Handgrip-induced airway dilation in asthmatic patients with bronchoconstriction induced by MCh inhalation

Author:

Fontana Giovanni A.1,Pantaleo Tito2,Lavorini Federico1,Bongianni Fulvia2,Mannelli Massimo3,Bridge Peter D.4,Pistolesi Massimo1

Affiliation:

1. Dipartimento di Area Critica Medico Chirurgica,

2. Scienze Fisiologiche, and

3. Fisiopatologia Clinica, Università degli Studi di Firenze, I-50134 Florence, Italy; and

4. Department of Respiratory Paediatrics, Barts and The London NHS Trust, London E1 1BB, United Kingdom

Abstract

We investigated the effects of static and rhythmic handgrip on the time course of recovery of airway resistance measured with the interrupter technique (Rint) following bronchoconstriction induced by methacholine (MCh) inhalation in 17 asthmatic patients. On three separate occasions, a 100 ± 5% increase in baseline Rint was induced by MCh inhalation. Subsequently, patients either rested [control trials (CTs)] or performed 3-min bouts of static or rhythmic handgrip. Respiratory and cardiovascular variables were continuously monitored. Rint changes were assessed at 1-min intervals for 30 min after rest and both types of handgrip. Plasma catecholamine concentrations were also determined at scheduled intervals. Bronchoconstriction increased ventilation ( P < 0.01) but did not affect cardiovascular variables and plasma catecholamine concentrations. Handgrip provoked an increase in cardiovascular variables ( P < 0.01) and plasma norepinephrine concentrations ( P < 0.05) but caused no additional changes in ventilation. Rint only partially recovered within 30 min after CTs, whereas it consistently decreased 1 min after both handgrip paradigms and remained lower than after CTs ( Palways <0.01) for the whole 30-min observation period. Sympathetic activation and withdrawal of cholinergic input to the airway smooth muscle reflexly induced by activation of skeletal muscle and carotid sinus receptors may be the primary events accounting for the bronchodilator response induced by handgrip. Mediators co-released in response to sympathetic activation may also have contributed.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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