Divyan Bavan
Introduction
Inhalation is dependent on the expansion of the lungs. When the external intercostal muscles and diaphragm contract, the thoracic volume increases. This leads to an increased pressure gradient between the alveoli and the pleural space, causing the lungs to expand. Expansion leads to the alveolar pressure dropping below atmospheric pressure, enabling air to enter the lungs. Compliance determines the extent of expansion, and thus the amount of air taken in. This feature measures the lungs’ ability to expand; it is expressed as the change in volume divided by the change in pressure. Two main properties of the lung contribute to its compliance: tissue elasticity and surface tension. Furthermore, compliance also changes as a consequence of lung volume. Compliance is thus not a static feature of the lungs, but rather dynamic. This can be disrupted by various diseases which can increase or decrease compliance past normal physiological values. By understanding these three components of compliance—contributors, dynamics, and disruption—it is possible to build an understanding for its importance to breathing.
The Contributors to Compliance
As mentioned previously, the two main contributors are tissue elasticity and surface tension. The former is the product of elastin and collagen fibres within the extracellular matrix of pulmonary cells. Elastin is a protein fibre that is composed of cross-linked tropoelastin monomers. It is able to extend to 150% of its original length, contributing to the lung’s overall compliance (Kamrani et al., 2023). Similarly, collagen is a protein fibre also found in the lungs. However, it is non-elastic and reduces the lungs’ compliance (Kamrani et al., 2023). This creates an antagonistic relationship between elastin and collagen that will become important for understanding dynamic compliance.
The second contributor to lung compliance is surface tension. This property states that there is an inward force into the alveoli due to the air-water interface. The force follows Laplace’s law, which states that the surface tension decreases with the radius of the bubble, in this case the alveoli. The force would create a recoil that contributes to the overall lung compliance. This was shown by von Neergaard in 1929. In his experiment, von Neergaard placed lungs in water to eliminate the air-water interface. He demonstrated that this greatly increased compliance when compared with air-filled lungs, suggesting that surface tension decreases compliance (Lumb, 2017). However, this would suggest that air flows into larger alveoli preferentially, which would destabilize the lungs. This substance is pulmonary surfactant (Koeppen and Stanton, 2017; Lumb, 2017).
Pulmonary surfactant is responsible for lowering the surface tension of the alveoli. It does this in a variable manner. Surfactant decreases tension in smaller alveoli more than larger alveoli, balancing out the surface tension. This is because surfactant molecules are more densely packed together over smaller surface areas, decreasing the surface tension further. The result is a prevention of imbalance in airflow distribution. Surfactant is produced by alveolar type II cells and stored in lamellar bodies. It is then released and spread across the alveolar surface. It is made up of primarily lipids, which account for 85-90% of its composition. More specifically, its primary lipid—dipalmitoyl phosphatidylcholine—is a key molecule for decreasing surface tension (Koeppen and Stanton, 2017).
Dynamic Compliance
While compliance can be measured statically, it can also be measured dynamically. This means measuring compliance while air is flowing through the system, compared to static compliance where there is no flow. This is measured by plotting a pressure-volume curve for both inhalation and exhalation. This value is always lower than the static compliance. This is because the change in alveolar surface area is not large enough to bring more surfactant. The product of this is increased surface tension and lower compliance. However, exercise, yawning, and sighing can increase surfactant material and thus, increase dynamic compliance as well (Koeppen and Stanton, 2017).
Another way to look at dynamic compliance is by understanding the pressure-volume curve of the lungs in general. At low volumes, the lungs have low compliance. This is due to lower numbers of alveoli being open. This means more pressure is required to get to a critical point. Once this point is reached, a larger number of alveoli become active, increasing compliance. This is the inflection point of the pressure-volume curve. Finally, as the lung volume reaches it maximum, compliance starts to decrease again. This is due to collagen fibres limiting the stretch. This mechanism shows that compliance can change throughout the respiratory cycle, making it critical for physiological function (do Amaral et al., 2011).
Disruptions in Compliance
Many diseases disrupt lung compliance. This makes it harder to breathe and can often lead to downstream effects. One example of this is emphysema. This disease is associated with damage to the alveoli and is often caused by exposure to toxic chemicals. The result of this is activation of the immune system and its effector cells. These cells, primarily neutrophils, release proteases such as elastase. This is coupled to a loss in antiproteases such as α1-antitrypsin. Together, these factors lead to a marked decrease in the presence of elastin. This leads to higher lung compliance as elastin maintains the elastic recoil of the lungs. Since this is an important property for exhalation, it becomes harder to exhale and thus, breathe with emphysema (Lumb, 2017; Pahal et al., 2025).
The opposite can also be true. In cystic fibrosis, compliance is markedly decreased. This disease is caused by a mutation on a gene in chromosome 7: the cystic fibrosis transmembrane regulator. Its primary role is to transport chloride ions and thus, control salt concentrations. Mutations in this gene can cause this protein to malfunction, leaving salt concentrations unregulated. This can inactivate the antibiotic human β-defensin (HBD), which causes bacteria to grow more easily within the lungs. The result of this is increased damage to the alveoli, scarring the lungs. This causes fibrosis—the placement of collagen in response to inflammation—and lowers the lungs’ ability to expand (Lumb, 2017).
While cystic fibrosis is a famous example of how lung compliance can be affected, it is not the only one. Several factors can cause pulmonary fibrosis: drugs, inorganic dusts, radiation, and others. For example, asbestos can cause inflammation of the airways through macrophage-mediated uptake. Once taken up by the macrophage, it damages its lysosome and spreads its contents throughout the environment. This damages the lungs, causing fibrosis over years of exposure. While this is an explainable version of pulmonary fibrosis, most cases are not understandable. These cases fall under the class of idiopathic pulmonary fibrosis (Lumb, 2017).
Conclusion
It is evident that compliance is critical for the normal functioning of the lungs. It is responsible for determining how much air is taken up for a given pressure change and thus represents how easily the lungs can expand. Static compliance is dependent on two main factors—tissue elasticity and surface tension. The former depends on the proteins elastin and collagen, while the latter is influenced by presence of surfactant on the alveoli. Dynamic compliance on the other hand is determined by calculating compliance while air is flowing through the lungs. It also shows how compliance changes over specific lung volumes. This is important for understanding how breathing patterns may be changed in diseases which affect compliance. As discussed, several diseases—emphysema, cystic fibrosis, and idiopathic pulmonary fibrosis, among others—affect lung compliance. Therefore, researching lung compliance further is critical for determining the best ways to treat these diseases.
Works Cited
do Amaral, R.A., et al. “The Physical Origin of Sigmoidal Respiratory Pressure–Volume Curves: Alveolar Recruitment and Nonlinear Elasticity.” Physica A: Statistical Mechanics and Its Applications, vol. 390, no. 10, 19 Jan. 2011, pp. 1791–1799, www.sciencedirect.com/science/article/pii/S0378437111000021, https://doi.org/10.1016/j.physa.2010.12.023.
Kamrani, Payvand, et al. “Anatomy, Connective Tissue.” National Library of Medicine, StatPearls Publishing, 5 Mar. 2023, www.ncbi.nlm.nih.gov/books/NBK538534/.
Koeppen, Bruce M, and Bruce A Stanton. Berne and Levy Physiology. 7th ed., Saintt Louis Elsevier Health Sciences, 2017.
Lumb, Andrew B. Nunn’s Applied Respiratory Physiology. 8th ed., Edinburgh ; New York, Elsevier, 2017.
Pahal, Parul , et al. “Emphysema.” National Library of Medicine, StatPearls Publishing, 2025, www.ncbi.nlm.nih.gov/books/NBK482217/.