Key result
In maximally constricted normal lungs, slow vital capacity was significantly smaller than forced vital capacity when performed as the first maneuver, with a mean difference of 13%.
Why the study?
Does the rate of expiration affect vital capacity in methacholine-constricted lungs in healthy subjects?
Does the rate of expiration affect vital capacity in methacholine-constricted lungs in healthy subjects?
Vital capacity in constricted lungs depends on the dynamic force-length properties of smooth muscle, with slow vital capacity being significantly lower than forced vital capacity when performed as the first maneuver after constriction.
Answers are grounded in this paper and cite their sources.
Slow vital capacity may underestimate volume in constricted airways; hypothesis-generating for smooth muscle dynamics, untested in patients.
Measurements of dynamic force-length behavior of maximally activated strips of smooth muscle during oscillatory length changes show that force decreases well below the isometric force during the shortening phase of the oscillation. The magnitude of the decrease depends on the rate of shortening; for slower shortening, the decrease is smaller and force is larger. Modeling of expiratory flow, based on these data, predicts that vital capacity in constricted lungs depends on the rate of expiration. In maximally constricted lungs, forced vital capacity (FVC) is predicted to be 16% smaller than control, and vital capacity for a very slow expiration (SVC), 31% less than control. These predictions were tested by measuring FVC and SVC in constricted normal subjects. In the first group of 9 subjects, four maneuvers were made following the delivery of two doses of methacholine in the order: SVC, FVC, FVC, SVC. In a second group of 11 subjects, two maneuvers were performed at each dose in the order: FVC, SVC. At the highest dose of methacholine, FVC for both trials in group 1 and for the one trial in group 2 were all approximately 13% less than control, a slightly smaller decrease than predicted. SVC for the 1st trial in group 1 was 27% less than control, also slightly smaller than predicted. The difference between FVC and SVC for this trial, 13%, was close to the predicted difference of 15%. However, SVC for the 2nd trial in group 1 (preceded by 3 vital capacity maneuvers) and for group 2 (preceded by 1) were no different from FVC. We conclude that vital capacity in constricted lungs depends on the dynamic force-length properties of smooth muscle and that the history dependence of the dynamic properties of smooth muscle is more complicated than has been inferred from oscillatory force-length behavior.
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Olson et al. (2010) studied Healthy (methacholine-induced bronchoconstriction) (n=20). Slow vital capacity (SVC) maneuver vs. Forced vital capacity (FVC) maneuver was evaluated on Difference between FVC and SVC at highest dose of methacholine (Group 1, Trial 1) (13% difference, p=<0.05). In maximally constricted normal lungs, slow vital capacity was significantly smaller than forced vital capacity when performed as the first maneuver, with a mean difference of 13%.
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