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Exercise increases sulfur dioxide-induced bronchoconstriction in asthmatic subjects.

Research paper by D D Sheppard, A A Saisho, J A JA Nadel, H A HA Boushey

Indexed on: 01 May '81Published on: 01 May '81Published in: The American review of respiratory disease



Abstract

We undertook a study to determine whether moderate exercise modifies the bronchoconstriction produced by sulfur dioxide (SO2) in subjects with mild asthma. In 7 subjects, we compared the changes in specific airway resistance (SRaw) produced by 10 min of exercise alone (400 kpm/min on a cycle ergometer), inhalation of SO2 alone, and the combination of exercise and SO2. During all studies, a subject breathed SO2 and/or air from a mouthpiece. In 6 additional subjects, we compared the increase in SRaw produced by inhalation of SO2 during exercise with that produced by eucapnic hyperventilation with SO2. Neither inhalation of 0.05 ppm of SO2 at rest nor exercise or hyperventilation alone had any effect on SRaw. Inhalation of SO2 during exercise, however, significantly increased SRaw (from 8.46 +/- 3.58 L x cm H2O/L/s (mean +/- SD) to 18.16 +/- 10.05 at 0.05 ppm and from 8.07 +/- 2.69 to 10.48 +/- 4.49 at 0.25 ppm (p less than 0.05)). In the 2 most responsive subjects, inhalation of 0.10 ppm of SO2 during exercise also significantly increased SRaw. The SRaw increased by the same amount whether SO2 was inhaled during exercise or during eucapnic hyperventilation at the same minute ventilation, but the time course of the increase in SRaw was different. The SRaw was at or near maximal values at the first measurement (30 s) after hyperventilation but not until 2 to 4 min after exercise. When 4 subjects took larger breaths after inhaling SO2 during eucapnic hyperventilation to more closely match the volume of the breaths taken after exercise, the time courses of SO2-induced bronchoconstriction after hyperventilation and after exercise were nearly identical. These results suggested that exercise increases the bronchoconstriction produced by a given concentration of SO2 in subjects with asthma by increasing the minute volume of ventilation and that the delay in bronchoconstriction after exercise is due to the large tidal volumes that persist for some minutes during recovery.