1. To examine the effect of lung inflammation on lung volumes and carbon monoxide transfer and their relationship to the ventilatory and gas exchange responses to exercise, a prospective study was performed in patients having Hodgkin's disease, with no evidence of intrathoracic involvement, who received prophylactic mantle-field radiotherapy to the chest.

2. From 6 weeks to 6 months from the start of therapy, vital capacity (FVC) was on average 10.4% lower than during the baseline period and the total transfer of carbon monoxide (TLCO) was 10.5% lower. Minute ventilation (V̇E) at any given work load during an incremental exercise test was on average 10.5% higher than baseline. The stimulation of ventilation after radiotherapy was present at all work rates, but greater at high work rates.

3. A number of other changes in the ventilatory and gas exchange responses to exercise were also seen. Most of these lay outside the range of variability observed in a group of normal subjects tested concurrently with the patients.

4. There was a poor, but statistically significant, positive correlation between reduction in FVC and increase in V̇E after radiotherapy and between reduction in carbon monoxide transfer and increase in V̇E.

5. A significant correlation between reduction in FVC and change in respiratory rate was also seen after radiotherapy, together with a significant inverse correlation between increase in respiratory rate and fall in tidal volume.

6. The ratio of V̇E to oxygen consumption, the ventilatory equivalent for oxygen, was calculated at each work rate. There was a negative correlation between the mean increase in this parameter, averaged over all work rates, and the reduction in FVC and TLCO, i.e. the greatest stimulation of breathing relative to metabolic demand occurred in those patients with the least change in lung volume.

7. In the period after 6 months lung volumes and carbon monoxide transfer fell further, or remained the same, but V̇E returned towards pretreatment levels.

8. It is suggested that changes in ventilatory response to work after lung inflammation, are the result of a balance between an increased drive to breathe and changes in the mechanical properties of the lungs.

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