Diaphragm motor units and their response to altered use

Our results suggest that when the diaphragm is rendered relatively inactive (as would occur during mechanical ventilation), overall contractile strength of the muscle is reduced due to a selective atrophy of type II muscle fibers. However, our results question whether this adaptation of the diaphragm to inactivity would compromise normal ventilation. The cross-sectional area of type I fibers increased following 2 weeks of inactivity, as did their estimated contribution to the maximum force-generating capacity of the diaphragm. Accordingly, the overall fatigue resistance of the diaphragm improved following this period of inactivity. If we are correct in assuming that normal ventilatory forces are achieved by the recruitment of only fatigue-resistant motor units (type S and FR), then the adaptations associated with prolonged inactivity would not affect the animal's ability to generate the required ventilatory forces. Only during brief, more forceful nonventilatory behaviors would diaphragm function be compromised. Imposition of a mechanical load on the diaphragm can produce variable effects on maximal contractile strength. For example, our studies showed that with compensatory loading P(o) (normalized for muscle weight or cross-sectional area) increased, whereas with emphysema, normalized P(o) decreased. In both cases, the relative contribution of type I fibers to total cross-sectional area and maximum force-generating capacity decreased. We speculate that for some reason, the specific tension of type F units is reduced in the emphysemic diaphragm. It is possible that emphysema was associated with other metabolic symptoms (such as chronic hypoxia that may have influenced diaphragm adaptations to the imposed mechanical loads. It should be recognized that although these models can never exactly replicate a pathologic condition, they do provide important insight and information that can be subsequently used clinically.