Background Children with uncontrolled asthma are less tolerant to exercise due to ventilatory limitation, exercise-induced bronchoconstriction (EIB), or physical deconditioning. The contribution of these factors in children with controlled mild-to-moderate asthma is unknown. Objective To explore the underlying mechanisms of reduced exercise capacity in children with controlled mild-to-moderate asthma. Methods This was a cross-sectional study of 45 children and adolescents (age 8–18 years) with controlled mild-to-moderate asthma (asthma control test score 21–25) and 61 age-matched healthy controls. All participants completed a physical activity questionnaire and performed spirometry and cardiopulmonary exercise testing (CPET; maximal incremental protocol). Spirometric indices and CPET parameters were compared between the two groups. The effect of EIB (FEV 1 decrease >10% post CPET), ventilatory limitation and physical deconditioning on maximum oxygen uptake ( O 2 peak), was assessed by multivariable linear regression. Results 62.2% of children with asthma and 29.5% of controls (P = 0.002) were categorized as inactive. Reduced exercise capacity ( O 2 peak <80%) was noted in 53.3% of asthmatics and 16.4% of controls (P < 0.001). EIB was documented in 11.1% of participants with asthma. Physical deconditioning was noted in 37.8% of children with asthma and in 14.8% of controls (P = 0.013). Physical deconditioning emerged as the only significant determinant of O 2 peak, irrespective of asthma diagnosis, body mass index, ventilatory limitation and EIB. Conclusion Children with controlled mild-to-moderate asthma are less tolerant to strenuous exercise than their healthy peers. The decreased exercise capacity in this population should mainly be attributed to physical deconditioning, while the contribution of ventilatory limitation and EIB is rather small.

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BackgroundVolumetric capnography (VCap) is a simpler alternative of multiple-breath washout (MBW) to detect ventilation inhomogeneity (VI) in patients with cystic fibrosis (CF). However, its diagnostic performance is influenced by breathing dynamics. We introduce two novel VCap indices, the Capnographic Inhomogeneity Indices (CIIs) that may overcome this limitation and explore their diagnostic characteristics in a cohort of CF patients.MethodsWe analysed 320 N2-MBW trials from 50 CF patients and 65 controls (age 4-18 years) and calculated classical VCap indices, such as slope III (SIII) and the capnographic index (KPIv). We introduced novel CIIs based on a theoretical lung model, and assessed their diagnostic performance compared to classical VCap indices and the lung clearance index (LCI).ResultsBoth CIIs were significantly higher in CF patients compared with controls (mean±SD CII1 5.9±1.4% versus 5.1±1.0%, p=0.002; CII2 7.7±1.8% versus 6.8±1.4%, p=0.002) and presented strong correlation with LCI (CII1 R2=0.47 and CII2 R2=0.44 in CF patients). Classical VCap indices showed inferior discriminative ability (SIII 2.3±1.0%/L versus 1.9±0.7%/L, P=0.013; KPIv 3.9±1.3% versus 3.5±1.2%, P=0.071), while the correlation with LCI was weak (SIII R2=0.03; KPIv R2=0.08 in CF patients). CIIs showed lower intra-subject inter-trial variability, calculated as coefficient of variation for three and relative difference for two trials, than classical VCap indices, but higher than LCI (CII1 11.1±8.2% and CII2 11.0±8.0% versus SIII 16.3±13.5%; KPIv 15.9±12.8%; LCI 5.9%±4.2%).ConclusionCIIs detect VI better than classical VCap indices and correlate well with LCI. However, further studies on their diagnostic performance and clinical utility are required.

Chronic periodontitis and chronic obstructive pulmonary disease (COPD) are chronic inlammatory diseases in which neutrophilic inlammation plays a major role. There are a few studies showing that these two entities share various predisposing factors and pathogenetic mechanisms; however, a direct connection between them has not yet been achieved. Epidemiology data may also show a connection between the two conditions. Neutrophilic inlammation in periodontitis and COPD is orchestrated by CD8+ lymphocytes and macrophages, leading to the aggregation of neutrophils and causing an imbalance to the proteases and antiproteases equilibrium. Finally, further research is needed to clarify the common pathogenesis of the two diseases to optimize their therapeutic management.

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