Review Article

Understanding Changes in the Respiratory System with Ageing

조한얼 1 , *
Han Eol Cho 1 , *
Author Information & Copyright
1연세대학교 의과대학 재활의학교실, 연세대학교 신경근질환 재활연구소
1Department of Rehabilitation Medicine, Gangnam Severance Hospital and Rehabilitation Institute of Neuromuscular Disease, Yonsei University College of Medicine, Seoul 06273, Korea
*교신저자 : 조한얼, 06273 서울특별시 강남구 언주로 211 강남세브란스병원 재활의학과 Tel: 82-2-2019-3500, Fax: 82-2-2019-4881, Email:

© Copyright 2024 The Korean Space Science Society. This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: Nov 08, 2023; Accepted: Nov 24, 2023

Published Online: Dec 31, 2023


Aging leads to functional decline across multiple organ systems due to physiological, anatomical, and immunological changes. The respiratory system also undergoes various changes due to aging. In this comprehensive review, we focus on the aging respiratory system, categorizing the changes into pulmonary function, structural anatomy, gas exchange, defense mechanisms, immune system alterations, and exercise capacity. Aging significantly affects pulmonary function. Lung development peaks around age 25 for males and age 20 for females, with notable deterioration starting around age 35. Multiple factors can expedite this decline, including smoking, air pollution, and pre-existing respiratory conditions. Changes in lung capacity, elasticity, and ventilation become evident, with a gradual decrease in vital capacity and forced expiratory volume in one second. Respiratory muscle strength diminishes, and gas exchange efficiency declines, especially after age 40. Structural and anatomical changes include decreased chest wall compliance, leading to barrel chest, and weakened respiratory muscles. The static elastic recoil of the lung decreases, resulting in senile emphysema. Immunological changes involve altered bronchoalveolar lavage fluid composition, reflecting activated T-cells in the lower respiratory tract. Sustained low-grade inflammation in the lower respiratory tract may lead to lung parenchymal damage, impairing gas exchange. Exercise capacity decreases with age, albeit with variations based on health and physical activity levels. Understanding these alterations in the aging respiratory system is vital for effective management, especially in an aging global population.

Keywords: Ageing; Immunology; Physiology; Pulmonary function; Respiratory system


Aging leads to functional decline in various organs and systems of the body through a multitude of physiological, anatomical, and immunological changes. The aging process affects the respiratory system, just like it does with other parts of the body. However, while many physicians are familiar with common pulmonary diseases that often occur in elderly patients, there is a lack of awareness regarding the normal physiological changes that occur in patients as a part of aging. The differentiation between the effects of natural aging-related physiological changes and damage caused by external factors, such as chronic exposure to pollutants, recurrent lung infections, smoking, lifestyle habits, occupational environments, and socioeconomic factors, is particularly challenging within the respiratory system, compared to other organ systems.

In this review, we aim to investigate the changes in the aging respiratory system. We will categorize these changes into alterations in pulmonary function, structural anatomical changes, modifications in gas exchange, defense mechanisms, immune system changes, and alterations in exercise capacity. By gaining a precise understanding of how aging affects the respiratory system, we can enhance our comprehension of how to manage and prevent deterioration in respiratory function among elderly patients. This understanding will aid in the development of treatment strategies customized for elderly patients.

Main Text

1) Alteration in pulmonary function

Pulmonary function changes with age. Lung growth and maturation occur over approximately the first 20 years of life, reaching their peak around the age of 25 for males and around 20 for females [1]. After the age of 35, a significant deterioration in pulmonary function becomes increasingly evident (Fig. 1). Factors like smoking, exposure to air pollution, and the presence of respiratory diseases can expedite this rapid decline in pulmonary function [2-4]. Upon closer inspection of age-related changes in pulmonary function, forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) gradually decrease, while residual volume (RV) and functional residual capacity (FRC) increase. Total lung capacity (TLC) remains relatively constant throughout one's lifetime.

Fig. 1. Changes in pulmonary function with age.
Download Original Figure

As individuals age, FVC decreases due to increased stiffness of the chest wall, loss of elasticity in lung tissue, and weakening of respiratory muscles. There is an average reduction of about 20-25 ml in FVC after the age of 40 [5,6]. FEV1 also decreases, with the rate of decline accelerating with aging. It is reported that the annual decrease in FEV1 is approximately 20-35 ml between the ages of 25-40. When individuals reach the age of 70 or older, the annual decrease is around 40-60 ml [6-10]. Nevertheless, due to substantial individual variability in FEV1, it is difficult to accurately estimate the decline rate because various regression equations are suggested.

It is important to note that the FEV1/FVC ratio decreases with age in both males and females [11] which is why using the FEV1/FVC ratio (<0.7) to define bronchial obstruction may lead to an overdiagnosis of COPD in the elderly [12,13]. There has been a discussion about using a lower limit of normal value, based on the lower 5% of the population, as the diagnostic criterion for COPD to complement this issue. However, the choice of the regression equation for FEV1 greatly influences the lower limit of normal value. Moreover, there is a lack of longitudinal studies using this approach. In light of these considerations, the GOLD guidelines recommend the use of a fixed ratio instead of the lower limit of normal value [1]. This recommendation is based on the understanding that a fixed ratio is not inferior to the lower limit of normal value when it comes to predicting prognosis [14]. Additionally, it is vital to recognize that irreversible airway obstruction is not exclusive to COPD, and clinical presentation and risk factors should be factored in when diagnosing COPD. The simplicity and consistency of diagnosis hold paramount importance in clinical practice. Peak flow rate (PFR) also decreases with age [15] is known that in older individuals, the decreased lung elastic recoil results in increased airway resistance, leading to a reduction in PFR. As for RV and FRC, they tend to increase with age. This is due to a decrease in the elastic recoil of the lungs, which leads to an increase in the size of alveoli. It is known that TLC, which is the sum of FVC and RV, remains relatively constant throughout one's lifetime [5,16].

2) Structural anatomical changes
(1) Reduced chest wall compliance

Chest wall compliance decreases with age. The chest wall comprises the ribs, surrounding muscles, and connective tissue. With aging, calcification and structural changes occur in the ribs and rib joints due to osteoarthritis, causing the chest wall to become rigid and leading to an increase in the anteroposterior diameter at the most expanded position [1]. This condition is known as "barrel chest." Additionally, overinflation of the lungs due to conditions like COPD also influences changes in the chest wall. Kyphosis also contributes to these structural changes. Conditions such as osteoporosis and vertebral fractures induce dorsal kyphosis, leading to a curvature of the thoracic spine that increases the anteroposterior diameter of the chest wall [17]. When chest wall compliance decreases, chest expansion during inhalation is restricted, leading to an increase in the work of breathing. The increased anteroposterior chest wall diameter induces alterations in diaphragmatic curvature and reduces the contractile strength of the diaphragm, ultimately affecting pulmonary function.

(2) Respiratory muscle dysfunction

The diaphragm is the most vital muscle in the respiratory process, particularly during the inhalation phase. The diaphragm's strength is reported to decline with advancing age. The contractile force of the diaphragm can be measured through transdiaphragmatic pressure (Pdi), which decreases by approximately 25% in older adults compared to young adults [17].

Maximum expiratory pressure (MEP) and maximum inspiratory pressure (MIP), which reflect respiratory muscle strength, also decrease with age [18-20]. MIP and MEP also decrease with age. MIP was reported to decrease annually by an average of 0.8 to 2.7 cmH2 O between the ages of 65 and 85 [17,21]. Respiratory muscle weakness can become more pronounced with age, especially in cases where there is an additional burden on the respiratory muscles due to conditions such as pneumonia or heart failure.

The maximum voluntary ventilation (MVV) also decreases, with a study reporting a 12% decrease in older athletes over a 6-year period [22]. The weakening of respiratory muscle strength with age is attributed to the atrophy of respiratory muscles linked to the aging process, particularly the selective reduction of fast-twitch fibers (Type IIb) [23]. These changes can potentially lead to conditions such as reduced ventilation, decreased exercise tolerance, impaired cough ability, and respiratory failure.

(3) Decrease in the static elastic recoil of the lung

As individuals age, there is a homogeneous degeneration of elastic fibers surrounding alveoli, resulting in excessive dilation of alveolar without the destruction of alveolar walls [24]. This results in an annual decrease in static elastic recoil pressure of 0.1-0.2 cmH2O [25]. Especially, Small airways with a diameter of less than 2 mm close prematurely, causing alveolar overdistention. Chest X-rays of elderly often show uniform hyperlucent lungs with flattened diaphragms, resembling emphysema-like findings. These changes are referred to as senile emphysema, which differs histologically from typical emphysema as it lacks alveolar wall destruction [26]. Understanding these changes can assist in making appropriate interpretations of chest X-rays in the elderly.

3) Changes in gas exchange

Aging reduces the diffusion capacity of the lungs. The diffusing capacity for carbon monoxide (DLCO) decreases annually by 0.2-0.32 ml/min/mmHg in men and 0.06-0.18 ml/min/mmHg in women. This decline becomes more prominent after the age of 40 [6]. The changes in gas exchange due to aging are known to be influenced by imbalances in the ventilation-perfusion ratio, a decrease in alveolar surface area [27], a decrease in pulmonary capillary density [28], and a decrease in blood flow within the pulmonary capillaries [29]. The decline in pulmonary diffusion capacity resulting from age-related alterations in gas exchange can lead to respiratory difficulties.

4) Defense mechanism impairments and immunological change

In the elderly, respiratory diseases tend to exhibit a higher frequency due to impairments in defense mechanisms. Responses to diseases are often diminished, resulting in more severe clinical courses and leaving behind numerous complications. The aging-related impairments in pulmonary defense mechanisms and immunological changes are manifested as follows.

(1) Decreased Airway Clearance Ability

Aging leads to a reduced ability to clear airway secretions, making it more challenging to effectively remove mucus and foreign particles (Fig. 2). As mentioned earlier, the weakening of respiratory muscles due to aging is directly related to a decrease in cough strength. Furthermore, changes in chest and lung compliance reduce the efficiency of coughing. Other contributing factors to the reduced ability to clear airway secretions with age include a decline in cough reflex [30] and impaired ciliary function in the airways [31]. This decline in airway clearance ability can lead to respiratory conditions such as pneumonia, bronchiectasis, and chronic obstructive pulmonary disease.

Fig. 2. Changes affecting poor airway clearance in elderly patients.
Download Original Figure
(2) Changes in Regulation of Breathing

Minute ventilation is calculated by multiplying tidal volume and respiratory rate. There is no difference in minute ventilation between the elderly and young adults, but the elderly tend to exhibit smaller tidal volumes and higher respiratory rates [32].

Aging significantly reduces responses of heart rate and ventilation to hypoxia (low oxygen levels) and hypercapnia (high carbon dioxide levels) in a resting state. One study reported a 50% reduction in the response to hypoxia and a 40% reduction in the response to hypercapnia in elderly patients compared to younger patients.

Aging is associated with a significant reduction in the heart rate and pulmonary ventilation responses to hypoxia and hypercapnia. One study reported a 50% reduction in the response to hypoxia and a 40% reduction in the response to hypercapnia in elderly patients compared to younger patients [33]. Reduced perception of respiratory abnormalities may be attributed to the diminished efferent neural output in response to hypoxia and hypercapnia [34].

Also, aging impairs the reactivity to increased airway resistance. Airway reactivity is studied using methacholine showed that elderly individuals require a lower dose of methacholine to induce bronchoconstriction [35]. Furthermore, the recovery after treatment with beta-2 agonists takes more time in the elderly [36], and ability to perceive bronchoconstriction are also impaired in the elderly [37]. These changes not only contribute to an increase in asthma-related mortality among the elderly but also reduce awareness of the onset of respiratory diseases such as pneumonia.

(3) Immunological changes

When examining bronchoalveolar lavage (BAL) fluid from healthy elderly individuals, researchers observed a decreased proportion of macrophages, increased levels of the immune globulins IgA and IgM, and an elevated CD4+/CD8+ lymphocyte ratio. These findings suggest the presence of activated T-cells in the lower respiratory tract mucosa due to repetitive antigen exposure [38]. Sustained low-grade inflammation in the lower respiratory tract can lead to proteolysis and oxidant-mediated injury in the lung parenchyma, resulting in a decrease in alveoli and impairment of gas exchange through the alveolar membrane.

5) Decrease in exercise capacity

As people age, exercise capacity generally declines, but the extent of this decline can vary depending on an individual's health and regular physical activity. Maximum oxygen consumption (VO2 max) is known to peak between the ages of 20 and 30 and then gradually decrease by about 1% per year [22]. The rate of this decline can vary based on an individual's level of physical activity, with more significant reductions observed in sedentary adults. Factors contributing to the decline in VO2 max due to aging may include decreased heart rate responsiveness, reduced maximal cardiac output, and a decrease in peripheral muscle mass.

In contrast to the resting state, older individuals are more sensitive to hypercapnia during exercise compared to young adults. A study involving 224 patients aged 56-85 observed that respiratory responses to a constant carbon dioxide production increased with age. [39] This was found to be unrelated to oxygen saturation or metabolic acidosis and is speculated to be due to an increase in dead space ventilation.


The content summarized in the preceding review has been organized in Table 1. These changes in the respiratory system can impair its function in elderly patients, rendering them more vulnerable to various respiratory disorders. This underscores the importance of exercising caution. The global increase in the elderly population is inevitable, and Korean society, in particular, is facing the challenges of becoming an ultra-aged society with a rapidly growing elderly population. Age-related respiratory system changes are a natural physiological process. Understanding and recognizing these changes is crucial not only for preventing and managing respiratory-related diseases in elderly patients but also for enhancing their health and quality of life.

Table 1. Summary of Age-Related Changes in the Respiratory System
Pulmonary function FEV1 Decreased
FVC Decreased
Total lung capacity Unchanged
Functional residual capacity Increased
Residual volume Increased
FEV1/FVC Decreased
Peak flow rate Decreased
Anatomical change Air space size Increased
Chest wall compliance Decreased
Total respiratory system compliance Decreased
Elastic recoil Decreased
Respiratory muscle strength Transdiaphragmatic pressure Decreased
Maximal inspiratory pressure Decreased
Maximal expiratory pressure Decreased
Maximal voluntary ventilation Decreased
Gas exchange Diffusing capacity for carbon monoxide Decreased
Defensive mechanism and regulation of breathing Cough ability Decreased
Cough reflex Decreased
Responses to hypoxia and hypercapnia Decreased
Reactivity to airway resistance Decreased
Minute ventilation Unchanged
Tidal volume Decreased
Respiratory rate Increased
Immunology (Bronchoalveolar lavage) Proportion of macrophages Decreased
CD4+/CD8+ ratio Increased
IgA and IgM Increased
Exercise capacity Maximum oxygen consumption Decreased
Dead space ventilation Increased
Responses to hypercapnia during exercise Increased

FEV1: forced expiratory volume in one second, FVC: forced vital capacity.

Download Excel Table



Sharma G, Goodwin J. Effect of aging on respiratory system physiology and immunology. Clin Interv Aging. 2006;1:253-60.


Lange P, Celli B, Agustí A, Boje Jensen G, Divo M, Faner R, et al. Lung-function trajectories leading to chronic obstructive pulmonary disease. N Engl J Med 2015;373:111-22.


Bui DS, Lodge CJ, Burgess JA, Lowe AJ, Perret J, Bui MQ, et al. Childhood predictors of lung function trajectories and future COPD risk: a prospective cohort study from the first to the sixth decade of life. Lancet Respir Med 2018;6:535-44.


Agusti A, Faner R. Lung function trajectories in health and disease. Lancet Respir Med 2019;7:358-64.


Knudson R. Physiology of the aging lung. The lung scientific foundations. New York: Raven; 1991. p. 1749-59.


Janssens JP, Pache JC, Nicod LP. Physiological changes in respiratory function associated with ageing. Eur Respir J 1999;13:197-205.


Burrows B, Lebowitz MD, Camilli AE, Knudson RJ. Longitudinal changes in forced expiratory volume in one second in adults. Methodologic considerations and findings in healthy nonsmokers. Am Rev Respir Dis 1986;133:974-80.


Morris JF, Koski A, Johnson LC. Spirometric standards for healthy nonsmoking adults. Am Rev Respir Dis 1971;103:57-67.


Kerstjens HA, Rijcken B, Schouten JP, Postma DS. Decline of FEV1 by age and smoking status: facts, figures, and fallacies. Thorax 1997;52:820-7.


Enright PL, Kronmal RA, Higgins M, Schenker M, Haponik EF. Spirometry reference values for women and men 65 to 85 years of age. Cardiovascular health study. Am Rev Respir Dis 1993;147:125-33.


Hankinson JL, Odencrantz JR, Fedan KB. Spirometric reference values from a sample of the general U.S. population. Am J Respir Crit Care Med 1999;159:179-87.


Güder G, Brenner S, Angermann CE, Ertl G, Held M, Sachs AP, et al. GOLD or lower limit of normal definition? A comparison with expert-based diagnosis of chronic obstructive pulmonary disease in a prospective cohort-study. Respir Res 2012;13:13.


van Dijk W, Tan W, Li P, Guo B, Li S, Benedetti A, et al. Clinical relevance of fixed ratio vs lower limit of normal of FEV1/FVC in COPD: patient-reported outcomes from the CanCOLD cohort. Ann Fam Med 2015;13:41-8.


Bhatt SP, Balte PP, Schwartz JE, Cassano PA, Couper D, Jacobs DR Jr, et al. Discriminative accuracy of FEV1:FVC thresholds for COPD-related hospitalization and mortality. Jama 2019;321:2438-47.


Nunn AJ, Gregg I. New regression equations for predicting peak expiratory flow in adults. Bmj 1989;298:1068-70.


Stocks J, Quanjer PH. Reference values for residual volume, functional residual capacity and total lung capacity. ATS Workshop on Lung Volume Measurements. Official Statement of the European Respiratory Society. Eur Respir J 1995;8:492-506.


Pierce JA, Ebert RV. The barrel deformity of the chest, the senile lung and obstructive pulmonary emphysema. Am J Med 1958;25:13-22.


Wilson SH, Cooke NT, Edwards RH, Spiro SG. Predicted normal values for maximal respiratory pressures in caucasian adults and children. Thorax 1984;39:535-8.


Black LF, Hyatt RE. Maximal respiratory pressures: normal values and relationship to age and sex. Am Rev Respir Dis 1969;99:696-702.


McElvaney G, Blackie S, Morrison NJ, Wilcox PG, Fairbarn MS, Pardy RL. Maximal static respiratory pressures in the normal elderly. Am Rev Respir Dis 1989;139:277-81.


Enright PL, Kronmal RA, Manolio TA, Schenker MB, Hyatt RE. Respiratory muscle strength in the elderly. Correlates and reference values. Cardiovascular Health Study Research Group. Am J Respir Crit Care Med 1994;149:430-8.


McClaran SR, Babcock MA, Pegelow DF, Reddan WG, Dempsey JA. Longitudinal effects of aging on lung function at rest and exercise in healthy active fit elderly adults. J Appl Physiol (1985) 1995;78:1957-68.


Bordoni B, Morabito B, Simonelli M. Ageing of the diaphragm muscle. Cureus 2020;12:e6645.


Gillooly M, Lamb D. Airspace size in lungs of lifelong non-smokers: effect of age and sex. Thorax 1993;48:39-43.


Turner JM, Mead J, Wohl ME. Elasticity of human lungs in relation to age. J Appl Physiol 1968;25:664-71.


Bickerman HA. Senile emphysema. J Am Geriatr Soc 1956;4:526-34.


Verbeken EK, Cauberghs M, Mertens I, Clement J, Lauweryns JM, Van de Woestijne KP. The senile lung. Comparison with normal and emphysematous lungs. 1. Structural aspects. Chest 1992;101:793-9.


Butler C 2nd, Kleinerman J. Capillary density: alveolar diameter, a morphometric approach to ventilation and perfusion. Am Rev Respir Dis 1970;102:886-94.


Guénard H, Marthan R. Pulmonary gas exchange in elderly subjects. Eur Respir J 1996;9:2573-7.


Newnham DM, Hamilton SJ. Sensitivity of the cough reflex in young and elderly subjects. Age Ageing 1997;26:185-8.


Bailey KL. Aging Diminishes Mucociliary Clearance of the Lung. Adv Geriatr Med Res. 2022;4(2):e220005.


Krumpe PE, Knudson RJ, Parsons G, Reiser K. The aging respiratory system. Clin Geriatr Med 1985;1:143-75.


Kronenberg RS, Drage CW. Attenuation of the ventilatory and heart rate responses to hypoxia and hypercapnia with aging in normal men. J Clin Invest 1973;52:1812-9.


Peterson DD, Pack AI, Silage DA, Fishman AP. Effects of aging on ventilatory and occlusion pressure responses to hypoxia and hypercapnia. Am Rev Respir Dis 1981;124:387-91.


Hopp RJ, Bewtra A, Nair NM, Townley RG. The effect of age on methacholine response. J Allergy Clin Immunol 1985;76:609-13.


Connolly MJ, Crowley JJ, Charan NB, Nielson CP, Vestal RE. Impaired bronchodilator response to albuterol in healthy elderly men and women. Chest 1995;108:401-6.


Connolly MJ, Crowley JJ, Charan NB, Nielson CP, Vestal RE. Reduced subjective awareness of bronchoconstriction provoked by methacholine in elderly asthmatic and normal subjects as measured on a simple awareness scale. Thorax 1992;47:410-3.


Meyer KC, Ershler W, Rosenthal NS, Lu XG, Peterson K. Immune dysregulation in the aging human lung. Am J Respir Crit Care Med 1996;153:1072-9.


Poulin MJ, Cunningham DA, Paterson DH, Rechnitzer PA, Ecclestone NA, Koval JJ. Ventilatory response to exercise in men and women 55 to 86 years of age. Am J Respir Crit Care Med 1994;149:408-15.