Acute effects of inspiratory pressure threshold loading upon airway resistance in people with asthma

https://doi.org/10.1016/j.resp.2009.03.003Get rights and content

Abstract

Large inspiratory pressures may impart stretch to airway smooth muscle and modify the response to deep inspiration (DI) in asthmatics. Respiratory system resistance (Rrs) was assessed in response to 5 inspiratory manoeuvres using the forced oscillation technique: (a) single unloaded DI; (b) single DI at 25 cmH2O; (c) single DI at 50% maximum inspiratory mouth pressure [MIP]; (d) 30 DIs at 50% MIP; and (e) 30 DIs at 50% MIP with maintenance of normocapnia. Rrs increased after the unloaded DI and the DI at 25 cmH2O but not after a DI at 50% MIP (3.6 ± 1.6 hPa L s−1 vs. 3.6 ± 1.5 hPa L s−1; p = 0.95), 30 DIs at 50% MIP (3.9 ± 1.5 hPa L s−1 vs. 4.2 ± 2.0 hPa L s−1; p = 0.16) or 30 DIs at 50% MIP under normocapnic conditions (3.9 ± 1.5 hPa L s−1 vs. 3.9 ± 1.5 hPa L s−1; p = 0.55). Increases in Rrs in response to DI were attenuated after single and multiple loaded breaths at 50% MIP.

Introduction

The ability of a deep inspiration (DI) to modify lower airway calibre has been known for a number of years. Nadel and Tierney (1961) were the first to demonstrate a marked decrease in airway resistance (bronchodilation) in healthy subjects after a DI during a period of induced bronchoconstriction. They suggested that increased stretching of airway smooth muscle, caused by greater transluminal airway pressures, induced a change in the airway lumen diameter. The response to DI in people with asthma differs from that of healthy people. Typically, in people with asthma, DI results in either a diminished or absent bronchodilation or even an increase in airway resistance (Kapsali et al., 2000, Brown et al., 2001, Salome et al., 2003). The bronchoconstriction seen after DI may be explained by changes in the excitation–contraction mechanism of the airway smooth muscle (Fredberg et al., 1997). Slowly cycling cross bridges may become ‘latched’, stiffer and possess low hysteresis. Under such conditions the airway is less responsive to stretch and, if airway hysteresis is low relative to parenchymal hysteresis, further airway narrowing after DI is likely (Burns et al., 1985).

Another factor that may contribute to the magnitude of airway re-narrowing after a DI is the extent to which the airway dilates in response to the pressure generated by DI. In support of this Jensen et al. (2001) demonstrated that not only did the airways of patients with asthma dilate less after DI, they also re-narrowed more. It has previously been proposed that the opening of narrowed airways in people with asthma may require negative pressures in excess of those generated by DI (Gunst et al., 1988). Recently it has been demonstrated that positive pressure inflation is able to reduce airway obstruction in asthma patients who are unable to do so with an active DI (Slats et al., 2008). The authors suggest that the positive pressures may have applied a greater stretching force on the airway than that which could be achieved under physiological conditions (Slats et al., 2008).

An alternative method of increasing airway stretch may be to breathe against an inertial inspiratory load, which may lead to a temporal dislocation between intra-airway pressure and pleural pressure as the inertial load is overcome. Studies of pressure threshold inspiratory muscle training have observed improvements in FEV1 (Weiner et al., 1992) and peak expiratory flow rate post-IMT (Lima et al., 2008). In addition, medication usage has been shown to reduce, suggesting an improvement in the severity of disease per se (Weiner et al., 2002). These data are therefore consistent with the notion that pressure threshold loading may impart a unique stretching stimulus to the airway. If this is the case, acute inspiratory loading may modify the bronchoconstrictor response to DI in people with asthma.

The aim of this study was to determine the acute effect of DI and various inspiratory loads upon respiratory system resistance (Rrs) in people with moderate asthma. We hypothesised that inspiratory loading, combined with DI would elicit either no change, or an acute decrease in Rrs.

Section snippets

Participants

After local ethics committee approval and written informed consent, 9 non-smoking adults (1 female) with a physician diagnosis of asthma and a history of respiratory complications volunteered to participate in the study. Participants were being prescribed with medication to control their asthma symptoms. All of the participants demonstrated an obstructive ventilatory defect as defined by a reduced FEV1/FVC ratio below the 5th percentile of the predicted value (Pellegrino et al., 2005).

Baseline respiratory system resistance and response to acute inspiratory loading

Repeated-measures ANOVA revealed no significant between-trial differences in baseline Rrs. Test–retest reliability revealed an intraclass correlation coefficient of 0.87 (95% likely range: 0.71–0.96). Rrs increased by 15.7 ± 11.0% in response to DI (3.7 ± 1.8 hPa L s−1 vs. 4.2 ± 1.7 hPa L s−1; p = 0.016) and 20.8 ± 26.1% in response to a single inspiration at 25 cmH2O (3.5 ± 1.7 hPa L s−1 vs. 4.0 ± 1.5 hPa L s−1; p = 0.03). No increase was observed in response to a single inspiration at 50% MIP (3.6 ± 1.6 hPa L s−1 vs. 3.6 ± 1.5 

Discussion

The finding of increased Rrs after DI agrees with previous studies in people with asthma (Brown et al., 2001, Salome et al., 2003). The attenuation of this response, seen after both a single loaded breath at 50% MIP and 30 loaded breaths at 50% MIP, is new. Furthermore, the magnitude of the latter response appears to be modulated by changes in airway carbon dioxide during loaded breathing. The attenuated response to DI was not seen during a single breath at 25 cmH2O. These data confirm our

References (31)

  • A. Bruton et al.

    Hypocapnia and asthma: a mechanism for breathing retraining?

    Chest

    (2005)
  • G.P. Burns et al.

    The apparent response of airway function to deep inspiration depends on the method of assessment

    Respir. Med.

    (2001)
  • P. Weiner et al.

    Inspiratory muscle training in patients with bronchial asthma

    Chest

    (1992)
  • W.A. Briscoe et al.

    The relationship between airway resistance, airway conductance and lung volume in subjects of different age and body size

    J. Clin. Invest.

    (1958)
  • N.J. Brown et al.

    Airway distensibility in adults with asthma and healthy adults, measured by forced oscillation technique

    Am. J. Respir. Crit. Care Med.

    (2007)
  • R.H. Brown et al.

    Airway response to deep inspiration: role of inflation pressure

    J. Appl. Physiol.

    (2001)
  • R.H. Brown et al.

    High-resolution computed tomographic evaluation of airway distensibility and the effects of lung inflation on airway caliber in healthy subjects and individuals with asthma

    Am. J. Respir. Crit. Care Med.

    (2001)
  • C.B. Burns et al.

    Effects of deep inhalation in asthma: relative airway and parenchymal hysteresis

    J. Appl. Physiol.

    (1985)
  • G.P. Burns et al.

    A novel hypothesis to explain the bronchconstrictor effect of deep inspiration in asthma

    Thorax

    (2002)
  • M.P. Caine et al.

    Development and evaluation of a pressure threshold inspiratory muscle trainer for use in the context of sports performance

    J. Sp. Eng.

    (2000)
  • C.J. Duggan et al.

    Bronchodilatation induced by deep breaths in relation to transpulmonary pressure and lung volume

    Thorax

    (1990)
  • J.J. Fredberg et al.

    Airway smooth muscle, tidal stretches, and dynamically determined contractile states

    Am. J. Respir. Crit. Care Med.

    (1997)
  • J.J. Fredberg et al.

    Perturbed equilibrium of myosin binding in airway smooth muscle and its implications in bronchospasm

    Am. J. Respir. Crit. Care Med.

    (1999)
  • M. Green et al.

    Tests of respiratory muscle strength

    Am. J. Respir. Crit. Care Med.

    (2002)
  • S.J. Gunst et al.

    Parenchymal interdependence and airway response to methacholine in excised dog lobes

    J. Appl. Physiol.

    (1988)
  • Cited by (7)

    • Technical standards for respiratory oscillometry

      2020, European Respiratory Journal
    View all citing articles on Scopus
    View full text