The mechanical advantages of the external and internal intercostals depend partly on the orientation of the muscle but mostly on interspace number and the position of the muscle within each interspace. Thus the external intercostals in the dorsal portion of the rostral interspaces have a large inspiratory mechanical advantage, but this advantage decreases ventrally and caudally such that in the ventral portion of the caudal interspaces, it is reversed into an expiratory mechanical advantage. The internal interosseous intercostals in the caudal interspaces also have a large expiratory mechanical advantage, but this advantage decreases cranially and, for the upper interspaces, ventrally as well. The intercartilaginous portion of the internal intercostals (the so-called parasternal intercostals), therefore, has an inspiratory mechanical advantage, whereas the triangularis sterni has a large expiratory mechanical advantage. These rostrocaudal gradients result from the nonuniform coupling between rib displacement and lung expansion, and the dorsoventral gradients result from the three-dimensional configuration of the rib cage. Such topographic differences in mechanical advantage imply that the functions of the muscles during breathing are largely determined by the topographic distributions of neural drive. The distributions of inspiratory and expiratory activity among the muscles are strikingly similar to the distributions of inspiratory and expiratory mechanical advantages, respectively. As a result, the external intercostals and the parasternal intercostals have an inspiratory function during breathing, whereas the internal interosseous intercostals and the triangularis sterni have an expiratory function.
We used a high-resolution ultrasound to make electrical recordings from the transversus abdominis muscle in humans. The behavior of this muscle was then compared with that of the external oblique and rectus abdominis in six normal subjects in the seated posture. During voluntary efforts such as expiration from functional residual capacity, speaking, expulsive maneuvers, and isovolume "belly-in" maneuvers, the transversus in general contracted together with the external oblique and the rectus abdominis. In contrast, during hyperoxic hypercapnia, all subjects had phasic expiratory activity in the transversus at ventilations between 10 and 18 l/min, well before activity could be recorded from either the external oblique or the rectus abdominis. Similarly, inspiratory elastic loading evoked transversus expiratory activity in all subjects but external oblique activity in only one subject and rectus abdominis activity in only two subjects. We thus conclude that in humans 1) the transversus abdominis is recruited preferentially to the superficial muscle layer of the abdominal wall during breathing and 2) the threshold for abdominal muscle recruitment during expiration is substantially lower than conventionally thought.
We investigated pulmonary mechanics in 25 patients, 9 to 55 years of age, with a variety of generalised neuromuscular diseases and variable degrees of respiratory muscle weakness. The average degree of inspiratory muscle force was 39 2 % (range 8-83 %) of predicted. The lung volume restriction far exceeded that expected for the degree of muscle weakness: the observed decrement in respiratory muscle force should, theoretically, decrease vital capacity to 78 % of its control value, while the mean VC in our patients was only 500% of predicted. Analysis of lung pressure-volume curves indicated that the two principal causes of the disproportionate loss of lung volume were a reduction in lung distensibility probably caused by widespread microatelectasis, and a decrease in the outward pull of the chest wall. Because it reflects both direct (loss of distending pressure) and secondary (alterations in the elastic properties of the lungs and chest wall) effects of respiratory muscle weakness on lung function, we conclude that, in these patients, the vital capacity remains the most useful measurement to follow evolution of the disease process or response to treatment.
This article examines the mechanics of the muscles that drive expansion or contraction of the chest wall during breathing. The diaphragm is the main inspiratory muscle. When its muscle fibers are activated in isolation, they shorten, the dome of the diaphragm descends, pleural pressure (P(pl)) falls, and abdominal pressure (P(ab)) rises. As a result, the ventral abdominal wall expands, but a large fraction of the rib cage contracts. Expansion of the rib cage during inspiration is produced by the external intercostals in the dorsal portion of the rostral interspaces, the intercartilaginous portion of the internal intercostals (the so-called parasternal intercostals), and, in humans, the scalenes. By elevating the ribs and causing an additional fall in P(pl), these muscles not only help the diaphragm expand the chest wall and the lung, but they also increase the load on the diaphragm and reduce the shortening of the diaphragmatic muscle fibers. The capacity of the diaphragm to generate pressure is therefore enhanced. In contrast, during expiratory efforts, activation of the abdominal muscles produces a rise in P(ab) that leads to a cranial displacement of the diaphragm into the pleural cavity and a rise in P(pl). Concomitant activation of the internal interosseous intercostals in the caudal interspaces and the triangularis sterni during such efforts contracts the rib cage and helps the abdominal muscles deflate the lung.
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