Abstract:The aim of study was to compare heart rate deflection point (HRDP) determined by visual and DMAX methods to Maximal lactate steady state (MLSS). Thirteen runners carried out incremental test Vameval and constant load tests (CLT). Velocity of HRDP (14,3 ± 1,13km.h -1 ) was significantly higher compared to DMAX (13,2 ± 1,35km.h -1 ) but they were not significantly correlated. However, both velocities, HRDP and DMAX, were not different from MLSS (13,8 ± 0,90km.h -1 ) while only HRDP has been significant correlated with MLSS (r = 0,75). On eight runners during CLT the blood lactate concentration did not show stability at HRDP velocity which to let us to conclude that HRPD is not appropriated to estimate MLSS. However, it may be used as aerobic capacity index
Airway remodeling is a hallmark of asthma, characterized by structural changes in the airways, including epithelial metaplasia, subepithelial fibrosis, angiogenesis and thickening of smooth muscle. Airway remodeling promotes irreversible loss of lung function and subside the airway hyperresponsiveness and is associated with severity of the disease. In addition, airway remodeling is caused by an unresolved chronic inflammatory response, involving exacerbated release of profibrotic mediators. Aerobic exercise (AE) is the main component of pulmonary rehabilitation and in pre-clinical studies in models of asthma, AE reduced airway remodeling, by reducing the release of pro-fibrotic mediators and increasing the release of anti-fibrotic mediators. However, no clinical study has tested whether AE could promote any effect on airway remodeling in asthmatic patients. METHODS:Treadmill aerobic exercise (AE) (12 weeks, 3x/week, 40min/session, 60-80%MaxHR) was applied to 17 persistent moderate asthmatic patients (42.11AE19.13). Body mass index (BMI), lung function, induced sputum, breath condensate, whole blood analysis and CD4þ cells proliferation, 6MWT, exhaled nitric oxide, was evaluated.RESULTS: AE improved VEF3 (L) (p<0.03) and PEF (L/min) (p<0.005) and PEF (%) (p<0.004), reduced the number of total leukocytes, eosinophils, neutrophils, lymphocytes and macrophages (p<0.01), as well as the levels of IL-1beta, IL-4, IL-5, IL-6, IL-8, IL-13, IL-17, IL-23 (p<0.01) in induced sputum. AE also reduced the levels of IL-1beta, IL-5, IL-6, IL-13, VEGF (p<0.01), while increased the levels of anti-inflammatory IL-1ra and IL-10 (p<0.01) and anti-fibrotic Relaxin 3 (p<0.01) in breath condensate. Systemically, AE reduced the number of eosinophils, neutrophils and lymphocytes (p<0.01), as well as the levels of IL-1beta, IL-5, IL-6, IL-13, VEGF (p<0.01), while increased anti-inflammatory IL-1ra, IL-10 (p<0.01) and anti-fibrotic Relaxin 3 (p<0.01) in plasma. AE improved 6MWT (p<0.01) and reduced exhaled nitric oxide (p<0.01) and CD4þ cells proliferation (p<0.01). CONCLUSIONS:In conclusion, AE improves airway and systemic inflammation reducing pro-inflammatory cytokines, while increased anti-inflammatory and anti-fibrotic mediators systemically and into the lungs.CLINICAL IMPLICATIONS: These findings present unprecedented findings on auxiliary treatment and prevention of the health consequences of people with asthma through the practice of physical exercise. From a social point of view, it demonstrates a lowcost and easily accessible intervention, while from a scientific point of view, it will promote research ideas in a promising field.
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