|Helping the Chronically Short of Breath
Jenevieve Roper & Len Kravitz, Ph.D.
What is COPD?
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the U.S. Approximately 13 million people are diagnosed with this incurable disease and another estimated 12 million people may have it and do not know (American Lung Association, 2013). The progressive obstruction of the airflow makes breathing difficult. The two major forms of COPD are chronic bronchitis and emphysema. Chronic bronchitis is a long-term inflammation (swelling) of the bronchi (air passageways), which causes a buildup up mucus (or phlegm) from the bronchial tubes. Sufferers develop a nagging cough with regular throat clearing of mucus secretion. Contrariwise, emphysema is the long-term destruction of the alveoli (air sacs) of the lungs, causing progressive shortness of breath from an inefficient gas exchange of oxygen and carbon dioxide. Smoking is the primary risk factor for COPD; however, those exposed to certain gases or fumes and large amounts of pollution or second hand smoke are also at risk for COPD.
For the most part, COPD is preventable, however, approximately 100,000 Americans have alpha1 antitripsin deficiency-related (AAT) emphysema, which is an autoimmune disease characterized by a deficiency of the liver protein AAT (a protein that promotes healing of lung tissue as cells age and/or are damaged) (American Lung Association, 2013). This type of emphysema is inherited and cannot be prevented. A blood screening is needed to determine if a person is deficient in AAT.
Individuals with COPD have difficulties exercising as lack of airflow causes shortness of breath. However progressive exercise should be encouraged, as there are many health benefits for COPD clients.
Pathophysiology of COPD
Excessive secretions of mucus and airway inflammation are two prominent symptoms of COPD (Rodriguez-Roisin, 2005). A thick bronchial tube lining will decrease the diameter of the bronchial airway and increase the resistance to the airflow, causing difficult breathing. Inflammation of this lining will further decrease the diameter of the airway, thus impairing the amount of air transported. McDounough et al. (2011) determined that the number of small airways and terminal bronchioles (smallest passageways in bronchial tubes) decrease as COPD progresses.
Emphysema is the long-term damage/destruction of the alveoli. Alveoli are the site of gas exchange, where oxygen is transferred to the blood from the lungs and carbon dioxide is transferred to the lungs from the blood for release. As emphysema progresses, more and more alveoli are wiped out, limiting the amount of gas exchange that occurs. This makes the extraction of oxygen from the lungs more difficult; an individual who suffers with it will continuously feel short of breath. The cause of the destruction of the alveoli is currently under investigation. Some research suggests that changes in elastin (a protein the provides elasticity in alveoli) may cause the alveoli to lose their physiological function (Lang et al., 1994). Other evidence identifies fibrosis (thickening and scarring) of the alveoli as the cause of emphysema (Lang et al., 1994). This fibrosis of the alveolar walls may be a consequence for inhaling smoke, gases and fumes. The fibrosis eventually leads to the destruction of the alveoli.
Exercise and COPD
Exercise has been shown to have several beneficial effects in individuals with COPD. A recent study determined that cardiovascular exercise increased PGC-1_ in individuals with COPD, and this increase was greater in subjects who exercised above their lactate threshold compared to those who exercised below their lactate threshold (Puente-Maestu et al, 2011). PGC-1_ is a cellular protein that has been shown to increase mitochondrial (energy powerhouse of cell) number and function, leading to improved exercise endurance. This explains why individuals with COPD who engage in regular endurance exercise are able to improve their functional endurance capacity in addition to their quality of life (Probst et al., 2011).
Additionally, aerobic exercise has been shown to improve the plasma metabolic profile in individuals with COPD. Rodriguez et al. (2012) recently determined that COPD patients had markedly lower levels of certain amino acids circulating prior to exercise, indicating that there may be some systemic side effects to the disease, including abnormal muscle bioenergetics (i.e., an increase of anaerobic metabolism and a decrease oxidative metabolism versus a decrease of anaerobic metabolism and increase of oxidative metabolism seen in healthy subjects). The authors indicated that exercise induces favorable changes in the function of these energy systems that will benefit most COPD patients.
The American Lung Association suggests that exercise programs should include stretching, aerobic exercise, and strengthening/resistance exercise as these will help strengthen respiratory muscles, improve circulation, and improve COPD symptoms. Stretching the upper body will help maintain/improve the elasticity of the respiratory muscles. Aerobic exercise (all modes) will help improve blood circulation (and oxygen circulation), lower blood pressure, and strengthen the heart and cardiovascular system. Total body strengthening/resistance training is encouraged from a health perspective of engaging and improving the musculoskeletal system to successfully handle the load challenges of daily living. Since symptoms vary considerably in COPD individuals, exercise professionals are encouraged to guide their exercise program design by individualizing established guidelines as proposed by the American College of Sports Medicine (150 minutes of moderate-intensity exercise per week; train each major muscle group two or three days each week using a variety of exercises; do flexibility exercises at least two or three days each week to improve range of motion) (ACSM, 2011).
Personal trainers should focus on increasing the duration and intensity of exercise gradually as shortness of breath will initially impede the exercise workout for the COPD client.
Also, even though the benefits of higher intensity aerobic exercise have been shown with some COPD individuals, high intensity exercise may cause oxidative stress (i.e. release of free radicals) in some blood vessels. This oxidative stress may in turn cause more damage to the already inefficient airways in the lungs. Therefore, exercise program design incorporating high intensity interval training should be completed with care and caution depending on the individual's health status.
Side Bar I. Facts About COPD
1. Female smokers are about 13 times more likely to die from COPD as women who have never smoked and male smokers are around 12 times as likely to die from COPD.
2. Women exceed men in the number of deaths attributable to COPD. In 2007, almost 64,000 females died compared to almost 60,000 males.
3. Smoking causes 85 to 90 percent of COPD deaths.
4. COPD limits a person's ability to work, exercise, do household chores, engage in social activities, sleep and participate in family activities.
5. Chronic bronchitis, which affects people of all ages (although highest in &Mac179; 65 yr) is clinically defined by the presence of a mucus-producing cough most days of the month, for at least three months of a year over a two-year period (without other underlying disease defining the condition).
6. Emphysema, which takes years to develop from smoking, leads to incurable damage or destruction of the alveoli in the lungs lose; thus dramatically reducing the ability of the lungs transfer oxygen to the blood.
7. Emphysema and chronic bronchitis often co-exist in persons with COPD.
8. Bronchodilator medications help to relax and open air passages in the lungs. Inhaled or oral steroids are used to decrease inflammation in the airways for some COPD clients. Other medications can lesson the symptoms (and frequency) and improve the ability of the client to exercise.
Source: American Lung Association, 2013
ACSM (2011), ACSM Issues New Recommendations on Quantity and Quality of Exercise
Accessed April 2, 2013
American Lung Association, Chronic Obstructive Pulmonary Disease (COPD) Fact Sheet (2013)
Accessed: April 1, 2013
Rodr&Mac245;guez, D.A., Alcarraz-Vizan, G., Diaz-Moralli, S. et al. (2012). Plasma metabolic profile in COPD patients: effects of exercise and endurance training, Metabolomics, 8, 508-516.
Lang, M.R., Fiaux, G.W., Gillooly, M. et al. (1994). Collagen content of alveolar wall tissue in emphysematous and non-emphysematous lungs. Thorax, 49:319-326.
McDonough, J.E., Yuan, R., Suzuki, M. et al. (2011). Small-airway obstruction and emphysema in chronic obstructive pulmonary disease. New England Journal of Medicine, 365(17), 1564-1675.
Probst, V.S. PhD, Kovelis, D. Hernandes, N.A. et al. (2011). Effects of 2 exercise training programs on physical activity in daily life in patients with COPD. Respiratory Care, 56(11), 1799-1807.
Puente-Maestu, L., Lazaro, A., Tejedor, A. et al. (2011). Effects of exercise on mitochondrial DNA content in skeletal muscle of patients with COPD. Thorax, 66:121-127.
Rodr&Mac245;guez-Roisin, R. (2005). The airway pathophysiology of COPD: Implications for treatment. Journal of Chronic Obstructive Pulmonary Disease, 2; 253-262.
Jenevieve Roper, M.S. is a doctoral student in Exercise Science at the University of New Mexico. Her research interests include running mechanics and injury prevention. She is a recreational sand volleyball player, runner, and fitness enthusiast.
@bio:Len Kravitz, PhD, is the program coordinator of exercise science and a researcher at the University of New Mexico, Albuquerque, where he won the Outstanding Teacher of the Year award. He has received the prestigious Can-Fit-Pro Lifetime Achievement Award and American Council on Exercise Fitness Educator of the Year.