathogenic mechanisms in a complex, heterogeneous disease. Lancet 372: 1107–1119, 2008.
4. Anderson SD, Daviskas E. The mechanism of exercise-induced asthma is.... J Allergy Clin Immunol 106: 453–459, 2000.
5. Anderson SD, Holzer K. Exercise-induced asthma: Is it the right diagnosis in elite athletes? J Allergy Clin Immunol 106: 419–428, 2000.
6. An SS, Fredberg JJ. Biophysical basis for airway hyperreponsiveness. Can J Physiol Pharmacol 85: 700–714, 2007.
7. Asthma and Allergic Foundation of America. Exercise induced asthma. Available at: Accessed: December 15, 2012.
8. Barnes PJ. Intrinsic pathology of asthma (Monograph). Eur Respir Monogr 23: 84–113, 2003.
9. Bel EH. Clinical phenotypes of asthma. Curr Opin Pulm Med 10: 44–50, 2004.
10. Bhakta NR, Woodruff PG. Human asthma phenotypes: From the clinic, to cytokines, and back again. Immunol Rev 242: 220–232, 2011.
11. Bousquet J, Jeffrey PK, Busse WW, Johnson M, Vignola AM. Asthma: From bronchoconstriction to airways inflammation and remodeling. Am J Respir Crit Care Med 161: 1720–1745, 2000.
12. Boyd A, Yang CT, Estell K, Ms CT, Gerald LB, Dransfield M, Bamman M, Bonner J, Atkinson TP, Schwiebert LM. Feasibility of exercising adults with asthma: A randomized pilot study. Allergy Asthma Clin Immunol 8: 13, 2012. Available at: Accessed: December 15, 2012.
13. Cabral AL, Conceição GM, Fonseca-Guedes CH, Martins MA. Exercise-induced bronchospasm in children: Effects of asthma severity. Am J Respir Crit Care Med 159: 1819–1823, 1999.
14. Carlsen KH, Engh G, Mørk M. Exercise-induced bronchoconstriction depends on exercise load. Respir Med 94: 750–755, 2000.
15. Centers for Disease Control and Prevention. Asthma action plan. Available at: Accessed: March 3, 2013.
16. Centers for Disease Control and Prevention National Center for Health Statistics, NCHS Data Briefs No. 94. Trends in asthma prevalence, health care use, and mortality in the United States, 2001–2010, 8 pp. (PHS) 2012-1209. May 2012. Available at: http:// Accessed: March 1, 2013.
17. Chandratilleke MG, Carson KV, Picot J, Brin MP, Esterman AJ, Smith BJ. Physical training for asthma. Cochrane Database Syst Rev 5: CD001116, 2012.
18. Chetta A, Castagnaro A, Foresi A, Del Donno M, Pisi G, Malorgio R, Olivieri D. Assessment of breathlessness perception by Borg scale in asthmatic patients: Reproducibility and applicability to different stimuli. J Asthma 40: 323–329, 2003.
19. Cieslewicz G, Tomkinson A, Adler A, Duez C, Schwarze J, Takeda K, Larson KA, Lee JJ, Irvin CG, Gelfand EW. The late, but not early, asthmatic response is dependent on IL-5 and correlates with eosinophil infiltration. J Clin Invest 104: 301–308, 1999.
20. Clark CJ, Cochrane LM. Assessment of work performance in asthma for determination of cardiorespiratory fitness and training capacity. Thorax 43: 745–749, 1988.
21. Crapo RO, Casaburi R, Coates AL, Enright PL, Hankinson JL, Irvin CG, MacIntyre NR, McKay RT, Wanger JS, Anderson SD, Cockcroft DW, Fish JE, Sterk PJ. Guidelines for methacholine and exercise challenge testing-1999. Am J Respir Crit Care Med 161: 309–329, 2000.
22. Dogra S, Kuk J, Baker J, Jamnik V. Exercise is associated with improved asthma control in adults. Eur Respir J 37: 318–323, 2011.
23. Douwes J, Gibson P, Pekkanen J, Pearce N. Non-eosinophilic asthma: Importance and possible mechanisms. Thorax 57: 643–648, 2002.
24. Durstine JL, Moore GE, Painter P, Roberts S. ACSM's Exercise Management for Persons with Chronic Diseases and Disabilities. Champaign, IL: Human Kinetics, 2009. pp. 146–148.
25. Fireman P. Understanding asthma pathophysiology. Allergy Asthma Proc 24: 79–83, 2003.
26. Garfinkel SK, Kesten S, Chapman KR, Rebuck AS. Physiologic and nonphysiologic determinants of aerobic fitness in mild to moderate asthma. Am Rev Respir Dis 145(4 Pt 1): 741–745, 1992.
27. Global Initiative for Asthma. Global strategy for asthma management and prevention 2007. Available at:|1=2&I2=1&intld=1389. Accessed: December 1, 2012.
28. Godfrey S, Bar-Yishay E. Exercise-induced asthma revisited. Respir Med 162: 331–344, 1993.
29. Gotshall RW. Airway response during exercise and hyperpnoea in non-asthmatic and asthmatic individuals. Sports Med 36: 513–527, 2006.
30. Haldar P, Pavord ID. Noneosinophilic asthma: A distinct clinical and pathologic phenotype. J Allergy Clin Immunol 119: 1043–1052, 2007.
31. Handoyo S, Rosenwasser LJ. Asthma phenotypes. Curr Allergy Asthma Rep 9: 439–445, 2009.
32. Holgate ST. Pathogenesis of asthma. Clin Exp Allergy 38: 872–897, 2008.
33. Holgate ST, Arshad HS, Roberts GC, Howarth PH, Thurner P, Davies DE. A new look at the pathogenesis of asthma. Clin Sci (Lond) 118: 439–450, 2010.
34. International Olympic Committee World Anti-Doping Agency. The world anti-doping code. The 2013 prohibited list, international standard. Available at: Accessed: March 3, 2013.
35. James AL, Elliot JG, Jones RL, Carroll ML, Mauad T, Bai TR, Abramson MJ, McKay KO, Green FH. Airway smooth muscle hypertrophy and hyperplasia in asthma. Am J Respir Crit Care Med 185: 1058–1064, 2012.
36. Khan DA. Exercise-induced bronchoconstriction: Burden and prevalence. Allergy Asthma Proc 33: 1–6, 2012.
37. Kiley J, Smith R, Noel P. Asthma phenotypes. Curr Opin Pulm Med 13: 19–23, 2007.
38. Kim HY, DeKruyff RH, Umetsu DT. The many paths to asthma: Phenotype shaped by innate and adaptive immunity. Nat Immunol 11: 577–584, 2010.
39. Lucas S, Platts-Mills T. Physical activity and exercise with asthma: Relevance to etiology and treatment. J Allergy Clin Immunol 115: 928–934, 2005.
40. Moore WC, Pascual RM. Update in asthma 2009. Am J Respir Crit Care Med 181: 1181–1187, 2010.
41. National Collegiate Athletic Association. NCAA banned drug list. Available at: Accessed: March 3, 2013.
42. National Heart and Lung Institute, US Department of Health and Human Services. Guidelines for the diagnosis and management of asthma (EPR-3). Available at: Accessed: December 3, 2012.
43. National Heart, Lung, and Blood Institute. National Institute of Allergy and Infectious Diseases American Academy of Allergy, Asthma & Immunology American Thoracic Society European Respiratory Society Asthma Phenotypes Task Force 2010. Defining phenotypes: Expanding our understanding of asthma challenges in treating a heterogeneous disease. Available at: Accessed: December 12, 2012.
44. Nici L, Donner C, Wouters E, Zuwallack R, Ambrosing N, Bourbeau J, Carone M, Celli B, Engelen M, Fahy B, Garvey C, Goldstein R, Gosselink R, Lareau S, MacIntyre N, Maltais F, Morgan M, O'Donnell D, Prefault C, Reardon J, Rochester C, Schols A, Singh S, Troosters T. ATS/ERS pulmonary rehabilitation writing committee: American Thoracic Society/European Respiratory Society statement on pulmonary rehabilitation. Am J Respir Crit Care Med 173: 1390, 2006.
45. Parsons JP, Baran CP, Phillips G, Jarjoura D, Kaeding C, Bringardner B, Wadley G, Marsh CB, Mastronarde JG. Airway inflammation in exercise-induced bronchospasm occurring in athletes without asthma. J Asthma 45: 363–367, 2008.
46. Parsons JP, Craig TJ, Stoloff SW, Hayden ML, Ostrom NK, Eid NS, Colice GL. Impact of exercise-related respiratory symptoms in adults with asthma: Exercise-Induced Bronchospasm Landmark National Survey. Allergy Asthma Proc 32: 431–437, 2011.
47. Pascoe CD, Wang L, Syyong HT, Paré PD. A brief history of airway smooth Muscle’s role in airway hyperresponsiveness. J Allergy (Cairo) 2012: 768982, 2012. Available at: Accessed: December 16, 2012.
48. Pearce N, Pekkanen J, Beasley R. How much asthma is really attributable to atopy? Thorax 54: 268–272, 1999.
49. Provost-Craig MA, Arbour KS, Sestili DC, Chabalko JJ, Ekinci E. The incidence of exercise-induced bronchospasm in competitive figure skaters. J Asthma 33: 67–71, 1996.
50. Ram FS, Robinson SM, Black PN, Picot J. Physical training for asthma. Cochrane Database Syst Rev 4: CD001116, 2005.
51. Rundell KW, Im J, Mayers LB, Wilber RL, Szmedra L, Schmitz HR. Self-reported symptoms and exercise-induced asthma in the elite athlete. Med Sci Sports Exerc 33: 208–213, 2001.
52. Rundell KW, Jenkinson DM. Exercise-induced bronchospasm in the elite athlete. Sports Med 32: 583–600, 2002.
53. Stickland MK, Rowe BH, Spooner CH, Vandermeer B, Dryden DM. Effect of warm-up exercise on exercise-induced bronchoconstriction. Med Sci Sports Exerc 44: 383–391, 2012.
54. Tan RA, Spector SL. Exercise-induced asthma: Diagnosis and management. Ann Allergy Asthma Immunol 89: 226–235, 2002.
55. United States Anti-Doping Agency. Athlete guide to the 2013 prohibited list. Available at: Accessed: March 3, 2013.
56. Weersink EJ, Postma DS, Aalbers R, de Monchy JG. Early and late asthmatic reaction after allergen challenge. Respir Med 88: 103–114, 1994.
57. Weiler JM, Bonini S, Coifman R, Craig T, Delgado L, Capão-Filipe M, Passali D, Randolph C, Storms W. American Academy of Allergy, Asthma & Immunology Work Group report: Exercise-induced asthma. J Allergy Clin Immunol 119: 1349–1358, 2007.
58. Weiler JM, Anderson SD, Randolph C, Bonini S, Craig TJ, Pearlman DS, Rundell KW, Silvers WS, Storms WW, Bernstein DI, Blessing-Moore J, Cox L, Khan DA, Lang DM, Nicklas RA, Oppenheimer J, Portnoy JM, Schuller DE, Spector SL, Tilles SA, Wallace D, Henderson W, Schwartz L, Kaufman D, Nsouli T, Shieken L, Rosario N, American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology; Joint Council of Allergy, Asthma and Immunology. Pathogenesis, prevalence, diagnosis, and management of exercise-induced bronchoconstriction: A practice parameter. Ann Allergy Asthma Immunol 105(6 Suppl): S1–S47, 2010.
59. Wenzel SE. Asthma: Defining of the persistent adult phenotypes. Lancet 368: 804–813, 2006.
60. Wilber RL, Rundell KW, Szmedra L, Jenkinson DM, Im J, Drake SD. Incidence of exercise-induced bronchospasm in Olympic winter sport athletes. Med Sci Sports Exerc 32: 732–737, 2000.
61. Woodruff PG, Modrek B, Choy DF, Jia G, Abbas AR, Ellwanger A, Koth LL, Arron JR, Fahy JV. T-helper type 2-driven inflammation defines major subphenotypes of asthma. Am J Respir Crit Care Med 180: 388–395, 2009.

airway hyperresponsiveness; inflammation; exercise-induced asthma; allergen

Supplemental Digital Content

© 2013 by the National Strength & Conditioning Association