We examined expiratory muscle fatigue during expiratory resistive loading in 11 normal subjects. Subjects breathed against expiratory resistances at their own breathing frequency and tidal volume until exhaustion or for 60 min. Respiratory muscle strength was assessed from both the maximum static expiratory and inspiratory mouth pressures (PEmax and PImax). At the lowest resistance, PEmax and PImax measured after completion of the expiratory loaded breathing were not different from control values. With higher resistance, both PEmax and PImax were decreased (P less than 0.05), and the decrease lasted for greater than or equal to 60 min. The electromyogram high-to-low frequency power ratio for the rectus abdominis muscle decreased progressively during loading (P less than 0.01), but the integrated EMG activity did not change during recovery. Transdiaphragmatic pressure during loading was increased 3.6-fold compared with control (P less than 0.05). These findings suggest that expiratory resistive loaded breathing induces muscle fatigue in both expiratory and inspiratory muscles. Fatigue of the expiratory muscles can be attributed directly to the high work load and that of the inspiratory muscles may be related to increased work due to shortened inspiratory time.

We investigated whether fatigue of the expiratory muscle, that is, the abdominal muscle, may account for a change in the respiratory effort sensation in normal subjects during expiratory threshold loading. The respiratory effort sensation was scored using a modified Borg scale. Expiratory muscle fatigue was assessed both from changes in the maximal static expiratory pressure and in the centroid frequency (fc) of the abdominal muscle electromyogram (EMG). Expiratory threshold loading (magnitude of threshold; 40 to 60% of the maximal expiratory pressure at FRC, breathing frequency = 15/min, and duty cycle = 0.5) was continued until exhaustion or for 30 min. Loading was repeated following a 15-min recovery period after the end of the first expiratory loading. The maximal static expiratory pressure during loading (Pmmax) decreased initially and then remained decreased. Decreases were smaller with the 40% load (22 +/- 6%, SEM) than with the 60% load (37 +/- 3%) (p less than 0.05). The decrease during the second run of the 60% load was greater than during the first (p less than 0.01 by ANOVA). The maximal expiratory pressure at TLC before the second run of the 60% load was decreased by 9 +/- 3% compared with the control (p less than 0.02) but that with the 40% load was not. The fc with the 60% load decreased initially by 8 +/- 1% and then remained constant, although no change was observed with the 40% load.(ABSTRACT TRUNCATED AT 250 WORDS)

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The effect of ozone dose (the product of ozone concentration and exposure time) on airway responsiveness was examined in unanesthetized, spontaneously breathing guinea pigs. Airway responsiveness was assessed by measuring specific airway resistance (sRaw) as a function of increasing concentration of inhaled methacholine (Mch) aerosol (the concentration of Mch required in order to double the baseline sRaw: PC200Mch). The airway responsiveness was measured before and at 5 min, 5 h, and 24 h after exposure. A 30-min exposure to 1 ppm ozone (dose 30 ppm.min) did not change PC200Mch at any time after exposure. Both a 90-min exposure to 1 ppm ozone and a 30-min exposure to 3 ppm ozone, which are identical in terms of ozone dose (90 ppm.min), decreased PC200Mch to a similar degree. A 120-min exposure to 3 ppm ozone (360 ppm.min) produced a much greater decrease of PC200Mch at 5 min and 5 h after exposure, compared with low-dose exposure. There was a significant correlation between ozone dose and the change in airway responsiveness. In all groups, the baseline sRaw was increased by approximately 50% at 5 min after exposure, but there was no correlation between the changes in PC200Mch and the baseline sRaw. This study suggests that ozone-induced airway hyperresponsiveness in guinea pigs is closely related to ozone dose.

The effect ofsmoking a cigarette on bronchial responsiveness was studied in healthy nonsmokers. Twenty two subjects performed a methacholine inhalation test before and after smoking a single cigarette. Ten of the subjects took part in a further study in which propranolol was inhaled before the smoking challenge to diminish the baseline adrenergic tone of the airway. After they had smoked a single filtered or non-filtered cigarette the indices of bronchial responsiveness (the cumulative dose of methacholine starting a decrease in the reciprocal of resistance, Grs (Dmin), and the cumulative dose causing a 35% drop in the Grs (PD35Grs)) did not change significantly. With the inhalation of propranolol mean (SD) log Dmin decreased from 1-37 (0 44) units to 0 74 (0 57) (p < 0-01) and log PD35Grs from 193 (0-38) to 1l51 (0 38) (p < 0-01). Smoking a single cigarette after the inhalation of propranolol did not, however, cause any further change in bronchial responsiveness. This study suggests that smoking a single filtered or non-filtered cigarette does not change bronchial responsiveness in non-smokers, and that changes in adrenergic tone of the airway do not modify the effect of smoking a single cigarette on bronchial responsiveness.Bronchial responsiveness to non-specific stimuli such as histamine, methacholine, and acetylcholine is increased in people with bronchial asthma and in those with chronic obstructive lung disease.' Even in normal individuals conditions such as a viral infection of the respiratory tract,2 ozone exposure,3 and airway cooling4 influence bronchial responsiveness. What remains controversial is the effect of chronic smoking on bronchial responsiveness.'Smoking a cigarette induces bronchoconstriction in small and large airways.9"' In guinea pigs inhalation of cigarette smoke increased bronchial responsiveness." It is not known, however, whether smoking one cigarette affects bronchial responsiveness in man. In the present study we have tested the hypothesis that the smoking of a single cigarette increases bronchial responsiveness.