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Search: WFRF:(Devereux Graham) > Tufvesson Ellen

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1.
  • Bolger, Claire, et al. (author)
  • Hyperpnea-Induced Bronchoconstriction and Urinary CC16 Levels in Athletes
  • 2011
  • In: Medicine & Science in Sports & Exercise. - 1530-0315. ; 43:7, s. 1207-1213
  • Journal article (peer-reviewed)abstract
    • BOLGER, C., E. TUFVESSON, M. SUE-CHU, G. DEVEREUX, J. G. AYRES, L. BJERMER, and P. KIPPELEN. Hyperpnea-Induced Bronchoconstriction and Urinary CC16 Levels in Athletes. Med. Sci. Sports Exerc., Vol. 43, No. 7, pp. 1207-1213, 2011. Purpose: Exercise-induced bronchoconstriction (EIB) is a common condition in both individuals with asthma and otherwise healthy elite athletes. Although excessive water loss by peripheral airways during hyperpnea is regarded as the initial trigger for EIB, the cascade of events that follows remains unclear. Our goal was to establish whether transient disruption of the airway epithelial barrier occurs after a short period of hyperpnea of dry air in athletes with EIB. Methods: Urinary concentration of the pneumoprotein Clara cell (CC16) was used as an assumed biomarker of lung epithelial cell damage or dysfunction. Samples were collected at baseline and for 90 min after an 8-min eucapnic voluntary hyperpnea (EVH) test in 50 female individuals (28 athletes and 22 untrained). Results: Nineteen subjects (10 athletes) demonstrated a sustained bronchoconstriction after EVH (mean +/- SE forced expiratory volume in the first second (FEV1) fall from baseline = 23.4% +/- 2.6%). The remaining subjects had a negative challenge result with an FEV1 fall of 5.9% +/- 0.6%. An increase (P < 0.001) in urinary CC16 concentration was noticed after EVH in all but one subject, with no group difference (median CC16 increase before to after challenge: athletes EVH- 0.083 ng.mu mol(-1), athletes EVH+ 0.223 ng.mu mol(-1), untrained EVH- 0.074 ng.mu mol(-1), untrained EVH+ 0.571 ng.mu mol(-1); P > 0.05). Conclusions: Urinary levels of CC16 are increased after EVH in all individuals (trained and untrained, with and without EIB) suggestive of dehydration-induced perturbation of the distal respiratory epithelium during episodes of hyperventilation.
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2.
  • Bolger, Claire, et al. (author)
  • Urinary cc16 levels in winter versus summer sport athletes after eucapnic voluntary hyperpnoea
  • 2009
  • Conference paper (peer-reviewed)abstract
    • Exercise induced bronchoconstriction (EIB) is highly prevalent in elite athletes, especially in those training in cold dry environments. Dehydration of the airways plays a key role in this process. EIB has recently been linked to airway epithelial injury in asthmatic individuals. The aim of the study is to determine whether a short period of hyperpnoea of dry air causes airway epithelial disruption in winter and/or summer sport athletes. We hypothesise that urinary level of the Clara cell protein (CC16) – an indirect marker of permeability/cellular integrity of the lung epithelial barrier – will be increased after a eucapnic voluntary hyperpnoea (EVH) test and that this increase will be larger in winter compared to summer athletes. Forty two female athletes – 28 summer athletes (age 31.1+/-1.7yr (SEM), training volume 9+/-1.1h/wk) and 14 winter athletes (age 21.4+/-0.8yr, training volume 12.0 ± 1.10h/wk) – took part in this study. They all performed an 8-min EVH test at a target ventilation rate of 30 times their baseline forced expiratory volume in one second (FEV1). After the challenge, FEV1 was measured in duplicate at 2, 5, 10, 15, 20, 30, 60 and 90min. A sustained decrease in FEV1 of at least 10% from baseline was considered positive. Urine samples were collected at baseline and at 30, 60 and 90min recovery. CC16 concentration was measured by enzyme immunoassay. Ten summer athletes had a positive test (max FEV1 fall = 19.6+/-2.4%), whilst eighteen of the summer athletes and all the winter athletes were negative (max FEV1 fall = 5.7+/-0.7% and 5.3+/-0.7%, respectively). CC16 increased significantly after the challenge in all three groups (P<0.01) with no difference between groups: delta CC16 (max post-EVH minus baseline) in summer EVH negative athletes was 0.241+/-0.1 ng/μmol creatinine, 0.292+/-0.085 ng/μmol creatinine in summer EVH positive athletes, and 0.123+/-0.047ng/μmol creatinine in winter EVH negative athletes (P=0.415)In conclusion, a short period of hyperpnoea of dry air is associated with an increased rate of CC16 excretion in urine in both winter and summer athletes. This suggests that the integrity of the airway epithelium might be compromised by loss of airway surface lining fluid when athletes inhale dry air at high flow rates. This appears to occur irrespective of the degree of bronchoconstriction or regular training environment.
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