BACKGROUND: This study investigated whether the inspiratory muscles are susceptible to fatigue during acute airway narrowing because of increased airway resistance and hyperinflation. METHODS: Asthmatic subjects performed up to four series (on separate days) of 18 maximal static inspiratory efforts of 10 seconds' duration with 10 second rest intervals (50% duty cycle; total duration six minutes): at functional residual capacity (FRC) (control); after histamine induced bronchoconstriction, which decreased forced expiratory volume in one second (FEV1) to a mean of 55% (SD 11%) of the initial value; at a voluntarily increased lung volume (initial volume held at 140% control); and after inhalation of histamine at a voluntarily increased lung volume. RESULTS: For the group of subjects the mean (SD) maximal inspiratory pressure (MIP) in the control experiments was 114 (22) cmH2O and the initial volume was 3.5 (1.2) 1. After histamine inhalation the initial lung volume for contractions increased to 118% (5%) of the control volume. In the high lung volume experiments initial volumes were 140% (12%) of the control (volume without histamine) and 140% (15%) (with histamine). The relation between MIP and initial absolute lung volume was determined for each subject before fatigue developed. When the inspiratory pressures for each contraction in the endurance test were normalised to the pressure expected for that lung volume, no significant differences were found between the four experimental conditions for MIP, or between pressures sustained over the 18 contractions. CONCLUSIONS: Histamine induced bronchoconstriction and hyperinflation had no detectable effect on inspiratory muscle strength or endurance in these asthmatic subjects.
BACKGROUND: This study investigated whether the inspiratory muscles are susceptible to fatigue during acute airway narrowing because of increased airway resistance and hyperinflation. METHODS: Asthmatic subjects performed up to four series (on separate days) of 18 maximal static inspiratory efforts of 10 seconds' duration with 10 second rest intervals (50% duty cycle; total duration six minutes): at functional residual capacity (FRC) (control); after histamine induced bronchoconstriction, which decreased forced expiratory volume in one second (FEV1) to a mean of 55% (SD 11%) of the initial value; at a voluntarily increased lung volume (initial volume held at 140% control); and after inhalation of histamine at a voluntarily increased lung volume. RESULTS: For the group of subjects the mean (SD) maximal inspiratory pressure (MIP) in the control experiments was 114 (22) cmH2O and the initial volume was 3.5 (1.2) 1. After histamine inhalation the initial lung volume for contractions increased to 118% (5%) of the control volume. In the high lung volume experiments initial volumes were 140% (12%) of the control (volume without histamine) and 140% (15%) (with histamine). The relation between MIP and initial absolute lung volume was determined for each subject before fatigue developed. When the inspiratory pressures for each contraction in the endurance test were normalised to the pressure expected for that lung volume, no significant differences were found between the four experimental conditions for MIP, or between pressures sustained over the 18 contractions. CONCLUSIONS:Histamine induced bronchoconstriction and hyperinflation had no detectable effect on inspiratory muscle strength or endurance in these asthmatic subjects.