Abstract
BackgroundAlthough the prevalence of inspiratory muscle strength training has increased in clinical medicine, its effect on diaphragm fiber remodeling is not well-understood and no relevant animal respiratory muscle strength training-rehabilitation experimental models exist. We tested the postulate that intrinsic transient tracheal occlusion (ITTO) conditioning in conscious animals would provide a novel experimental model of respiratory muscle strength training, and used significant increases in diaphragmatic fiber cross-sectional area (CSA) as the primary outcome measure. We hypothesized that ITTO would increase costal diaphragm fiber CSA and further hypothesized a greater duration and magnitude of occlusions would amplify remodeling.Methodology/Principal FindingsSprague-Dawley rats underwent surgical placement of a tracheal cuff and were randomly assigned to receive daily either 10-minute sessions of ITTO, extended-duration, 20-minute ITTO (ITTO-20), partial obstruction with 50% of cuff inflation pressure (ITTO-PAR) or observation (SHAM) over two weeks. After the interventions, fiber morphology, myosin heavy chain composition and CSA were examined in the crural and ventral, medial, and dorsal costal regions. In the medial costal diaphragm, with ITTO, type IIx/b fibers were 26% larger in the medial costal diaphragm (p<0.01) and 24% larger in the crural diaphragm (p<0.05). No significant changes in fiber composition or morphology were detected. ITTO-20 sessions also yielded significant increases in medial costal fiber cross-sectional area, but the effects were not greater than those elicited by 10-minute sessions. On the other hand, ITTO-PAR resulted in partial airway obstruction and did not generate fiber hypertrophy.Conclusions/SignificanceThe results suggest that the magnitude of the load was more influential in altering fiber cross-sectional area than extended-duration conditioning sessions. The results also indicated that ITTO was associated with type II fiber hypertrophy in the medial costal region of the diaphragm and may be an advantageous experimental model of clinical respiratory muscle strength training.
Highlights
The diaphragm is the primary muscle of the inspiratory pump, and in humans it contracts every three to five seconds to sustain alveolar ventilation
Our findings indicate intrinsic transient tracheal occlusion (ITTO) could be a useful experimental model of the respiratory muscle hypertrophy induced by the initial occlusion-load phase of inspiratory muscle strength training (IMST)
Neither fiber composition nor morphology was affected by group assignment. This experiment provides novel information regarding the effects of short duration, high intensity respiratory muscle overload training with ITTO, on diaphragmatic muscle fiber remodeling
Summary
The diaphragm is the primary muscle of the inspiratory pump, and in humans it contracts every three to five seconds to sustain alveolar ventilation. Inspiratory muscle strength training (IMST) with high pressure threshold loads has been shown to increase the pressure generating capacity of the inspiratory pump and facilitate weaning from MV in hospitalized patients [7,8,9,10]. Shorter yet physiologically challenging durations of resistive breathing increase diaphragmatic slow MHC gene expression, with concurrent plasma membrane damage and sarcomere disruption [15,16]. These studies suggested that the high magnitude and long duration of the loads damaged diaphragmatic fibers. We hypothesized that ITTO would produce fast-fiber hypertrophy in the costal diaphragm, compared to a sham-trained control group. We hypothesized that partial airway obstruction would not cause fiber hypertrophy
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