Handgrip-induced airway dilation in XXXX @entity1 with bronchoconstriction induced by MCh inhalation.

@entity748 @entity1 @entity2922 @entity1063 @entity2710 @entity17695
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 @entity2710 ( @entity17695 ) inhalation in 17 @entity748 @entity1 . On three separate occasions, a 100 +/- 5% increase in baseline Rint was induced by MCh inhalation. Subsequently, @entity1 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 @entity2922 concentrations were also determined at scheduled intervals. Bronchoconstriction increased ventilation (P < 0.01) but did not affect cardiovascular variables and plasma @entity2922 concentrations. Handgrip provoked an increase in cardiovascular variables (P < 0.01) and plasma @entity1063 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 (P always <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.
