Carmo Palmares

Differential responses of adiposity, inflammation and autonomic function to aerobic versus resistance training in older adults

BACKGROUND Increased body fat, autonomic dysfunction and low-grade chronic inflammation are interrelated risk factors implicated in the etiology of several chronic conditions normally presented by older adults. OBJECTIVE This study aims to assess the effectiveness of different training protocols on reducing body fat, improving autonomic function, and decreasing low-grade systemic inflammation in community-dwelling elderly adults. METHODS Fifty participants (11 men, 68±5.5years) were randomly allocated into resistance or aerobic training or control groups. Evaluations were done at baseline and following the 8-month intervention period on their body composition (assessed by DXA), inflammatory biomarkers (high-sensitivity C-reactive protein [hs-CRP], tumor necrosis-alpha [TNF-α], interferon-gamma [IFN-γ], interleukins-6 and -10 [IL-6, IL-10]), lipoproteic profile, fasting glycemia, blood pressure, heart rate variability (HRV; frequency and time domains) and aerobic fitness (assessed by six-minute walk distance [6MWD]). A paired t-test was used to detect changes (%Δ=[(post-test score-pretest score)/pre-test score]×100) within groups, while between-group differences were analyzed using the one-way ANOVA or General Linear Models. RESULTS A significant change (Δ%) both in total (-5.4±6.3% and -3.3±2.9%, respectively) and central body fat (8.9±11.3% and -4.8±4.5%) was observed in resistance and aerobic training groups, respectively; along with a change in resting systolic and diastolic blood pressures (-9.2±9.8% and -8.5±9.6%), heart rate (-4.6±6.5%), hs-CRP (-18.6±60.6%), and 6MWD (9.5±6.9%) in response to aerobic training. CONCLUSIONS The present findings provide further evidence for the benefits of aerobic and resistance training on reducing body fat. Aerobic training was demonstrated to reduce hs-CRP and blood pressure in community-dwelling elderly participants with no serious medical conditions.

Substance P antagonist improves both obesity and asthma in a mouse model

Evidence suggests a causal relationship between obesity and asthma; however, the underlying mechanisms remain unknown. Substance P (SP), involved in neurogenic inflammation by acting through its receptor NK1‐R, seems to participate in obese–asthma phenotype in mice.

Increased circulating platelet microparticles as a potential biomarker in asthma.

Endothelial (EMPs) and platelet microparticles (PMPs) have been studied as biomarkers in several inflammatory diseases and as central players in intercellular communication.

Competitive swimmers with allergic asthma show a mixed type of airway inflammation

To the Editors: Elite swimmers are at increased risk of asthma 1. This has been attributed to airway inflammation and increased airway responsiveness induced by high-intensity long-term exercise and repeated exposure to the chlorine-rich atmosphere in swimming pools during training and competition 2, 3. Recently, increased levels of leukotriene (LT)B4 in exhaled breath condensate and normal exhaled nitric oxide fraction ( F eNO) levels have been reported in five elite swimmers, suggesting possible underlying neutrophilic airway inflammation 4. Previous analysis of induced sputum in nonasthmatic elite swimmers showed increased proportion of eosinophils and neutrophils compared with healthy controls 3. We aimed to characterise the airway inflammation in competitive asthmatic swimmers. Athletes from the FC Porto main swimming team and 20 nonathlete asthmatics were recruited; participants gave informed consent. Subjects were classified by their asthma and training status as asthmatic swimmers (n = 6, two female, aged 17±2 yrs, competing 8±3 yrs, training 16±4 h·week−1), asthmatics (n = 20, eight female, aged 14±3 yrs) and swimmers (n = 20, six female, aged 17±2 yrs, competing 8±3 yrs, training 17±3 h·week−1). All asthmatics and nine (45%) of the swimmers were atopic according …

Neurogenic inflammation in allergen-challenged obese mice: a missing link in the obesity-asthma association?

ABSTRACT Aim: A number of studies have shown an association between obesity and asthma. Controversy remains on the mechanisms supporting this association. In this study we aimed to assess neurogenic inflammation in a model of diet-induced obesity and allergen-challenged mice. Methods: High fat diet-induced (HFD) obese Balb/c mice were sensitized and challenged with ovalbumin (OVA). Glucose, insulin, OVA-specific IgE and substance P (SP), and the main tachykinin involved in neurogenic inflammation, were quantified in sera. Cell counts were performed in bronchoalveolar lavage fluid (BALF). The extent of peribronchial infiltrates was estimated on lung tissue sections and inflammation was score based on inflammatory cell counts surrounding the bronchi. Results: Obesity per se and allergen-sensitization per se increased serum SP (P = .027, P = .004, respectively). Further increased was observed in obese-sensitized mice (P = .007). Obese-sensitized mice also showed higher insulin (P = .0016), OVA-specific IgE (P = .016), peribronchial inflammatory score (P = .045), and tendency for higher glycemia. The interaction of obesity and asthma on SP levels was confirmed (P = .005, R2 = 0.710). SP was positively correlated with metabolic (glycemia, r = 0.539, P = .007) and allergic inflammation parameters (BALF eosinophils, r = 0.445, P = 0.033; BALF mast cells, r = 0.574, P = .004; peribronchial inflammation score, r = 0.661, P < .001; and OVA-specific IgE, r = 0.714, P < .001). Conclusions: Our findings provide support to the neurogenic inflammation link between obesity and asthma in mice. These two conditions independently increased SP and the presence of both pathologies further increased this level. Neurogenic inflammation may be a previously unrecognized mechanism beyond the obese-asthma phenotype. Further studies are need to confirm this role of SP in human obesity-asthma association.

Airway vascular damage in elite swimmers

We postulated that high level swimming can promote airway inflammation and thus asthma by enhancing local vascular permeability. We aimed to test this hypothesis by a cross-sectional study comparing swimmers (n = 13, 17 ± 3 years, competing 7 ± 4 years, training 18 ± 3 h per week), asthmatic-swimmers (n = 6, 17 ± 2 years, competing 8 ± 3 years, training 16 ± 4 h per week), and asthmatics (n = 19, 14 ± 3 years). Subjects performed induced sputum and had exhaled nitric oxide, lung volumes, and airway responsiveness determined. Airway vascular permeability index was defined as the ratio of albumin in sputum and serum. Results from the multiple linear regression showed each unit change in airway vascular permeability index was associated with an increase of 0.97% (95%CI: 0.02 to 1.92; p = 0.047) in sputum eosinophilis, and of 2.64% (95%CI:0.96 to 4.31; p = 0.006) in sputum neutrophils after adjustment for confounders. In a general linear model no significant differences between airway vascular permeability between index study groups existed, after controlling for sputum eosinophilis and neutrophils. In conclusion, competitive swimmers training in chlorine-rich pools have similar levels of airway vascular permeability than asthmatics. Although competitive swimming has been associated with asthma, airway inflammation and airway hyperesponsiveness do not seem to be dependent on increased airway vascular permeability.

Esputo induzido nas doencas pulmonares intersticiais --- Um estudo piloto

INTRODUCTION Induced sputum with hypertonic saline has been suggested as a safer and cheaper alternative to bronchoalveolar lavage for evaluation of patients with interstitial lung diseases (ILD). OBJECTIVE To evaluate the safety and feasibility of sputum induction in ILD and to compare sputum cellular profiles with paired bronchoalveolar lavage fluid results. MATERIAL AND METHODS Twenty patients underwent sputum induction with 4.5% saline within 2 weeks of bronchoalveolar lavage. Total, differential cell counts and cellular viability were assessed. Wilcoxon test and Spearmans rank correlation coefficient were used and a p<0,05 was considered statistically significant. RESULTS From a total of 20 subjects (mean age 49.4±16.4 years, 70% male) a satisfactory sputum sample was obtained in 15 subjects (75%). Induction was stopped in one subject, due to a significant decrease in PEF. The cell profiles for induced sputum and bronchoalveolar lavage fluid (BALF) were different (P <.05), except for eosinophils, and there were no significant correlations between the two methods. Compared to sputum reference values there was an increase of lymphocytes (3.2% vs 0.5%) and eosinophils (1.4% vs 0.0%). Comparing sarcoidosis and hypersensitivity pneumonitis sputum, both diseases had an increase in lymphocytes (4.4 vs 3.9%), with a significant higher neutrophil count in hypersensitivity pneumonitis (65.4% vs 10.6% P <0.05), a finding also seen in BALF. CONCLUSION Induced sputum is feasible and safe in interstitial lung diseases. Although sputum cellular counts are not correlated with bronchoalveolar lavage fluid, sputum cellular profiles may help to distinguish different ILD.