The main mediator of air flow during respiration is the bronchiole. These tiny airways are wrapped in smooth muscle, which allows them to contract or relax in order to restrict or increase air flow in the lung. The trachea and bronchioles are cartilaginous rather than muscular, and are unable to constrict, while the wall of the alveolar sac is also devoid of smooth muscle, made up only of epithelial cells, capillaries, and connective tissue.  

The system by which debris is removed from the lung is termed the mucociliary escalator. This is made up of two parts: the mucus produced by respiratory goblet cells, and the wave-like movement of cilia covering the bronchioles and bronchi of the lung. Bacteria and particles  of debris are caught in the mucus coating the cilia, which is then passed in waves upward toward the trachea. Once it clears the trachea and enters the pharynx, it can either be coughed out or swallowed.  

Type II alveolar cells secrete pulmonary surfactant, a lipoprotein complex that is essential for lung function. This surfactant acts to break up the surface tension of fluid coating the lung airspaces, allowing for alveolar compliance and reducing the buildup of fluid in the lung. Lack of surfactant can lead to atelectasis, or collapse of part of the lung.

The most important muscle of respiration is the diaphragm, followed by the intercostals. The sternocleidomastoid and scalenes are considered accessory muscles of respiration. 

Carbon dioxide has paracrine effects in the airway, causing the smooth muscle of bronchioles to relax. When the partial pressure of carbon dioxide in the alveoli increases, the bronchioles dilate. This allows for increased ventilation.

The diaphragm is innervated by the phrenic nerve. This nerve exits the spine at C3-C5. In the case of spinal cord trauma, if injury occurs above C3, the diaphragm is no longer able to function on its own and breathing assistance is generally required.

Vital capacity is the maximum volume of air a person can exhale after maximum inhalation. Residual volume is the air that remains in the lung after forced exhalation, while functional residual capacity is the volume of air that remains in the lung after a relaxed exhalation. 

Dead space is the volume of air that remains in the trachea, bronchi, and bronchioles during respiration. It does not enter the alveoli and so does not participate in gas exchange. In the average adult, the amount of air left in the dead space after expiration is . 

Tidal breathing is the term for relaxed inhalation and exhalation (as opposed to maximum inspiration and forced exhalation). The average volume of air breathed into and out of the respiratory system during tidal breathing is . 

There are many factors that can cause bronchioconstriction. Some of them are normal physiological responses, such as parasympathetic input or decreased partial pressure of carbon dioxide in the alveoli. Other causes are pathological, such as allergic bronchioconstriction or asthma triggered by cold air.