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1 Erasme University Hospital
2 University of Minnesota
* To whom correspondence should be addressed. E-mail: a_detroyer{at}yahoo.fr.
When the lung is inflated acutely, the capacity of the diaphragm to generate pressure, in particular pleural pressure (Ppl), is impaired because the muscle during contraction is shorter and generates less force. At very high lung volumes, the pressure-generating capacity of the diaphragm may be further reduced by an increase in the muscle radius of curvature. Lung inflation similarly impairs the pressure-generating capacity of the inspiratory intercostal muscles, both the parasternal intercostals and the external intercostals. In contrast to the diaphragm, however, this adverse effect is largely related to the orientation and motion of the ribs, rather than the ability of the muscles to generate force. During combined activation of the two sets of muscles,
Ppl is larger than during isolated diaphragm activation, and this added load on the diaphragm reduces the shortening of the muscle and increases muscle force. In addition, activation of the diaphragm suppresses the cranial displacement of the passive diaphragm that occurs during isolated intercostal contraction and increases the respiratory effect of the intercostals. As a result, the
Ppl generated during combined diaphragm-intercostal activation is greater than the sum of the pressures generated during separate muscle activation. Although this synergistic interaction becomes particularly prominent at high lung volumes, lung inflation, either bilateral or unilateral, places a substantial stress on the inspiratory muscle pump.
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