Effect of Albuterol on Maximal Exercise Capacity in Cystic Fibrosis

Serisier, David J.; Coates, Andrew; Bowler, Simon

doi:10.1378/chest.06-1697

Cited by 17 publications

(5 citation statements)

References 35 publications

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“…In the present study, acute intravenous salbutamol had no eVects on muscle strength. However, other studies showed a slight improvement in muscle strength after oral salbutamol (van Baak et al 2000) and a greater improvement during chronic use of salbutamol in healthy subjects (Yang and McElligott 1989;Martineau et al 1992) or patients Murphy et al 1999b;Caruso et al 2005;Serisier et al 2007). Interestingly, both type I and II muscle Wbre types showed increased contractility and hypertrophic response after chronic 2 agonist administration (Dodd et al 1996;Ryall et al 2004;Bard et al 2006;Lynch and Ryall 2008).…”

Section: Discussionmentioning

confidence: 93%

Effects of β2-adrenergic stimulation on exercise capacity in normal subjects

et al. 2011

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β2-Adrenergic receptor agonists are believed to present with ergogenic properties. However, how combined respiratory, cardiovascular and muscular effects of these drugs might affect exercise capacity remain incompletely understood. The effects of salbutamol were investigated in 23 healthy subjects. The study was randomised, placebo-controlled in double-blind and followed a cross-over design. Salbutamol was given at the dose of 10 μg/min in 11 subjects and 20 μg/min iv in the other 12 subjects. Measurements included muscle sympathetic nerve activity (MSNA), ventilatory responses to hyperoxic hypercapnia (7% CO(2) in O(2,) central chemoreflex), isocapnic hypoxia (10% O(2) in N(2), peripheral chemoreflex) and isometric muscle contraction followed by a local circulatory arrest (metaboreflex), cardiopulmonary exercise test (CPET) variables and isokinetic muscle strength. Salbutamol 10 μg/min increased heart rate and blood pressure, while MSNA burst frequency remained unchanged. Peripheral chemosensitivity increased, as evidenced by an increased ventilatory response to hypoxia, but ventilatory responses to hypercapnia or muscle ischaemia remained unchanged. The effects of salbutamol 20 μg/min were similar. Both doses of salbutamol did not affect CPET. Only the higher dose of salbutamol decreased the anaerobic threshold, but this was not associated with a change in VO(2) max. Salbutamol increased the slopes of ventilation as a function of VO(2) (P < 0.05) and VCO(2) (P < 0.001) during CPET. Maximal isokinetic muscle strength was not affected by salbutamol. In conclusion, the acute administration of either low or high dose salbutamol does not affect exercise capacity in normal subjects, in spite of an earlier anaerobic threshold and increased chemosensitivity.

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Section: Discussionmentioning

confidence: 93%

Effects of β2-adrenergic stimulation on exercise capacity in normal subjects

et al. 2011

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“…Eggleston et al attempted to evaluate how responses to bronchial provocation testing with methacholine related to the medium‐term effects of treatment with albuterol, finding that 4 weeks of bronchodilator treatment lead to an increased PEFR compared with placebo only among those patients with bronchial hyperresponsiveness. Conversely, no relationship was found between responses to histamine, and treatment outcomes in a short‐term study of adult CF patients …”

Section: Asthma Therapy In Cfmentioning

confidence: 91%

“…Trials of short‐acting B‐agonists have demonstrated a beneficial short‐term effect on lung function, with salbutamol (or albuterol) generally being found to increase FEV 1 , particularly when administered more than once a day . However, these improvements in lung function did not necessarily correlate with improvements in functional status or exercise capacity . Eggleston et al attempted to evaluate how responses to bronchial provocation testing with methacholine related to the medium‐term effects of treatment with albuterol, finding that 4 weeks of bronchodilator treatment lead to an increased PEFR compared with placebo only among those patients with bronchial hyperresponsiveness.…”

Section: Asthma Therapy In Cfmentioning

confidence: 99%

Asthma and cystic fibrosis: A tangled web

Kent

Lane

Beek

et al. 2014

Pediatric Pulmonology

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Successfully diagnosing concomitant asthma in people with cystic fibrosis (CF) is a challenging proposition, and the utility of conventional diagnostic criteria of asthma in CF populations remains uncertain. Nonetheless, the accurate identification of individuals with CF and asthma allows appropriate tailoring of therapy, and should reduce the unnecessary use of asthma medication in broader CF cohorts. In this review, we discuss the diagnostic challenge posed by asthma in CF, both in terms of clinical evaluation, and of interpretation of pulmonary function testing and non-invasive markers of airway inflammation. We also examine how the role of cross-sectional thoracic imaging in CF and asthma can assist in the diagnosis of asthma in these patients. Finally, we critically appraise the evidence base behind the use of asthma medications in CF populations, with a particular focus on the use of inhaled corticosteroids and bronchodilators. As shall be discussed, the gaps in the current literature make further high-quality research in this field imperative.

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“…One of the proposed mechanisms by which virus infections limit the action of b 2 -agonists is via the production of mucus [69]. While it is possible that increased mucus in the airway lumen following virus infection could impair b 2 -agonist efficacy by reducing the amount of drug reaching the smooth muscle, b 2 -agonists have clinical benefit in respiratory diseases with abnormal mucus production such as cystic fibrosis [70,71] and COPD [72]. It is therefore likely that viral infection of the airway may affect the inherent ability of the airway smooth muscle to respond to b 2 -agonists.…”

Section: Do Respiratory Viral Infections Reduce B 2 -Agonist Efficacy?mentioning

confidence: 99%

Viral infections and asthma: an inflammatory interface?

et al. 2014

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Asthma is a chronic inflammatory disease of the airways in which the majority of patients respond to treatment with corticosteroids and b 2 -adrenoceptor agonists. Acute exacerbations of asthma substantially contribute to disease morbidity, mortality and healthcare costs, and are not restricted to patients who are not compliant with their treatment regimens. Given that respiratory viral infections are the principal cause of asthma exacerbations, this review article will explore the relationship between viral infections and asthma, and will put forward hypotheses as to why virus-induced exacerbations occur. Potential mechanisms that may explain why current therapeutics do not fully inhibit virus-induced exacerbations, for example, b 2 -adrenergic desensitisation and corticosteroid insensitivity, are explored, as well as which aspects of virus-induced inflammation are likely to be attenuated by current therapy. @ERSpublications Why do virus-induced asthma exacerbations occur? Mechanisms and interventions

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Effect of Albuterol on Maximal Exercise Capacity in Cystic Fibrosis

Cited by 17 publications

References 35 publications

Effects of β2-adrenergic stimulation on exercise capacity in normal subjects

Effects of β2-adrenergic stimulation on exercise capacity in normal subjects

Asthma and cystic fibrosis: A tangled web

Viral infections and asthma: an inflammatory interface?

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