During exercise and hyperventilation, exhalation becomes active. The main muscles involved in exhalation are the abdominal wall muscles (rectus abdominis, internal and external oblique, and transversus abdominis) and the internal intercostal muscles, which oppose the external intercostal muscles by pulling the ribs downward and inward. The work of breathing is done by the inspiratory muscles, which have a significant reserve during normal breathing. While respiratory muscles can be trained to do more work, there is a limit to their performance. Weakness in respiratory muscles can hinder chest wall movement and respiratory muscle fatigue is a major contributor to respiratory failure.

The lung epithelium starts forming as a pouch from the primitive foregut approximately 22 to 26 days after fertilization. This single lung bud then branches into the primitive right and left lungs. Over the next 2 to 3 weeks, further branching occurs, creating an irregular dichotomous branching pattern. Lynne Reid, a pathologist, described "three laws of lung development": (1) by week 16 of intrauterine life, the bronchial tree has developed; (2) alveoli develop after birth, with an increase in number until the age of 8 years and an increase in size until growth of the chest wall is completed at adulthood; and (3) the development of preacinar vessels (arteries and veins) parallels that of the airways, while intra-acinar vessels develop in tandem with the alveoli.

In diseases that affect the mechanical properties of the lung, the muscles of respiration are also impacted. For instance, in chronic obstructive pulmonary disease (COPD), increased airflow obstruction leads to an increase in the work of breathing. Exhalation, which is usually passive, now requires active contraction of expiratory muscles. Additionally, total lung capacity is increased in COPD, causing the diaphragm to be forced downward, resulting in shorter muscle fibers and a decreased radius of curvature. This leads to decreased function and efficiency of the diaphragm. Like other skeletal muscles, respiratory muscles can also experience fatigue with increased workload. Patients with neuromuscular diseases, such as Guillain-Barré syndrome and myasthenia gravis, may experience weakening of respiratory muscles. In these cases, respiratory failure can occur due to impaired chest wall movement, despite the lung and chest wall's mechanical properties being normal.
Exhalation during normal breathing is passive, but it becomes active during exercise and hyperventilation. The most important muscles of exhalation are those of the abdominal wall (rectus abdominis, internal and external oblique, and transversus abdominis) and the internal intercostal muscles, which oppose the external intercostal muscles (i.e., they pull the ribs downward and inward). The inspiratory muscles do the work of breathing. During normal breathing, this workload is low, and the inspiratory muscles have significant reserve. Respiratory muscles can be trained to do more work, but there is a limit to the work that they can perform. Respiratory muscle weakness can impair movement of the chest wall, and respiratory muscle fatigue is a major factor in the development of respiratory failure.
Lung Embryology, Development, Aging, and Repair
The epithelium of the lung arises as a pouch from the primitive foregut at approximately 22 to 26 days after fertilization of the ovum. This single lung bud branches into primitive right and left lungs. Over the next 2 to 3 weeks, further branching occurs to create the irregular dichotomous branching pattern. The pathologist Lynne Reid described “three laws of lung development”: (1) The bronchial tree has developed by week 16 of intrauterine
Diaphragm (domes descend, increasing longitudinal dimension of chest and elevating lower ribs)
A Muscles of inspiration
Internal intercostals, except parasternal intercartilaginous muscles (depress ribs)
Abdominal muscles (depress lower ribs, compress abdominal contents)
Muscles of expiration
Because respiratory muscles provide the driving force for ventilation, diseases that affect the mechanical properties of the lung affect the muscles of respiration. For example, in chronic obstructive pulmonary disease (COPD), the work of breathing is increased secondary to airflow obstruction. Exhalation no longer is passive but instead requires active, expiratory muscle contraction. In addition, total lung capacity is increased (see ). The larger total lung capacity forces the diaphragm downward, shortens the muscle fibers, life; (2) alveoli develop after birth, the number of alveoli increases until the age of 8 years, and the size of alveoli increases until growth of the chest wall is completed at adulthood; and (3) the development of preacinar vessels (arteries and veins) parallels that of the airways, whereas that of intra-acinar vessels parallels that of the alveoli.
and decreases the radius of curvature. As a result, the function and efficiency of the diaphragm are decreased. Respiratory muscles can fatigue just as other skeletal muscles do when the workload increases. Respiratory muscles can also weaken in patients with neuromuscular diseases (e.g., Guillain-Barré syndrome, myasthenia gravis). In these diseases, sufficient weakness of the respiratory muscles can impair movement of the chest wall and result in respiratory failure, even though the mechanical properties of the lung and chest wall are normal.