Objective: To test the hypothesis that chronic
hypercapnia changes the composition of the respiratory muscle by
continuous augmentation of ventilation.
methods: Eighteen male Wistar rats were housed in 10%
CO2 in air for 19 weeks, and their minute ventilation
(V̇e) was measured every 6 weeks. The diaphragm,
excited at 19 weeks of exposure, was classified as fiber type I, IIa,
or IIb. Cross-sectional areas of individual fibers were measured.
Fibers with a target-like appearance on reduced nicotinamide adenine
dinucleotide-tetrazolium reductase (NADH-TR) stain also were counted.
The data were compared with those of rats kept in room air.
Results: The mean (± SD) Paco2
after 19 weeks of sustained hypercapnia was 71.0 ± 4.7 mm Hg. The
V̇e remained at a high level until 12 weeks of
exposure, and then it significantly decreased at week 18. In a
comparison with the control rats, a larger number of type I fibers and
a smaller number of type IIb fibers were found in the diaphragm of the
chronically hypercapnic rats. In addition, the latter group’s
cross-sectional area revealed fibers of a significantly smaller
diameter. Target-like fibers were observed in 5% of the
NADH-TR-stained fibers in the chronically hypercapnic rats but were not
seen in the control rats.
Conclusion: By increasing
the ratio of fatigue-resistant fibers, the diaphragm was able to adapt
to a sustained load induced by hypercapnia. However, this adaptive
process was accompanied by a degenerative change in the