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To assess the effect of sleep on functional residual capacity (FRC) in normal subjects and asthmatic patients, 10 adult subjects (5 asthmatic patients with nocturnal worsening, 5 normal controls) were monitored overnight in a horizontal volume-displacement body plethysmograph. With the use of a single inspiratory occlusion technique, we determined that when supine and awake, asthmatic patients were hyperinflated relative to normal controls (FRC = 3.46 +/- 0.18 and 2.95 +/- 0.13 liters, respectively; P less than 0.05). During sleep FRC decreased in both groups, but the decrease was significantly greater in asthmatic patients such that during rapid-eye-movement (REM) sleep FRC was equivalent between the asthmatic and normal groups (FRC = 2.46 +/- 0.23 and 2.45 +/- 0.09 liters, respectively). Specific pulmonary conductance decreased progressively and significantly in the asthmatic patients during the night, falling from 0.047 +/- 0.007 to 0.018 +/- 0.002 cmH2O-1.s-1 (P less than 0.01). There was a significant linear relationship through the night between FRC and pulmonary conductance in only two of the five asthmatic patients (r = 0.55 and 0.65, respectively). We conclude that 1) FRC falls during sleep in both normal subjects and asthmatic patients, 2) the hyperinflation observed in awake asthmatic patients is diminished during non-REM sleep and eliminated during REM sleep, and 3) sleep-associated reductions in FRC may contribute to but do not account for all the nocturnal increase in airflow resistance observed in asthmatic patients with nocturnal worsening.

We have previously shown that patients with nocturnal worsening of asthma (nocturnal asthma) exhibit increased parenchymal inflammation at night. To evaluate the functional significance of this parenchymal inflammation, 10 subjects with nocturnal asthma (NA), four subjects with non-nocturnal asthma (NNA), and four normal control subjects underwent bronchoscopy with measurement of peripheral airways resistance (Rp) at 4:00 P.M. and at 4:00 A.M. Employing a wedged bronchoscope technique, Rp was measured. Flow was stopped, and the pressure reached after 10 s of decay was termed the plateau pressure. The time constant of this decay (tau) was measured, and the peripheral compliance (Cp) was calculated as tau/Rp. The NA group exhibited the highest Rp values at 4:00 P.M. and at 4:00 A.M. as compared with the NNA and control groups, but all groups were significantly different from each other at 4:00 P.M.: NA, 0.113 +/- 0.02 cm H(2)O/ml/min; NNA, 0.033 +/- 0.005 cm H(2)O/ml/min; Control subjects, 0.010 +/- 0.001 cm H(2)O/ ml/min; p = 0.0001; and at 4:00 A.M.: NA, 0.129 +/- 0.023 cm H(2)O/ ml/min; NNA, 0.035 +/- 0.007 cm H(2)O/ml/min; Control subjects, 0.009 +/- 0.002 cm H(2)O/ml/min; p = 0.0003. None of the groups exhibited statistically significant differences in Rp between 4:00 P.M. and 4:00 A.M. The plateau pressure increased significantly from 4:00 P.M. to 4:00 A.M., but only in the NA group (7.7 +/- 0.9 cm H(2)O at 4:00 P.M. versus 16.9 +/- 4.6 cm H(2)O at 4:00 A.M.; p = 0.0004). Cp was decreased in the NA group as compared with the NNA and control groups at both 4:00 P.M. (p = 0.0003) and 4:00 A.M. (p = 0.003). The Rp positively correlated with the residual volume at both 4:00 P.M. (r = 0.71, p = 0.004) and 4:00 A.M. (r = 0.59, p = 0.03). We conclude that the distal lung units, specifically the collateral channels, and may be functionally altered at night in NA.