Breathing is the spontaneous taking in and giving out of air from the lungs, the product of the visible movements of the ribcage and abdomen. In earlier years breathing was synonymous with life itself, for with the ‘last breath’ its absence signified death and departure of the soul. However, in the late nineteenth Century, the advent of a scientific understanding of its nature and basis and, later, the development of life support measures, meant that this view was no longer tenable, giving rise to new moral and ethical dilemmas as to when life support can be withdrawn.
Breathing is a remarkably robust process compared with other activities involving skeletal (voluntary) muscle. It performs some 400 million or so operational cycles in a sedentary lifetime and, except in disease, does so without fatigue, thus being able to increase in pace with the most strenuous exercise that the heart can support. Also, breathing continues in sleep and in coma and, fortuitously for patient and surgeon alike, even under anaesthesia that is sufficiently deep to abolish pain. Breathing occurs spontaneously and without conscious attention, notwithstanding its immediate cessation or augmentation in response to volition. Thus it is both the most highly automated of movements, yet, when powering vocalization during speech and singing, the most voluntary.
The neural mechanism responsible for the generation of the basic respiratory rhythm is now attributed to a network of neurons located in the brain stem. The search for such a rhythm generator, originally conceived as the ‘Respiratory Centre’, began early in the nineteenth century and notably, perhaps with Madame Guillotine in mind, initiated by the French scientist Le Gallois. In rabbits he successively transected the brain stem and spinal cord at different levels in different sequences. He discovered that if the lower brain stem remains connected to the spinal cord breathing continues, a result in sharp distinction to that following the human experiment by ‘Madame, ’ of sectioning in the neck between the brain stem and spinal cord!
In the fully automatic mode the rate and depth (tidal volume) of breathing movements is regulated on the basis of information from sensors in the brain (‘central’ chemoreceptors) and a variety of peripheral reflex mechanisms, using sensors detecting the concentrations of oxygen and carbon dioxide in the arterial blood (peripheral chemoreceptors) and mechanical events in the heart, lungs and arteries (heart, lung, and arterial mechanoreceptors), and also receptors elsewhere in the body. Collectively, these maintain homeostasis of the blood gases and pH, thus satisfying tissue metabolic requirements for oxygen uptake and the elimination of carbon dioxide in the face of changing behavioural demands.
The act of breathing can be considered from two points of view: mechanical properties, and the central nervous control mechanism. Insight into the former dictates the problem to be solved by the central nervous system, as through its ‘command’ signals breathing is maintained and regulated according to the metabolic or behavioural demands of the moment.
Mechanical factors
The lungs are paired, lobed structures which when inflated are in some ways balloon-like: when punctured or surgically removed from the thorax, they collapse under the combined influence of internal elastic forces and surface tension within the terminal air sacs (alveoli). As with a balloon they can be inflated through their neck (trachea) by air under positive pressure (greater than atmospheric pressure), and the relationship between pressure and volume can be determined experimentally. However, in the living body, the situation is different. For example, at the end of a normal expiration, there is a volume of air in the lungs known as the Functional Residual Capacity (FRC) ; at this point the pressure in the alveoli is atmospheric, there is no airflow, but nevertheless the lungs are held inflated within the chest; this is now by ‘suction’ from without. Suction exists because the outer surfaces of the lungs are exposed to a pressure less than atmospheric (‘negative’ pressure) within the thin film of fluid between the two layers of the pleura that cover the lungs and line the inside of the chest wall. This pleura fluid both separates the lungs from the chest wall and also links them to it, whilst allowing the lobes to move freely as they inflate and deflate. At FRC this surface pressure, of about -5.0 to -8.0 cm H2O, is determined by the balance between the elastic recoil forces of the lung pulling inwards and the net elastic recoil of the chest wall pulling outwards. Evidence of the latter is seen during surgery when opening of the chest is accompanied by the collapse of the lungs and the outwards motion of the ribcage. Entry of air into the pleural ‘space’ due to lung or chest wall puncture constitutes a ‘pneumothorax’; this is not life-threatening when only one lung collapses, but bilateral collapse is fatal unless artificial ventilation is immediately available.

Above: (a) the tidal flow in and out of the lungs at rest that is caused by (b) the pressure changes within the lungs (alveolar), caused in turn by (c) the pressure changes between lungs and chest wall (pleural). Below: tidal volume at rest, vital capacity, and tidal volume as it increases during muscular activity; the relation of these volume changes to total lung capacity, and to the volume remaining after a normal tidal breath (FRC) or after a full expiration (RV) (see text).
Even when the breath has been fully expelled by voluntary effort to reach the lungs' minimal volume (
Residual Volume, RV) the lungs still remain slightly inflated, with pleural pressure still negative at about -2.0 cm H
2O; the expiratory muscular effort to reach RV is needed to overcome the greatly increasing elastic recoil outwards of the chest wall as lung volume becomes low. Similarly, if voluntary effort is used to inflate the lungs to their maximal volume (
Total Lung Capacity, TLC) the lungs remain intimately applied to the chest wall, held there by a negative pressure of some -25 to -30 cm H
2O; this reflects the increased elastic recoil of the lungs at this higher volume; and the recoil of the chest wall itself is now also a force acting inwards, opposing the voluntary muscular effort to reach TLC. The total volume of air that can be breathed in from residual volume to TLC (or vice versa) is called the
Vital Capacity (VC), and is in the order of 5.0 litres in the adult. Lung volume, or changes in lung volume, are often expressed as a percentage of vital capacity. The tidal volume during quiet breathing, about 0.5 litres, therefore represents only 10% VC and is achieved by swings in pleural pressure of -2 to -3 cm H
2O (see figure).
In respiratory mechanics, the term ‘chest wall’ also includes the abdomen, because a major factor contributing to the balance of elastic forces is that of posture. This is due to the influence of gravity on the large mass of the abdominal organs, which hydraulically generates a negative pressure transmitted across a relaxed
diaphragm to the pleural space at the base of the lungs, so increasing their volume. Thus changing from the supine to the upright posture can increase FRC by some 15-20% of VC (approximately 0.75-1.0 litres). In fact, this major influence of posture can be utilized to achieve artificial ventilation by means of a tilting bed, but the tidal volume achieved is restricted.
The above considerations all refer to the principal ‘passive’ mechanical properties of the system. In quiet, effortless breathing (
eupnoea) the resistance to airflow in the lungs and airways is negligible, as also is the viscous resistance to movement of the lungs and surrounding structures, except in disease states. Changes in pleural pressure require appropriate
displacements of the structures immediately around the lungs — namely the ribcage and diaphragm — and, through hydraulic coupling, the abdominal wall. This would represent a formidable design challenge in engineering, as it would be the equivalent of asking for the hull of a ship or aircraft to change its volume and shape, although the latter is actually achieved in Concorde by articulation of its nose! The articulated ribcage does exactly this, and aided by cartilaginous extensions at the front which flexibly couple each rib pair to the breastbone or sternum, allows the inspiratory rise (inflation) and expiratory fall (deflation) of the chest in
‘thoracic’ breathing. Similarly, the diaphragm descends relatively freely within the upper abdomen, accommodated by an outward displacement of the abdominal wall — so-called
‘abdominal’ breathing — until this motion is limited by tension in the abdominal wall. Both expansion of the ribcage and descent of the diaphragm normally cause a decrease in pleural pressure, so either acting alone (as can occur following spinal injury or diaphragmatic paralysis) will cause a paradoxical movement of the other, reducing the change in lung volume. Such paradoxing of the ribcage is seen in the newborn, most markedly in the
respiratory distress syndrome, when the absence of surfactant which reduces surface tension within the lungs necessitates the development of much greater changes in pleural pressure to achieve an adequate tidal volume. During such inspiratory effort the reduction in pleural pressure due to the diaphragm is greater than the resisting force of the underdeveloped ribcage muscles, so that the chest collapses inwards instead of expanding. Under most circumstances, however, the 2 sets of muscles work in concert and, even when the ribcage may not appear to rise or expand in inspiration, it is stiffened sufficiently to withstand the fall in pleural pressure, enabling the diaphragm to work more efficiently. Similarly, when thoracic breathing is exaggerated the abdomen may move inwards even though the diaphragm is contracting.
The actual elevation and depression of the ribs in quiet breathing is due to the external and internal intercostal muscles, respectively, which bridge each adjacent pair of ribs, aided by other muscles at the front and back, while three layers of abdominal muscle generate active forces for expiratory flow when greater than resting tidal volumes are required. In quiet breathing neither the diaphragm nor all of the chest wall is fully actively engaged in generating the pressures reviewed above. When exercise requires breathing to be increased, the volume and velocity of airflow in and out is greatly accelerated. This is achieved by additional force production involving progressively more of the chest wall and diaphragm; in the athlete this may no longer be fully automatic, but patterned through training to achieve the best performance.
In addition to their role in breathing, the voluntary activation of respiratory muscles is also utilized for generating much higher forces and hence pressures within the system. For example, abdominal pressures in excess of 200 mm Hg help to stabilize the vertebral spine during weight lifting — some 100 times greater than the pressures required for tidal air movement during quiet, effortless breathing. (See
respiratory system).
Neural aspects
In order to achieve lung ventilation the central nervous control mechanism has to generate muscular forces, displacements, and hence pressure changes, to oppose the augmenting elastic recoil as lung volume increases. It does this through motor commands issued from the brain stem for a waxing and waning profile of pleural pressure change, with a time course matching the current demand for pulmonary ventilation; in resting breathing this would be approximately 1.0 sec for inspiration, and 2-3 sec for expiration depending on the overall respiratory rate (12-15/min). Inspiration is generated by a progressively increasing co-activation of the diaphragm and external intercostal muscles. This action can either be observed mechanically or more directly visualized by recording the electrical activity of the motor units in the relevant muscles, by electromyography (EMG). The EMG shows a strongly augmenting activity pattern paralleling that of the pressure change. At the end of inspiration such activity ceases fairly rapidly, allowing the lungs to deflate due to elastic recoil back to their starting lung volume at FRC. The cycle then repeats. It is generally held that during breathing at rest expiration is a mainly ‘passive’ process, although some activity in expiratory muscles may maintain the outflow of air.
The inspiratory augmentation in the EMG is due to the progressive recruitment in the number and discharge frequencies (e.g. ranging from 5-25 Hz) of the active motor units in the respective muscles. These discharge patterns correspond to respiratory phased ‘trains’ of nerve impulses in the motor nerve fibres to the muscles; in turn, their origin lies in the pattern of the electrical activity in the cell bodies of the motor neurons within the spinal cord. Recordings through minute electrodes inserted through the cell membrane of these motor neurons (intracellular recording) reveals the presence of rhythmic waxing and waning changes of electrical potential, which are given the name ‘central respiratory drive potentials’. Their time course and amplitude closely mirror a mechanical record of the changes in pleural pressure, and it is during the waxing phase that they generate the augmenting patterns of impulse activity in the motor axons that result in the motor unit activity recorded in the muscles.
The ‘central respiratory drive potentials’ of respiratory motor neurons, with their slow time course of 2-3 sec duration, reflect the summed synaptic action of impulses in respiratory motor pathways descending from the brain stem, wherein lies the neural network that generates the breathing rhythm. Again, intracellular recording from those ‘respiratory’ neurones whose axons descend into the spinal cord reveals central respiratory drive potentials, but, in contrast to the motoneurons, their discharge rates are much higher, ranging typically from 50-300/sec within each cycle, depending on the prevailing ‘demand’ for ventilation. This particular system of neurones corresponds to the ‘upper motor neuron system’, the corticospinal tract which conveys ‘volitional’ as well as automated commands for limb and digit movement from the ‘motor cortex’. It is these vital pathways which are interrupted following trauma to the highest part of the spinal cord in the neck (cervical spinal cord), leading to total paralysis of the whole body below the neck including both voluntary and automatic breathing movements. Death ensues within minutes unless artificial ventilation is immediately available. A spinal transection at the base of the neck (low cervical region) abolishes thoracic and expiratory-phased abdominal movements, whereas diaphragmatic movements are left intact because their motor neurons are located above the transection.
Much research, of necessity based on studies of anaesthetized animals, is devoted to unravelling the neural connectivity that sustains the respiratory rhythm, and how this is regulated by a variety of reflexes. Such insights should help, for example, to solve the mystery of the sudden infant death syndrome (SIDS or ‘cot death’), which is usually attributed to an abrupt cessation of breathing — its absence being the first indication of the tragedy to the unsuspecting parents. By recording the electrical activity of a wide range of neurons in the brain stem of anaesthetized animals, several distinctive patterns of neurone activity have been identified, each having different firing patterns within the respiratory cycle and different connectivities one to the other; it is from such information that deductions are made as to how this system could generate the respiratory rhythm. The brain stem emerges as a truly vital structure in the immediate maintenance of ‘life’ as now understood. Thus following major destruction or inactivation of the cerebral cortex through trauma or deprivation of oxygen, a still viable brain stem can maintain breathing when the former structures are so damaged as not to sustain the conscious state (vegetative state) ; conversely, if the viability of the brain stem is compromised, breathing ceases; however, although artificial ventilation and other life preserving measures may sustain the metabolic activities of the heart, lungs, and other tissues, the otherwise intact cerebral cortex now lacks the afferent inputs from, and also channelled through, the brain stem that are critical for consciousness itself, a state dependent on a fully-functioning cerebral cortex.
— Tom Sears
See respiratory system. See also life support; lungs; respiration.