| Grant number: | 14/21501-0 |
| Support Opportunities: | Regular Research Grants |
| Start date: | August 01, 2015 |
| End date: | July 31, 2017 |
| Field of knowledge: | Health Sciences - Physical Education |
| Principal Investigator: | Maria Fernanda Cury Boaventura |
| Grantee: | Maria Fernanda Cury Boaventura |
| Host Institution: | Pró-Reitoria de Pós-Graduação e Pesquisa. Universidade Cruzeiro do Sul (UNICSUL). São Paulo , SP, Brazil |
| Associated researchers: | João Bosco Pesquero ; Renata Gorjao ; Sandro Soares de Almeida |
Abstract
The intense and strenuous physical exercise promotes the release of inflammatory mediators (IL-6, CRP, IL-1ra, IL-10, IL-8) and markers of myocardial injury leading to an exacerbated immune stimulation followed by immunosuppression. Exacerbated inflammatory process can affect various physiological systems such as the cardiopulmonary system contributing to cardiopulmonary fatigue after competition. The long duration exercise causes changes in inspiratory muscles and contractility, relaxation, systolic and diastolic function of the left ventricle leading alteration in the internal diameter of the left ventricle, increases A wave and reduction in E / A ratio and myocardial hypertrophy denominated "athlete's heart". Researchers have been investigating if the release of inflammatory markers of myocardial injury after chronic endurance exercise is a physiological or pathological process of adaptation. The release of these markers can be the result of transient myocardial injury that would lead to an adaptation and enhancement of the function and structure of the heart. On the other hand, studies in animals have shown that the performance of long term leads to inflammation and myocardium fibrosis, which is associated with the occurrence of sudden death. Few studies have investigated the correlation between markers of myocardial injury, inflammation and cardiopulmonary function after exercise. The aim of our study is to investigate the behavior morphofunctional heart and its relation to markers of myocardial injury and inflammatory mediators in total peripheral blood of marathon runners after the race and in the recovery. Participate in the study 60 male runners between 25 and 50 years, without cardiovascular or pre-existing metabolic disease. We will carry out physical measurements (weight, height, BMI, bioimpedance and antropometric measures), electrocardiogram and ergo spirometry. The echocardiogram will be performed 24 hours before and immediately after the marathon. The electrocardiogram, ergo spirometry and spirometry will be repeated 3-15 days after the competition. Blood samples will be taken 24 hours before, immediately after and 72 hours after the marathon for BNP, cardiac troponin I, CK, CK-MB, myoglobin, LDH, glucose, lactate, total cholesterol and fractions, triglycerides, complete blood count, CRP and inflammatory cytokines and single nucleotide polymorphism of cardio-metabolic genes. We will evaluate the relationship between changes in cardiopulmonary function after the marathon, the characteristics of the "athlete's heart" and genotype, as well as the exercise load during the marathon; the behavior of the markers of myocardial injury, plasma cytokines after the race. (AU)
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