Exercise is known to affect the airway epithelium through dehydration, followed by a release of mediators, such as club cell (Clara) protein (CC16). The aim of this study was to follow the CC16 levels at repeated time points in plasma and urine after exercise in asthmatic subjects and controls, and to relate the findings to exhaled breath temperature (EBT) and exhaled nitric oxide (NO). Twenty-two asthmatics and 18 healthy subjects performed an exercise challenge test on a treadmill. Lung function, CC16 in plasma and urine, EBT and fractional exhaled NO were investigated before and repeatedly for 60 min after the exercise. The increase in CC16 concentration in plasma was seen already one minute after exercise (p < 0.001) and increased further after 20 (p = 0.009) until 60 min (p = 0.001). An increase in urinary levels of CC16 peaked after 30 min (p < 0.001), and declined after 60 min but were still higher than baseline (p = 0.002). There were no differences in plasma or urine CC16 levels between asthmatics and controls, but males had higher plasma levels compared to females (p < 0.001) at all time points. EBT peaked at 15 min (p < 0.001) and thereafter declined, and FENO50 (p < 0.0001), alveolar NO concentration (p = 0.049) and bronchial flux of NO (p = 0.0055) decreased after exercise. In conclusion, this study shows that CC16 in plasma increased during 60 min after exercise, not synchronized with CC16 levels in urine. CC16 levels in plasma correlated to EBT and exhaled NO, reflecting an overall epithelial involvement. There was no difference between asthmatics and healthy controls, showing a physiological rather than pathophysiological response.
<b><i>Background:</i></b> Exhaled breath temperature (EBT) has been suggested as a marker of airway inflammation in asthma. <b><i>Objectives:</i></b> The aim of the present study was to investigate EBT in asthmatic subjects compared to healthy controls after an exercise challenge test, and in subjects with exercise-induced bronchoconstriction compared to subjects without, and to compare with body temperatures. <b><i>Methods:</i></b> A total of 21 healthy controls and 20 asthmatics were included. Forced expiratory volume in 1 s (FEV<sub>1</sub>), EBT and oral, axillary and auricular temperatures were measured before and after an exercise challenge test. <b><i>Results:</i></b> FEV<sub>1</sub> % predicted (%p) was significantly lower in asthmatic subjects compared to healthy controls at all time points after exercise. The largest drop in FEV<sub>1</sub>%p correlated with EBT after 5 min. EBT increased markedly 5 min after exercise and remained high for at least 60 min. In asthmatics whose FEV<sub>1</sub> dropped by >10%, EBT was higher after 60 min compared to the remaining asthmatics. EBT correlated with oral temperature at all time points after exercise, with axillary temperature only at 15, 30 and 60 min, and not at all with auricular temperature. <b><i>Conclusions:</i></b> EBT is increased after exercise, and elevated EBT correlated with a drop in FEV<sub>1</sub>%p. The immediate increase in EBT did not differ between asthmatics and controls but remained elevated in the asthmatics whose FEV<sub>1</sub> dropped by >10%, indicating a different vascular response.
Background: It has been suggested that exhaled breath temperature (EBT) is increased in asthmatic subjects. Objectives: Our aim was to investigate EBT in asthmatics compared to healthy controls before and after eucapnic voluntary hyperventilation (EVH) and a methacholine challenge test (MCT). Methods: A total of 26 asthmatics and 29 healthy controls were included. Forced expiratory volume in 1 s (FEV1), EBT and oral, axillary and auricular temperatures were measured before and after EVH and MCT. Results: FEV1 % predicted (%p) was significantly lower in asthmatic subjects compared to healthy controls at all time points. EBT was significantly increased in all subjects 15-30 min after EVH and 5-45 min after MCT. Oral temperature displayed a similar pattern of increase, in contrast to axillary and auricular temperature, and correlated with EBT before and after both of the challenge tests. EBT after 5 min correlated with the largest drop in FEV1%p after EVH in asthmatic subjects. No significant differences or changes in EBT were found when comparing asthmatics to healthy controls before or after any of the tests. Conclusions: EBT is increased after both EVH and MCT, possibly reflecting a vascular response. This is related to both the fall in FEV1 and to oral temperature, suggesting an effect on the whole respiratory tract including the oral cavity. No differences in EBT are seen between asthmatics and healthy controls, indicating that the increase in EBT is mainly physiological rather than pathophysiological.
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