Pulmonary Disorders & Exercise Prescription
Pathophysiology of Asthma
Pathophysiology of EIB
Effects of Exercise on Asthma & EIB
Exercise Guidelines for Asthma & EIB
Pathophysiology of COPD
Exercise Guidelines for COPD
Pulmonary Hypertension [PH]
Exercise Effects & Guidelines for PH
Performing regular physical activity (PA) and exercise has been reported to have profound positive health benefits to those individuals suffering from chronic health conditions (e.g., heart disease, diabetes). Unfortunately, substantiation of the benefits of regular PA for individuals with chronic lung disease is less clear. Several studies have reported that subjects improved cardiorespiratory fitness, quality of life scores, reduced corticosteroid use whilst reporting a reduction in the severity of exercised induced bronchoconstriction (EIB) follow aerobic exercise (Pasnick et al., 2013). However, there is also evidence that aerobic endurance exercise may contribute to asthma and EIB.
For example, Sue-Chu et al., (1999) reported that elite cross-country skiers have asthma-like symptoms (“ski asthma”). The authors investigated these symptoms via bronchoscopy and bronchoalveolar lavage (BAL) on thirty (23 male) elite cross-country skiers, aged 16 ± 20 (mean 17.3) years, and 10 (seven male) healthy nonathletic control subjects, aged 21±31 (mean 24.4) years. Compared to controls there was a threefold increase in the macroscopic inflammatory index in the proximal airways of the elite skiers (median [interquartile range] 3.0 [2.0 ± 5.0] versus 1.0 [0.8 ± 2.3], p = 0.008).
Moreover, air pollution has been correlated with new-onset asthma and chronic obstructive pulmonary disease (COPD) (Gauderman et al., 2004; Hogg et al., 2004). This page investigates both the positive and negative effects of exercise relating to asthma, pulmonary hypertension, COPD, and cystic fibrosis
Asthma
Asthma is a chronic inflammatory lung disease that affects the airways of the lungs. It is estimated that in the UK, 5.4 million people are currently receiving treatment for asthma equating to one in every 12 adults and one in every 11 children. Asthma in adults is more common in women than men (Asthma UK, 2018 [ www.asthma.org.uk]). Asthma is not a curable condition, but is manageable; the severity of the symptoms varies from individual to individual, and the symptoms are frequently manageable in most patients.
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Exercise-related exacerbations commonly occur in almost 10% of the populace (Rundell et al., 2015); however, in several sports, the occurrence is much higher. For instance, Molis and Molis (2010) suggested that EIB is >25% greater in swimmers, Nordic skiers and ice rink athletes. Exercise-induced bronchoconstriction ensues in individuals with evident asthma and those without asthma. In both cases, the mechanism is inflammatory; however, the specific cause may differ from individual to individual (Weiler et al., 2010).
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Pathophysiology of Asthma
The prevalence of asthma in the UK and the United States has dramatically increased in the last three decades. This escalation according to Luks and colleagues (2010) is due [in part] to greater awareness and also overdiagnosis, and also the increase in airborne toxins. These include an array of combustion sources (vehicle traffic, coal and oil burning furnaces) and increased ozone levels that can aggravate existing asthma and be responsible to new-onset asthma who are genetically susceptible (McCreanor et al., 2007). Strannegard and Strannegard (1999) also proposed that alterations in diet, changes in bacteria, viral infections and microflora contribute to allergic diseases. This reduction of contact and viral infections with the microbial environment during early life may according to Holt and Bjorksten (1997) affect the maturation of a normal immune reaction. The lack of exposure to microbial during early childhood may also affect sensitisation to allergens (Berstad and Brandtzaeg, 2000). Immune reactions are prepared in utero and remodelled during postpartum allergen exposure. The sensitivity to environmental antigens is dependent on the immunologic memory instigated during antigen faced early in life (Holt, 2011).
According to Yakubovich, Cluver and Gie, (2016) reported that low socioeconomic standing (SES) promotes adverse conditions to high allergens (i.e., exposure to cockroaches, dust mites and also cigarette smoke). The authors investigated the association between socioeconomic factors and childhood asthma. A sample of 6002 children aged between 10-17 years from six low-income urban and rural sites in three SA provinces completed questionnaires that measured health status, sociodemographic and socioeconomic factors. Yakubovich and colleagues reported that child anxiety and community violence were associated with increased odds of having asthma. Children doing more outdoor housework and living in greater poverty had lower odds of having asthma. Severe asthma was predicted by child depression and greater household poverty. Most socioeconomic factors operated in 'risk pathways', where urban living was associated with individual factors (e.g., fewer outdoor tasks), which predicted greater odds of having asthma or severe exacerbations. This is further supported by the work of Volmer (2001) who reported that asthma severity and associated mortality are twice as common in individuals with low SES. Conversely, it has been reported that the prevalence and incidence of asthma are higher among people with high SES. This feasibly is due to the high SES populace receiving better health care and diagnosis compared to low SES.
Additional research has suggested that there is a greater prevalence of asthma among African Americans. McGowan et al., (2015) reported that asthma mortality rates are fourfold higher in African Americans compared to Caucasians. This is supported by Litonjua et al., (1999) who examined the effects of SES on the relationship between race/ethnicity and asthma prevalence in a cohort of 499 families (998 parents and 307 children) with a history of asthma or allergies from the Boston, Massachusetts area. In the parental cohort, Blacks and Hispanics were at greater risk for asthma than Caucasians. In the cohort of children, Black and Hispanic children were also at increased risk for asthma. The authors concluded that a large proportion of the racial/ethnic variances in asthma incidence is explained by aspects related to income, area of residence, and level of educational attainment.
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Various studies (Camargo et al., 1999; Castro-Rodriguez et al., 2001; Von Kries et al., 2001) have reported that asthma is a risk factor for obesity due to decreased physical activity levels, although Beasley and associates (2015) have also suggested that obesity is a risk for asthma. The airway obstruction and peak flow variability are increased in obese individuals while a decrease in body mass index and fat mass is associated with improved airway function. Asthma is a condition characterised by an increased sensitivity of the airway passages, which manifests itself as a reversible narrowing of the air passages, principally the bronchioles. The narrowing is produced by a swelling of the mucous membrane lining with copious thick mucus and a constriction of the smooth muscle surrounding the bronchioles. In asthma, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells may all be dynamically involved in the inflammatory process and airway hyperresponsiveness (Chung et al., 2014).
Symptoms of asthma include recurrent episodes of wheezing, breathlessness, chest tightness, and coughing (particularly during the morning and night), or in response to allergen exposure or exercise. Asthma incidences are correlated with airflow obstruction that normally resolves within 1 hour (Weiler et al., 2010). An acute response is characterised by activation of airway inflammatory cells, while the subacute reactions involve inflammation from resident inflammatory cells in the airway initiating more persistent inflammation. Chronic inflammation a trait of moderate to severe asthma is defined by resident inflammatory cells, airway remodelling, and persistent respiratory symptoms. Figure 1 reveals the structural changes in a person with asthma.
Figure 1. Schematic of a normal airway and a constricted airway of a person with asthma.
There is a range of factors or indices that are used to grade an individual’s asthma status; however, a key indicator of severity is the degree to which medication is required to relieve the symptoms (Chung et al., 2014 ). A categorisation system is displayed in Table 1.
Table 1. Components of Asthma Severity by Clinical Features Prior to Treatment
Pathophysiology of Exercise-Induced Bronchoconstriction
Exercise-induced bronchoconstriction (EIB) is defined by Parsnick et al., (2014) as a temporary contraction of the airways during or after the termination of exercise. This response normally resolves within an hour post-exercise. Most diagnostic criteria define EIB as a 10% or greater decrease in forced expiratory volume in the first second of maximal exhalation (FEV1). Exercise-induced bronchoconstriction can transpire in individuals with apparent asthma and those without. Exercise is the most common initiator of an asthma attack. This hyperresponsive reaction to exercise occurs in almost 90% of individuals who have asthma and, for those who have mild asthma, EIB may be the only evident expression of the disease (Anderson, Connolly and Godfrey, 1971).
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Exercise-induced bronchoconstriction prevalence has been estimated to be 4-to-20% in the general population (Parsons et al., 2013; Weiler et al., 2010; Weiler et al., 2000). In the athletic populace, the prevalence of EIB has been reported to be 11-to-55% (Weiler et al., 2010; Weiler et al., 2000), with the highest rates found in winter sports athletes (Weiler et al., 2000). Exercise-induced bronchoconstriction is normally triggered by water loss from the airway surfaces that are essential to the humidification of inspired air throughout the exercise (Anderson and Daviskas, 2000). Exercise-related inflammation and airway hyperresponsiveness can also be associated with the allergen reaction or inhalation of airborne contaminants during exercise.
Following the humidification process essential to dry air inhalation, water loss from the airway surfaces increases osmolarity in airway cells. This is followed by an inflow of water into the cells to re-establish osmolarity and initiate an inflammatory mediator release, which consequently causes bronchial smooth muscle constriction (Parsons et al., 2013; Weiler et al., 2010). The severity of the exercise-related response is determined by ventilation rate, ambient air water content and temperature during exercise, as well as the presence of any allergen (Parsons et al., 2013). Normally, water loss from the humidification process in the airways is constantly replenished by epithelial cells and submucosa (Chen and Horton, 1977). However, scientific evidence suggests that changes in the subepithelial basement membrane may be [in part] responsible for a decrease in the ability to sufficiently respond to this airway surface evaporative water loss (Laitinen and Haahtela, 1993). This may require the recruitment of smaller airways into the humidification process, augmenting airway hyperreactivity (Chen and Horton, 1977).
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Though the exercise setting may be the principal cause of the EIB response in individuals with and without apparent asthma, it has been suggested that the modality of exercise may play a role [when ventilation is affected. Rundell and associates (2000) compared a field-based exercise challenge and laboratory-based exercise challenge for pulmonary function test (PFT) exercise-induced asthma (EIB) screening of elite athletes. The authors reported that 91% of PFT positive and 48% of PFT normal athletes reported at least one symptom of EIA, with postrace cough most frequent. Rundell et al., (2000) concluded that self-reported symptoms by elite athletes are not reliable in identifying EIB. Additionally, a large number of false negatives may occur in this population if EIB screening is executed with inadequate exercise and environmental stress.
This is supported by Castricum et al., (2010), who investigated the effectiveness of the eucapnic voluntary hyperpnoea (EVH) challenge, the field swim challenge and the laboratory cycle challenge in the diagnosis of EIB in elite swimmers. Thirty-three elite swimmers were assessed on different days for the incidence of EIB using 3 different bronchial challenge tests: an 8-minute field swim challenge, a 6-minute laboratory EVH challenge, and an 8-minute laboratory cycle challenge. The authors reported that 1 of the 33 subjects had a positive field swim challenge with a fall in FEV1 of 16% from baseline. Eighteen of the 33 subjects had a positive EVH challenge, with a mean fall in FEV1 of 20.4% from baseline. Four of the subjects had a positive laboratory cycle challenge, with a mean fall in FEV1 of 14.8 % from baseline. Only 1 of the 33 subjects was positive to all 3 challenges. These results suggest that the EVH challenge is a highly sensitive challenge for ascertaining EIB in elite swimmers, in contrast to the laboratory and field-based exercise challenge tests, which significantly underdiagnose the condition.
Interestingly, a study by Seys et al., (2015) investigated airway epithelial damage and release of damage-associated molecular patterns (DAMPs) after intensive exercise in elite athletes and controls. Competitive swimmers (n = 26), competitive indoor athletes (n = 13) and controls (n = 15) without any history of asthma were recruited with lung function was assessed before, immediately after and 24 hours after a 90-minute intensive exercise protocol. Sputum induction was performed at baseline and 24 hours after exercise. Exercise-induced bronchoconstriction was assessed by the eucapnic voluntary hyperventilation test. Results indicated that baseline sputum uric acid, high mobility group box-1, CXCL8 mRNA, sputum neutrophils and serum Clara cell protein-16 (CC-16) were significantly higher in competitive swimmers compared with controls. Intensive swimming for 90 minutes resulted in increased sputum IL-1β, IL-6 and TNF mRNA in competitive swimmers, and of sputum IL-6 mRNA and sputum neutrophils in controls. The study also noted findings that the intensive training combined with exposure to by-products of chlorination induces airway epithelial damage in competitive swimmers.
Effects of Exercise in Individuals With Asthma and EIB
As discussed in the previous section there is qualifiable evidence that supports the premise that a greater prevalence of asthma and EIB can be found in swimmers and winter sports athletes. The specific causes are likely from high minute ventilation breathing of air with high trichloramine levels found in indoor pool air, cold air, air high in combustion contaminants. Studies have reported that performing exercise in high-ozone air may cause acute decreases in lung function in both asthmatic and non-asthmatic populace. (Rundell et al., 2015; Seys et al., 2015). Islam et al., (2007) has stated that continuing exposure to ozone while exercising attenuates the protective effect of better lung function against new-onset asthma in children.
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Most individuals with asthma are predisposed to EIB, yet their ability to exercise is often not limited (Rundell et al., 2015); however, in instances in which resting lung function is impaired, exercise can be compromised (Rundell et al., 2015). Nevertheless, most people with asthma can engage in exercise or various sports symptom-free, while improving their overall quality of life (del Giacco and Garcia-Larsen, 2016). Carson et al., (2013) noted that there is not a general consensus that exercise creates an improvement in baseline lung function. This is despite the extensive review by del Giacco and associates (2014) that concluded that moderate-intensity aerobic exercise improves cardiovascular fitness in a person with asthma or EIB (Figure 2).
Figure 2. del Giacco et al., (2015) dose-response relationship between physical activity and asthma risk
The effects of aerobic training have been studied by Dogra et al., (2011). The authors examined the effects of a 12-week supervised exercise intervention followed by a 12-week self-administered exercise on adults with partially controlled asthma and match controls. The exercise intervention focused on aerobic training, with one set of strength training per week included that targeted the major muscle groups. Exercise intensity was established from the subject’s maximum heart rate (HRmax) that was obtained during the aerobic fitness test. As a result of subjects previously being sedentary, the programme intensity increased with a 5% increase every three weeks from 70% to a minimum of 85% HRmax. Subjects were also shown the Borg Rating of Perceived Exertion scale at each 5-minute interval of exercise, so they understood the ‘‘feeling’’ related to that intensity of exercise. The result found that a 12-week supervised exercise intervention led to improvements in asthma control and quality of life in partially controlled adults with asthma who were motivated in exercise training. Moreover, supervised exercise followed by a period of self-administered exercise retained the developed asthma control levels and resulted in significant improvements in aerobic fitness and perceived asthma control. These results suggest that a well-designed exercise intervention can improve aerobic fitness, asthma control, and quality of life.
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After a 6-to-8-minute duration challenge test, a frequently reported EIB response occurs. However, during more prolonged sessions of exercise, there is a continuing regression in lung function followed by a decrease in FEV after stopping exercise (Beck et al., 1994). Beck and colleagues further noted that the mode of exercise (continuous vs. interval), intensity and duration will determine whether bronchoconstriction develops during or at the termination of exercise, or not at all. Research by Stirling et al., (1983) and Godfrey, (1988) have specified that lung function during the EIB challenge test typically involves bronchodilation during the exercise session followed by a reduction in expiratory flow rates 5-to-20 minutes post-exercise. Beck et al., (1994) has intimated that exercise bronchodilation is feasibly attributable to increased tidal volumes during exercise that causes the airways to be stretched open, therefore providing mechanical protection against EIB.
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Following a reduction in tidal volume as a result of exercise cessation or a decrease in intensity bronchoconstrictive effects dictate. It has been observed by Beck et al., (1994) that during 36-minutes of steady-state exercise, bronchodilation ensues after the initial few minutes of exercises followed by a continuous decline in lung function for the remaining exercise duration. Prior to the work of Beck and colleagues, the reduction in exercising lung function was not reported due to the challenge tests being of short duration. During interval exercise, the lung function of individuals with asthma varies with the intensity of exercise. The lung function increases with high intensity and decreases during the recovery interval. Moreover, Beck and associates assessed lung function during 36 minutes of interval exercise that involved 6-minute alternating moderate- and light-intensity bouts. Lung function established a continued reduction during the 36-minute exercise period, displaying improvement during the moderate-intensity period and a decline during light-intensity.
Current Exercise Recommendations for Individuals with Asthma and EIB
Evidence that has been drawn from prevalence rates of asthma and EIB in individuals who engage in exercise or sport in environments (i.e., cold and dry environments) supports the premise that exercise is feasible for clients with these conditions. Recommendations on exercise prescription for individuals with asthma or EIB should be centred upon the results obtained from exercise testing and assessment including a bronchial challenge test (see Coates et al., 2017 for ERS technical standards]). This is to ensure that the exercise professional is aware of the client’s threshold and response to exercise intensity, mode, duration, and the environmental setting.
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Importantly, individuals with asthma and EIB must ensure that they have sufficient control of their condition and symptoms before engaging in an exercise program. Aerobic exercise is frequently paired with pharmaceutical therapy in clients with moderate and severe asthma as a means of improving bronchial hyperresponsiveness, exercise capacity and quality of life (Eichenberger et al., 2013; França-Pinto et al., 2015)
Exercise professionals should not that they are aware that clients may use medication pre-exercise including a mast cell stabilising agent or inhaled anticholinergic agent (Parsons et al., 2013). In combination, clients with asthma or EIB regularly take a regular controller medication (Table 2) that may include a leukotriene receptor antagonist or an inhaled corticosteroid (Parsons et al., 2013). Eves and Davidson, (2011) propose that even though this is an appropriate strategy that reduces the associated risk of the exercise session triggering an adverse occurrence. Considerations should be given to any exacerbation of symptoms with the involvement of a multi-disciplinary team (including health professions) to determine a client-centred action plan and program.
Table 2. Examples of medication for asthma and EIB.
Studies and recommendations have proposed (Parsons et al., 2013; Stickland et al., 2012) that using interval or combination warm-up exercise as opposed to continuous high or light-intensity exercise may produce a refractory period of up to 2-hours that reduces the client’s tendency to develop EIB (MacKenzie et al., 1994).
When the client performs the aerobic aspect of the program the intensity and duration should begin at a lower level progressively advancing so as not to trigger or exacerbate any symptoms (Table 3). As the fitness profile of the client develops evidence suggests that the exercise professional should endeavour to assign an intensity of 40-to <60% V.O2 or heart rate reserve for 20-to-60 minutes three to five times a week using an exercise mode that involves rhythmic and continuous movement of large muscle groups (Andrianopoulos et al., 2014; del Giacco et al., 2015; Spruit et al., 2013). For clients with asthma or EIB, the design of an initial resistance training program is similar to the recommendation for beginners or untrained individuals (two-to-three sessions per week of two to four sets using moderate loading) (Andrianopoulos et al., 2014; Spruit et al., 2013).
Table 3. NSCA Recommendations for clients with asthma and EIB.
Chronic Obstructive Pulmonary Disease & Exercise
Chronic obstructive pulmonary disease (COPD) is a progressive lung disorder characterised by emphysema and chronic bronchitis which diminishes lung function. It is the result of the disease process consisting of narrowing of the airways (chronic bronchitis) and destruction of the lung tissue (emphysema), and the disease is usually accompanied by profuse mucus secretion. There is no known cure and only cancer and heart disease kill more people in developed countries than COPD.
Globally, COPD mortality is increasing (American Lung Association, 2020), and the disease is responsible for over £30 billion in the USA annual health care costs (CHEST, 2014). Females are 37% more likely to have COPD than males, and about half of the deaths are in women (82,158 versus 73,887). However, the COPD death rate is higher among men than women (42.9 versus 35.8 per 100,000) because the female population is larger than the male population (American Lung Association, 2020). The number of individuals with COPD have increased by approximately 41% since 1982 (Sin and Man, 2005). Presently, smoking cessation is the only intervention that has overwhelmingly been shown to reduce the rate of lung function decline (Tashkin and Murray, 2009). Symptoms of declined lung function include a chronic cough, sputum production, shortness of breath, exercise intolerance, muscle wasting, gas trapping, and frequent respiratory infections (Sin and Man, 2005).
Chronic obstructive pulmonary disease is caused by prolonged cigarette smoking, predominantly, and is common in the UK. It is estimated that 3 million individuals in the UK have COPD (NICE, 2016), with a further 2.1 million people estimated to be undiagnosed. The prevalence increases with age, with most patients being diagnosed in their 50s. COPD is closely associated with levels of deprivation: rates are higher in more deprived communities (NICE, 2016). COPD is the fifth largest killer in the UK and the second most common cause of emergency admission to hospital and one of the most expensive inpatient conditions treated by the NHS.
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Management is normally short-acting β2-adrenergic agonists (SABAs), long-acting β2-agonists (LABAs), anticholinergics, inhaled corticosteroids (ICSs), or a combination of these drugs (National Heart, Lung, and Blood Institute, 2020). Moreover, the National Heart, Lung, and Blood Institute (2020) suggests that these individuals should have a twelve-monthly flu shot and the pneumococcal vaccine. Identification, screening and diagnosis of comorbid COPD and asthma occur in 15-20% of individuals (Louie et al., 2013; McDonald et al., 2011). It has been reported that individuals experience a more rapid disease progression than with COPD and asthma alone (Gibson and Simpson, 2009; Kauppi et al., 2011).
Previous studies (Lange et al., 1998; Rijcken et al., 1995; Tashkin et al., 1996) have demonstrated that bronchial hyperresponsiveness (BHR) and the diagnosis of asthma have been associated with a greater deterioration in forced expiratory volume (FEV1) in both smokers and non-smokers. Hospers and colleagues (2000) suggested that the existence of BHR in individuals with COPD has been linked with an increase in exacerbations and mortality. Soriano et al., (2005) compared baseline rates of comorbidities in COPD and asthma patients to the risks to the UK general population. The authors reported in both COPD and asthma cohorts, the total sum of diagnoses related to major organ systems was higher than in their matched population controls. Among incident COPD patients, an occurrence of > 1% within the first year was observed after diagnosis for angina, cataracts, bone fractures, osteoporosis, pneumonia, and respiratory infections, the highest being angina with 4.0%. Compared to the non-COPD group, COPD patients were at increased risk for pneumonia, osteoporosis, respiratory infection, myocardial infarction, angina, fractures, and glaucoma [all p < 0.05].
Pathology and Pathophysiology of COPD
Pathology of COPD
Chronic obstructive pulmonary disease (COPD) is characterised by progressive emphysema, chronic bronchitis, or both, resulting in decreased forced expiratory volume (FEV1) and forced vital capacity (FVC). As a result of emphysema and obstruction to airflow in the smaller airways, there is a reduction in exhalation force available and a decline in lung capacity. The typical characteristics of COPD are inflammatory cells in the airways and airway wall thickening. Due to immune responses neutrophils, T lymphocytes, and B lymphocytes are activated and contribute to the decline in lung function.
However, (Hogg et al., 2004) have suggested that airway wall thickening is correlated strongly to the progression status of COPD. Hogg and associates examined the advancement of the pathological effects of airway obstruction in patients with COPD. The small airways were evaluated in surgically resected lung tissue from 159 patients. Results indicated that the advancement of COPD strongly correlated with an increase in the volume of tissue in the wall (P<0.001) and the accumulation of inflammatory mucous exudates in the lumen (P<0.001) of the small airways. The percentage of the airways that contained polymorphonuclear neutrophils, macrophages, CD4 cells, CD8 cells, B cells, and lymphoid aggregates containing follicles and the absolute volume of B cells and CD8 cells also increased as COPD progressed. The authors concluded that the evolution of COPD is related to the accretion of inflammatory mucous exudates in the lumen and infiltration of the wall by innate and adaptive inflammatory immune cells that form lymphoid follicles. These alterations are connected to a remodelling process that thickens the walls of these airways and attenuates mucociliary clearance.
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Pathophysiology of COPD
Approximately 80-90% of COPD is linked to smoking while the remainder is possibly due to exposure to noxious gases and elements (NHLBI, 2021). Salvi and Barnes (2009) have reported that the problem of non-smoking COPD is greater than previously thought with a projected range of 25-to-45% of people with COPD have never smoked.
Further factors that have been related to COPD include exposure to air toxins including dust, cooking fumes, and internal combustion fumes from automobiles and other transportation devices; a record of repeated lower respiratory tract infections during infancy; pulmonary tuberculosis; chronic asthma and poor sustenance. Sood and associates (2009) reported that exposure to wood smoke was associated with a 70% greater risk of COPD in both males and females and that this association persisted even after correction for age, tobacco smoking, and educational level. Equally, biomass or coal cooking has been acknowledged as an elevated risk for COPD in low- and middle-income countries (Gordon et al., 2014).
Inflammation of the airways also plays a central role in disease progression (Di Stefano et al., 1998; Gosman et al., 2014; Hogg et al., 2004). The amount of inflammation relates to the degree of airflow obstruction (Di Stefano et al., 1998) and can result from oxidant-induced damage. Approximately 3% of all COPD incidents have been correlated to a lack of alpha-1 antitrypsin (a genetic deficiency). The primary function of alpha-1 antitrypsin is to safeguard the lungs from inflammation caused by infection and inhaled irritants (Greulich and Vogelmeier, 2016; Vignaud, Cullin and Bouchecareilh, 2015).
Exercise Recommendations for Clients With COPD
At present, there is not a universal consensus on the optimum exercise program, as exercise intensity and duration should be modified to reflect the severity of symptoms (Garvey et al., 2016). Though various studies have displayed improvement in peripheral muscle strength, gas exchange, and aerobic endurance capacity with various exercise interventions (Garvey et al., 2016). It has been recommended that inclusion of resistance training with aerobic training is associated with significantly greater increases in muscle strength and mass (Garvey et al., 2016), but does not specify further improvement in exercise capacity, dyspnoea, or quality of life in clients with COPD (Bernard et al., 1999; Zambon-Ferraresi et al., 2015). Equally, adding resistance training to an aerobic endurance program offers an applicable approach due to muscle weakness which is one of the extrapulmonary indices of COPD (Zambon-Ferraresi et al., 2015).
Importantly evidence has suggested that resistance training, aerobic endurance training, and a combination of them both together have comparable value for clients with COPD (Jones and Nzekwu, 2006). Therefore, the exercise program can be devised around the client’s preference to augment their compliance. Progression in exercise tolerance and an increase in muscle strength are indicative of an effective rehabilitation program.
Aerobic Guidelines for Clients with COPD (Garvey et al., 2016)
Resistance Training Guidelines for Clients with COPD (Garvey et al., 2016)
Pulmonary Hypertension
Pulmonary hypertension is a hemodynamic and pathophysiological disorder that has been defined as having mean pulmonary arterial pressure greater than 25 mmHg at rest (Galie et al., 2013). Pulmonary hypertension can be further divided into six distinctive categories that represent a range of pathophysiological mechanisms (Galie et al., 2013). Therefore, managing an individual with a diagnosis of pulmonary hypertension does not merely involve following a wide-ranging procedure. Rather, considerations must be given to the type of pulmonary hypertension and the causal factors specific to each person.
Pulmonary arterial hypertension is a clinical condition categorised by pulmonary arterial hypertension in the absence of other causes of precapillary hypertension (Galie et al., 2013). There may be numerous underlying origins, including heredity, drug toxicity or can be idiopathic. Each cause of pulmonary arterial hypertension generates similar pathophysiological alterations in the cardiopulmonary system. Although, pulmonary arterial hypertension is uncommon, with an incidence of one in 100,000-to-1,000,000 individuals (Mocumbi, Thienemann and Sliwa, 2015). However, the financial effect of pulmonary arterial hypertension is considerable, with Gu and colleagues (2015) reporting approximately $2,500 to $12,000 per month of direct costs, plus unspecified indirect costs.
The condition of pulmonary hypertension is not unusual, with estimates of up to 1% of the worldwide population and is frequently linked with other chronic cardiopulmonary or infectious disorders (Hoeper et al., 2016; Mocumbi, Thienemann and Sliwa, 2015). The prevalence and primary cause of pulmonary hypertension have significant environmental disparity, due to variances including genetics, infectious disease, and primary medical treatment. Pulmonary hypertension is normally linked with hypoxic cardiopulmonary diseases, including COPD and diffuse parenchymal lung diseases (Papathanasiou et al., 2015; Rowan et al., 2016).
Pathology and Pathophysiology of Pulmonary Hypertension
The pulmonary circulatory system is a fast-moving, low-pressure, low-resistance system compared to the other workings of the circulation, with resting peak systolic pressure <25 mmHg and diastolic pressure <10 mmHg with the mean pulmonary arterial pressure at rest being 14 ± 3 mmHg.
Right atrial and ventricular pressure during diastole is approximately <5 mmHg, which is the pressure necessary to permit a positive pressure gradient for venous blood from the systemic circulation to return to the right side of the heart. In line with the principles of cardiovascular physiology, increases in blood pressure are attributed to an increase in cardiac output or an increase in vascular resistance. However, in pulmonary hypertension, vascular resistance is usually the underlying factor, though the cause of increased pulmonary vascular resistance is varied.
Preceding classification schema of pulmonary hypertension have apportioned it into primary and secondary conditions, but this has been discarded as it is overly simplistic (Galie et al., 2013). That said, there remains significant value in understanding how several pathological conditions can lead to the development of pulmonary hypertension. The pathogenesis of pulmonary hypertension leads to the diminished functional diameter of the lumen of pulmonary arteries and veins, depending on the classification of pulmonary hypertension. For example, primary vasoconstriction, thromboembolic blockages, and parasitic infestations may all reduce blood vessel diameter and consequently increase vascular resistance. In hypoxic settings, pulmonary arterial smooth muscle contracts to create vasoconstriction. This mechanism normally promotes perfusion matching (ventilation), however, in chronic hypoxic lung disease, the increased pulmonary vascular resistance from hypoxic pulmonary vasoconstriction leads to the development of pulmonary hypertension (Evans et al., 2015).
Pulmonary hypertension can lead to further systemic consequences including increased pulmonary vascular resistance, which requires greater demands (pressure) in the right ventricle for blood to be ejected into the pulmonary circulation. This produces overload in the right ventricle and subsequent dilation and eventually, right-sided heart failure. Blood pooling in the right side of the heart can lead to obstruction in the vena cava and hepatoportal circulation, which can cause liver dysfunction. Moreover, increased blood pressure can lead to pulmonary and systemic oedema.
Data from animal models suggest that respiratory function is compromised in pulmonary hypertension due to diaphragmatic muscle fibre weakness and atrophy (de Man et al., 2011), which contributes to dyspnoea and fatigue during exercise. Certainly, people with idiopathic pulmonary arterial hypertension experience inspiratory and expiratory muscle limitations (Meyer et al., 2005), feasibly due to respiratory muscle overload (Naeije, 2005). There is also supporting evidence that this dysfunction extends out with the diaphragm and impacts the skeletal muscles (Panagiotou, Peacock and Johnson, 2015).
As previously noted, pulmonary hypertension impacts negatively affect the heart, lungs, vascular system, and respiratory muscles. This limits the exercise capacity in pulmonary arterial hypertensive individuals and depressingly impacts their quality of life (Halank et al., 2013). Intriguingly, the authors noted that the resting hemodynamic parameters were not found to be related to the quality of life in individuals with pulmonary arterial hypertension. The symptoms of pulmonary hypertension are largely nonspecific, including dyspnoea, lethargy, signs of cardiovascular dysfunction (e.g., syncope, angina, several heart murmurs), and elevated systemic blood pressure.
Effects of Exercise in People with Pulmonary Hypertension
Pulmonary arterial pressure generally climbs during high-intensity exercise in healthy fit individuals due to increased cardiac output. The pulmonary circulation is typically a low-resistance system, with the pulmonary arteries having the restricted capacity to dilate beyond that of rest (Frostell et al., 1993). The lung is characteristically fully perfused at rest, however, during exercise the stimulation of more blood vessels in less perfused areas aids in accommodating some of the increase in cardiac output to counterbalance the changes in pulmonary arterial pressure. As cardiac output rises during high-intensity exercise, there is only partial space to reduce pulmonary vascular resistance in comparison to the systemic circulation. Consequently, pulmonary arterial pressure rises during high-intensity exercise (D’Andrea et al., 2015). However, in some cases, the exercise-induced increase in pulmonary arterial pressure is pathological and is referred to as exercise pulmonary hypertension.
Regrettably, the classification of exercise pulmonary hypertension is problematic in comparison to resting pulmonary hypertension. This is because an increase in mean pulmonary arterial pressure during exercise transpires in all healthy people. Exercise pulmonary hypertension is characterised by a high pulmonary arterial pressure increased by symptoms of pulmonary hypertension (e.g., breathlessness, which are not present at rest). This state may happen in people with mild left heart disease or pulmonary vascular dysfunction that is not severe enough to produce these outcomes under resting conditions (Herve et al., 2015). Formerly, a mean pulmonary arterial pressure value of >30 mmHg during exercise was indicative for exercise pulmonary hypertension, however, it is conceivable for fit and healthy individuals to achieve this measure during high-intensity exercise. Contemporary evidence suggests that a mean pulmonary arterial pressure of >30 mmHg, when pooled with a total pulmonary resistance of >3 mmHg·min−1·L−1, has high sensitivity and specificity for discriminating between healthy people and those individuals with pulmonary vascular disease or right heart disease (Herve et al., 2015).
Since exercise can induce pulmonary hypertension before it manifests at rest, exercise assessment may be beneficial in the identification of early-stage pulmonary hypertension by reporting subclinical impairments in right ventricle contractility in people with conditions associated with pulmonary hypertension (Chia et al., 2016). For example, in systemic sclerosis, pulmonary vascular resistance may be raised and need to be increased right heart contractility at rest, which leads to permanent failure to the right side of the heart. However, people may be symptomless at rest in the initial stages of the disease, but the observation of right ventricular impairment at rest can be helpful in validating pulmonary vascular dysfunction before it leads to irreversible right heart failure. Equally, pulmonary arterial hypertension is commonly detected late in the disease process (Humbert et al., 2006), and therefore it is possible that exercise testing may be useful in detecting it earlier.
Exercise assessment may be used to establish the severity of pulmonary arterial hypertension and offers valuable evidence regarding prognosis. Laboratory testing specifies that V.O2 peak of fewer than 10.4 ml· kg−1·min−1 is related to poorer prognosis, as is the inability to surpass a systolic blood pressure of >120 mmHg during peak exercise. Physiological field tests that assess functional aerobic capacity are also beneficial in assessing pulmonary hypertension, and the 6-minute walk test is frequently applied for this purpose. However, the interpretation of walk test scores must consider several confounding aspects that may impact test results, (i.e., age and musculoskeletal function). Consequently, wide-ranging recommendations, rather than individual targets, are suitable in understanding the functional capacity of individuals with pulmonary arterial hypertension. A V.O2peak of >15 ml·kg−1·min−1 and a 6-minute walk test result of >500 metres are considered aspects that contribute to a “stable and satisfactory” prognosis. In younger and healthier people, a test result of >500-metres walking distance may be attained even by those individuals with severe pulmonary arterial hypertension, which makes this assessment less meaningful in this populace.
Several measurements attained during exercise have been suggested to be a superior predictor of long-term survival compared to resting pulmonary hemodynamics (Hasler et al., 2016). During exercise, a low V.O2peak, high pulmonary vascular resistance, and a trivial alteration in heart rate relative to rest are all linked with poorer prognosis in people with pulmonary arterial hypertension (Wensel et al., 2013). Furthermore, cardiac index (cardiac output divided by body surface area) during exercise, but not rest, is connected to aerobic function in pulmonary arterial hypertension and is one of the significant predictors of survival in pulmonary arterial hypertension (Hasler et al., 2016). Equally, the association between mean pulmonary arterial hypertension and cardiac output during exercise is linked to transplant-free survival of pulmonary hypertension (Hasler et al., 2016). Pulse oximetry values that decrease more than 10% below resting values are also associated with a poorer prognosis.
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Exercise Recommendations for People with Pulmonary Hypertension
As discussed earlier pulmonary arterial hypertension is a prolonged disorder with no known cure. However, contemporary treatments to lessen symptoms and slow the progress of the disease may be quite effective. The exercise was formerly assumed to be harmful to individuals with pulmonary hypertension, as it was alleged that exercise increased stress on the cardiopulmonary system that could hasten heart failure. However, a substantial body of academic evidence reveals that exercise has a positive role to play in improving symptoms, exercise capacity, and activities of daily living in individuals with pulmonary arterial hypertension and other types of pulmonary hypertension (Arena et al., 2015; Babu et al., 2016; Galie et al., 2009; Grünig et al., 2012; Mereles et al., 2006)
A recent meta-analysis by Yuan et al., (2015) examined the effects of subjects with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension reported that exercise training increased the 6-minute walk distance and V.O2peak within three weeks of the start of the program and was maintained in studies of 12- to 15-week duration (Yuan et al., 2015). Additionally, the authors reported improved quality of life and physical functioning following 15 weeks of exercise. The exercise procedures comprised a combination of aerobic activity (i.e., treadmill walking, stationary cycling, or both) and resistance training.
The specifics of individual exercise training protocols differ, however, many share comparable fundamental constructs. A frequently followed model of exercise programming in pulmonary hypertension studies involves three weeks of in-hospital training followed by a 12-weeks homebased session. The preliminary three weeks allows individuals to become accustomed with the correct exercise procedures, learn how to assess exercise intensity, and develop confidence in their capability to perform the exercise independently. These initial three weeks may also integrate educational components concerning the adherence towards the program and the anticipated health benefits. It has been suggested that the collection of baseline and post training outcome data related to physical fitness (i.e., the 6-minute walk test) and quality of life may assist in educating the individual regarding the value of exercise.
The components of the exercise training protocols share several similarities. For example, Mereles and associates (2006) performed a study that investigated the effects of exercise and respiratory training in severe pulmonary hypertension subjects. The exercise procedures included interval training on a cycle ergometer, interchanging between 30 seconds of lower-intensity and 60 seconds of higher-intensity exercise for 10-to-25 minutes per day in an in-patient environment. In this specific protocol, the higher-intensity training was 60-to-80% of subjects heart rate achieved during preliminary maximal exercise testing. Limitations for exercise intensity were centred on the subject’s subjective physical exertion, a peak heart rate not more than 120 beats/min, and pulse oximetry values greater than 85%. Moreover, subjects walked 60 minutes per day, performed 30-minutes of light resistance training, and performed 30-minutes of specific respiratory muscle training five days per week. Upon discharge, subjects were requested to continue a comparable protocol, although the duration and frequency was decreased.
Subsequent exercise protocols for pulmonary hypertension have applied both interval and continuous training and varied the training methodology with regards to the aerobic exercise component. For example, several studies (Chang et al., 2012); Weinstein et al., 2013) had subjects walk for 30-to-45 minutes at 70-to-80% of their heart rate reserve, two-to- three sessions per week, while Grünig and colleagues (Grünig et al., 2012) incorporated cycle ergometer interval training and walking like Mereles et al., (2006) protocol. Fox and colleagues (2011) prescribed interval training for the initial six weeks of subject’s rehabilitation, followed by continuous aerobic exercise in the subsequent six weeks of rehabilitation, including stair climbing in both components of the program. Fox et al., (2011) method may be beneficial for individuals who may not be able to engage initially in extended periods of continuous physical activity. Furthermore, skeletal muscle dysfunction may be correlated with pulmonary arterial hypertension, and it has been suggested that the inclusion of resistance training protocols is warranted (Yuan et al., 2015).
Studies have also suggested that specific respiratory muscle training may yield specific benefit to clients with pulmonary hypertension and has been integrated within several training studies (Yuan et al., 2015). For example, Kabitz and associates (2013) reported increased respiratory muscle strength and exercise capacity following 15-weeks of exercise and respiratory training in subjects with pulmonary arterial hypertension. Similarly, Saglam and colleagues (2015) reported that six weeks of inspiratory muscle training improved subjects’ pulmonary parameters including their 6-minute walk distance, fatigue severity, and dyspnoeic symptoms.
Generally speaking, it is suggested within the academic literature that clients with pulmonary hypertension should be physically active within the tolerance of their symptoms (Galie et al., 2009) and perform a combination of continued light-to-moderate-intensity sessions (Arena et al., 2011), respiratory muscle training, and resistance exercise. These exercise protocols primary aim is to improve physical function and individuals’ quality of life. It is also recommended that these clients undergo medically supervised assessments to establish their symptom thresholds for exercise intensity and duration prior to starting an exercise program. High-intensity aerobic or resistance training that aggravates the client’s symptoms or could cause the Valsalva manoeuvre should be avoided (Galie et al., 2016). Lastly, it should be noted that exercise programs may be specific to each type of pulmonary hypertension.