Essay: Exercise is Medicine – Chronic Obstructive Pulmonary Disease (COPD)

INTRODUCTION:
Exercise is Medicine (EIM) is a global health initiative directed by the American College of Sport Medicine (ACSM) that promotes the incorporation of physical activity by qualified health care professionals into treatment programmes for patients (Exercise is Medicine, 2019). It is widely acknowledged that physical exercise is crucially important for one’s optimal health and EIM aims to endorse exercise as a prevention and treatment of a plethora of medical conditions and to integrate exercise as part of general health care. I will discuss the crucial role that physical activity has to play in prevention and treatment of chronic obstructive pulmonary disease (COPD), a diverse group of clinical syndromes that share the common feature of limitation of expiratory airflow (Devine, 2008).
CHRONIC OBSTRUCTIVE COMPULSIVE DISORDER:
Chronic obstructive pulmonary disease (COPD) is a long term progressive respiratory disease characterized by inflammation and severe limitation of airflow in and out of the lungs. COPD is a nonspecific umbrella term that encompasses a variety of pulmonary diseases, the main three being chronic bronchitis, emphysema and asthma I COPD (Mannino, 2002). It is characterized by airflow limitation due to the gradual loss of effective breathing. At first no symptoms or mild symptoms are present however as the disease progresses, shortness of breath, wheezing, chest tightness, ongoing (chronic) cough often with a lot of mucous occurs. As it worsens, breathing requires much more energy and it can get harder to complete simple activities or to exercise, this may lead to fatigue, weight loss and muscle loss. Exacerbations and comorbidities contribute to the overall severity of the disease to individual patients. Patients present with common problems like dyspnoea(laboured breathing), chronic cough and sputum production. Some less common symptoms include wheezing and chest tightness. Risk factors include smoking, air pollution, low birth weight, recurrent infections and low economic status.
Chronic Bronchitis is defined as an inflammatory change leading to muscularly dysfunction and increased goblet cell secretion and numbers. This damage inside the airways causes the lining to swell thicken. The combination of bronchoconstriction and mucus hyper secretion causes a persistent cough to develop in bronchitis as the body tries to expel this excessive mucus. The airway constriction and mucus leads to wheezing typically heard during expiration. When airway obstruction is occurring, alveolar hypoxia may also be occurring because oxygen is not getting through to the alveoli efficiently. Some symptoms include
an ongoing cough, shortness of breath and frequent respiratory infections.
Emphysema is a disease that destroys some alveolar walls and increases airspaces inside the lungs that provide less surface area for oxygen absorption from the atmosphere (Mannino, 2002). Airways and air sacs lose their flexibility making it harder for them to expand and contract. Symptoms include wheezing shortness of breath and chest tightness.
Asthma is the least common respiratory disease present in COPD relative to chronic bronchitis and emphysema. It is a chronic inflammatory disorder of the airway in which many cells and cellular elements play a role. Recurrent episode of wheezing, breathlessness and coughing are some signs and symptoms.
The American Thoracic Society (ATS) COPD guidelines composed definitions for asthma, chronic bronchitis, emphysema, COPD and airflow obstruction and classified eleven separate disorders, as seen in the figure below. These guideline also recognised COPD as a respiratory disease where irreversible airflow interference is the underlying aspect, allowing COPD to be more clearly identified. Below is a non-proportional Venn diagram clearly distinguishing the eleven separate disorders in patients and the ways in which they overlap.
(Gibson and Simpson, 2009)
CAUSE:
Normal lungs function by pulmonary ventilation where inhalation occurs that causes each air sac to fill with air, and exhalation causing them to deflate. External respiration then takes place where oxygen from the lungs is exchanged with carbon dioxide from the blood vessels surrounding the alveoli. The transport of respiratory gases proceeds this followed by internal respiration which involves the movement of oxygen from the blood vessels to the tissues and the movement of carbon dioxide from the tissues to the blood. When inhalation occurs, air from the atmosphere passes through the primary bronchus(trachea) followed by secondary bronchi, segmented bronchi, bronchioles and alveoli, the last point of division connected to blood vessels. The alveolar sac contains many alveoli and is connected to the terminal bronchiole by alveolar ducts. Normally during inspiration air moves freely through these sections of the respiratory system. Small capillaries surround the alveoli where gaseous exchange occurs. Normally the airways and alveoli are flexible and springy and during inhalation each air sac inflates and during exhalation they deflate.
In COPD patients, the airways become narrow and inflamed and produce excessive mucus that may clog the airways, making it difficult to breathe. The walls of air sacs in the lungs are damaged, losing their elastic quality and the air sacs lose their shape. As airspaces get larger, air becomes trapped leading to fewer air sacs to supply oxygen to the blood (Willsie, 2009).
It becomes harder for these air sacs to deflate like normal lungs as trapped air makes it increasingly difficult to get fresh air into the lungs, making breathing more challenging.
Causes include smoking, long term exposure to second-hand smoke, air pollution, dust or workplace fumes and biomass exposure. In developed countries COPD is caused mainly by cigarette smoking where over 25% of smokers develop COPD in their lifetime (Mannino, 2002). On the other hand in In developing countries, the leading cause is exposure to biomass fuel. An uncommon genetic disorder called alpha 1-antitrypsin deficiency is also sometimes associated with COPD. Respiratory infections such as influenza and Pneumonia can worsen symptoms therefore it becomes more important to obtain these vaccinations.
DIAGNOSIS:
Typically people with COPD possess all of the symptoms stated above and spirometry is the most effective way to determine airway obstruction caused by this disease. Patients inspire maximally before forcefully expiring; the total exhaled volume of air in one second (forced expiratory volume in one second, FEV1) and the total exhaled volume (forced expiratory vital capacity, FVC) are measured. (Yu et al., 2013). In 90% of COPDsufferers, two successive tests at short time increments display similar FEV1 values, differing from less than 225 mL between them (Salvi and Barnes, 2009).
In Ireland there are approximately 110,000 people who have been diagnosed with COPD, however it is estimated that there are around 2 00,000 undiagnosed sufferers of this disease as many believe their symptoms are mainly as a result of “smokers cough” and fail to seek professional help. It is one of the most prevalent respiratory diseases nationally and in most cases sufferers are people over the age of 35 (HSE.ie, 2019). One in five Irish adults smoke daily this is roughly equal to 714,000 people with the highest prevalence being in men aged between. 25 and 34 years old. (HSE.ie, 2019). COPD is the fourth leading cause of death in the United States, succeeding heart disease, cancer and cerebrovascular disease. Death rates from this disease doubled within 32 years from 1970 to 2002 and the amount of people who are affected and die from this disease are on the rise. COPD patient death rates from exacerbations in the US are approaching 60% at one year for those over the age of 65 (Devine, 2008). Multitudes of patients endure COPD for many years, eventually passing away prematurely as a result of its complications.
EXERCISE AS MEDICINE:
The nature of exercise training an individual patient needs is based on their own physiological condition. Exercise is very important for healthy people and for COPD patients as it’s a critical element of the pulmonary rehabilitation programme and exercising regularly improves quality of life and general health. The PR programme trains one to breathe more effectively , start at what capable of
At present, pulmonary rehabilitation (PR) is recommended by the present Global Obstructive Lung Disease document (GOLD) to help improve dyspnoea, functional capacity, and quality of life of COPD sufferers (Garvey et al., 2016). Medical professionals in this field who are establishing current guidelines for different exercises included in the PR programme may struggle with the variable degrees of severity amongst patients and the diversity of their symptoms also. As a result of this, pulmonary rehabilitation programmes vary worldwide and a PR programme should be developed to accommodate each individual patient. Below are tables based on three different exercise proposals and how they are carried out clinically from four principal qualifies associations ; 1) The American College of Sports Medicine (ACSM), The American Thoracic Society (ATS), The European Respiratory Society (ERS) and The American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR).
Instruction from the ACSM involve respiratory function tests and recordings to be carried out on COPD sufferers prior to initiation of PR programme such as the fraction of oxygen saturated haemoglobin in the arteries relative to the total haemoglobin by arterial blood gas tests and tracking dyspnea usuing the Borg CR10 Scale that measures physical activity intensity levels (Borg, 1982).
In some cases where patients have lost a lot of lung function due to severe COPD modified exercises are established to cater for individual patients with varying levels of lung function.
Aeroblic Exercise
Skeletal muscle dysfunction is influenced by skeletal muscle strength and endurance function and structure (fiber size, fiber type distribution, capillary density, and metabolic capacity) (Zeng et al., 2018). A prolonged lack of exercise promotes a decrease in physical activity in COPD sufferers. The activity of these muscles rely greatly on the physiologic structural elements of the particular muscle and the velocity at which a fiber contracts inversely regulates the fibers ability t resist fatigue.
Type I fibers are slow-twitch fibers and can endure long periods of exercise as they are highly resistant to fatigue. They are comprised of myosin heavy-chain (MyHC) type I. Type IIx fibers are fast-twitch fibers and are a subset or the fast twitch muscles which contain type IIa and type IIb. Type IIx fibers are the strongest and lowest endurance abibity as they fatigue much easier. Their composition differs from Type I fibers as they are composed of MyHC type IIx. It has been reported that a less than 27% of fiber type I proportionality is regarded as unusually low. Additionally, an amount of fiber type IIX that is greater than 29% is regarded as unusually large (Barreiro and Gea, 2016). In cases where the subject suffers from COPD, the amount of type I fibers are significantly lower than that of a healthy individual. Also a greater amount of type IIb fibers are present, thus demonstrating why COPD sufferers possess greater muscular fatigability and a lack of endurability (Whittom et al., 1998).
Muscle dysfunction and wastage are major systemic manifestations in COPD. Patients’ respiratory and limb muscles are often impaired and this adds to defective muscle function, low exercise ability and poorer health in general. Diminishing muscle fiber cross-sectional area is largely an accepted distinguisher of muscle atrophy and may be an indication of mortality associated with COPD (Gouzi et al., 2013).
Hyperinflation is another crucial aspect of COPD as hyperinflated lungs may lead to consequential destructive breathing issues. This is displayed by advancements in COPD symptoms following lung volume reduction surgery. Static and dynamic processes may both lead to hyperinflation in COPD, static being caused by a decline in elasticity as a result of emphysema. Dynamic hyperinflation is as a result of exercise and is found present more frequently and is caused by air becoming trapped in the lungs as a result of an imbalance in the volumes of air inhaled and exhaled (Ferguson, 2006). Inadequate exhalation generates continuous air retention referred to as ‘air trapping’, consequently leading to dyspnea (O’Donnell and Laveneziana, 2006).
TREATMENT & CURE:
There is currently no cure for COPD however patients affected by this disease can take steps to slow down its progression. The main one being smoking cessation. Lung function stabilizes after smoking cessation and will decline at a much slower rate. If one is a successive smoker, lung function declines more rapidly. The earlier the detection and diagnosis of the disease, the earlier treatment can commence and suitable treatment varies from patient to patient as it has to consider the severity of their symptoms. Bronchodilators and anti-inflammatory medication help improve the performance of the lungs and reduce the likelihood of developing exasperations. In more sever cases surgical procedures may be the best option to help increase patients’ quality of life. Pulmonary rehabilitation is the main factor that play enormous role in slowing down the disease progression, this involves lifestyle changes such as smoking cessation, improved nutrition and exercise. Physical exercise also lowers dyspnea and increases the time one takes to exhail, therefore decreasing dynamic hyperinflation.(Bhatia and Fromer, 2011)
CONCLUSION/DISCUSSION:
Research / future
Although no cure is readily available, many crucial steps can be taken to feel better, stay more active and slow disease progression. The two major lifestyle changes that contribute largely to slowing down the disease progression are smoking cessation and increase physical activity. Without a doubt physical exercise plays a crucial role in ones wellbeing and the prevention and treatment of various diseases, it seems astonishing that there still is an absence of more informative guidelines for this within the medical environment. It is important that appropriate pulmonary rehabilitation programmes are put in place and are tailored to cater for individualism to improve their quality of life.
Bhatia, R. and Fromer, L. (2011). Diagnosing and treating COPD: understanding the challenges and finding solutions. International Journal of General Medicine, p.729.
Barreiro, E. and Gea, J. (2016). Molecular and biological pathways of skeletal muscle dysfunction in chronic obstructive pulmonary disease. Chronic Respiratory Disease, 13(3), pp.297-311.
BORG, G. (1982). Psychophysical bases of perceived exertion. Medicine & Science in Sports & Exercise, 14(5), pp.377???381.
Devine, J. (2008). Chronic Obstructive Pulmonary Disease: An Overview. American Health Drug Benefits., 1(7), pp.34-42.
Exercise is Medicine. (2019). [online] Available at: https://www.exerciseismedicine.org [Accessed 18 Feb. 2019].
Ferguson, G. (2006). Why Does the Lung Hyperinflate?. Proceedings of the American Thoracic Society, 3(2), pp.176-179.
Garvey, C., Bayles, M., Hamm, L., Hill, K., Holland, A., Limberg, T. and Spruit, M. (2016). Pulmonary Rehabilitation Exercise Prescription in Chronic Obstructive Pulmonary Disease. Journal of Cardiopulmonary Rehabilitation and Prevention, 36(2), pp.75-83.
Gibson, P. and Simpson, J. (2009). The overlap syndrome of asthma and COPD: what are its features and how important is it?. Thorax, 64(8), pp.728-735.
Gouzi, F., Maury, J., Molinari, N., Pomiès, P., Mercier, J., Préfaut, C. and Hayot, M. (2013). Reference values for vastus lateralis fiber size and type in healthy subjects over 40 years old: a systematic review and metaanalysis. Journal of Applied Physiology, 115(3), pp.346-354.
HSE.ie. (2019). Ireland’s Health Services – HSE.ie. [online] Available at: https://www.hse.ie/eng/ [Accessed 18 Feb. 2019].
Mannino, D. (2002). COPD: Epidemiology, Prevalence, Morbidity and Mortality, and Disease Heterogeneity. Chest, 121(5), pp.121S-126S.
O’Donnell, D. and Laveneziana, P. (2006). Physiology and consequences of lung hyperinflation in COPD. European Respiratory Review, 15(100), pp.61-67.
Salvi, S. and Barnes, P. (2009). Chronic obstructive pulmonary disease in non-smokers. The Lancet, 374(9691), pp.733-743.
WHITTOM, F., JOBIN, J., SIMARD, P., LEBLANC, P., SIMARD, C., BERNARD, S., BELLEAU, R. and MALTAIS, F. (1998). Histochemical and morphological characteristics of the vastus lateralis muscle in patients with chronic obstructive pulmonary disease. Medicine & Science in Sports & Exercise, 30(10), pp.1467-1474.
Willsie, S. (2009). Severe exacerbations predict excess lung function decline in asthma. Yearbook of Pulmonary Disease, 2009, pp.3-4.
Yu, W., Fu, Tai, Yeung, Kwong, Chang, Tam and Yiu (2013). Spirometry is underused in the diagnosis and monitoring of patients with chronic obstructive pulmonary disease (COPD). International Journal of Chronic Obstructive Pulmonary Disease, p.389.
Zeng, Y., Jiang, F., Chen, Y., Chen, P. and Cai, S. (2018). Exercise assessments and trainings of pulmonary rehabilitation in COPD: a literature review. International Journal of Chronic Obstructive Pulmonary Disease, Volume 13, pp.2013-2023.