The Relationship of IL-8 and IL-10 Myokines and Performance in Male Marathon Runners Presenting Exercise-Induced Bronchoconstriction.

At present, it is unclear which exercise-induced factors, such as myokines, could diminish the negative impact of the reduction in pulmonary function imposed by the exercise in question. In this study, we aim to evaluate the prevalence of exercise-induced bronchoconstriction (EIB) and also to investigate the effect of myokines in the performance of marathon runners presenting EIB or not. Thirty-eight male recreational marathon runners (age 38.8 [33-44], height 175.7 [172.0-180.3]; weight 74.7 [69.3-81.6]) participated in this study, and through spirometry tests, a prevalence of 23.6% of EIB was found, which is in agreement with the literature. The volunteers who tested positive to EIB (EIB+) presented lower maximum aerobic capacity compared to those who tested negative (EIB-) (EIB+ 44.02 [39.56-47.02] and EIB- 47.62 [44.11-51.18] p = 0.03). The comparison of plasma levels of IL-1ß (EIB+ p = 0.296, EIB- p = 0.176, EIB+ vs. EIB- baseline p = 0.190 immediately after p = 0.106), IL-4 (undetectable), IL-6 (EIB+ p = 0.003, EIB- p ≤ 0.001, EIB+ vs. EIB- baseline p = 0.301 immediately after p = 0.614), IL-8 (EIB+ p = 0.003, EIB- p ≤ 0.001, EIB+ vs. EIB- baseline p = 0.110 immediately after p = 0.453), IL-10 (EIB+ p = 0.003, EIB- p ≤ 0.001, EIB+ vs. EIB- baseline p = 0.424 immediately after p = 0.876) and TNF-α (EIB+ p = 0.003, EIB- p ≤ 0.001, EIB+ vs. EIB- baseline p = 0.141 immediately after p = 0.898) were similar in both groups 24 h before and immediately after the marathon. However, negative correlations were found between the marathon finishing time and the levels of IL-8 (r = -0.81, p = 0.022), and IL-10 (r = -0.97, p ≤ 0.001) immediately after completing the marathon. In conclusion, for the first time, it is shown that the myokines IL-8 and IL-10 are related to improvement of the performance of marathon runners presenting EIB.

Association Between Hematological Parameters and Iron Metabolism Response After Marathon Race and ACTN3 Genotype.

α-Actinin-3 (ACTN3 R577X, rs.1815739) polymorphism is a genetic variation that shows the most consistent influence on metabolic pathway and muscle phenotype. XX genotype is associated with higher metabolic efficiency of skeletal muscle; however, the role of ACTN3 polymorphism in oxygen transport and utilization system has not yet been investigated. Therefore, the aim of this study was to determine the influence of ACTN3 polymorphisms on hematological and iron metabolism response induced by marathon race. Eighty-one Brazilian amateur male endurance runners participated in the study. Blood samples and urine were collected before; immediately after; and 1, 3, and 15 days after the marathon race. Urine, hematological parameters, iron metabolism, and ACTN3 genotyping analyses were performed. The marathon race induced a decrease in erythrocytes, Hb, and Ht, and an increase in hematuria, creatinine, myoglobin, red cell distribution width, mean corpuscular hemoglobin concentration, mean corpuscular hemoglobin, direct and indirect bilirubin and erythropoietin. Moreover, an elevation immediately or 1 day after the marathon race follows a reduction 3 or 15 days after the marathon race were observed on transferrin saturation and iron and transferrin levels. Hematological parameters and iron metabolism changes induced by marathon race were not observed in XX genotypes. Hematuria and decreased erythrocytes, Hb, Ht, and iron and transferrin levels were observed only in RR and/or RX genotypes but not in XX genotypes. The percentage of runners with hematuria, leukocyturia, iron deficiency, creatinine, myoglobin, and bilirubin imbalance was higher in RR compared to XX genotypes. ACTN3 polymorphism is associated with iron metabolism and hematological responses after endurance exercise. Despite these results being based on a small sample, they highlight a protective role of the XX genotype on hematological and renal changes induced by long-distance exercise. Therefore, these findings should be further replicated.

Angiotensin-Converting Enzyme Related-Polymorphisms on Inflammation, Muscle and Myocardial Damage After a Marathon Race.

Muscle damage is one of the most important factors that affect muscle fatigue during endurance exercise. Recent evidence suggests that the renin-angiotensin system impacts on skeletal muscle wasting. The aim of this study was to determine association between the AGT Met235Thr, ACE I/D and BDKRB2 -9/+9 polymorphisms with inflammation, myocardial and muscle injury induced by endurance exercise. Eighty-one Brazilian male runners participated in this study and completed the International Marathon of Sao Paulo. Muscle and myocardial damage markers (alanine transaminase, ALT, aspartate transaminase, AST, lactic dehydrogenase, LDH, creatine kinase, CK, Troponin, pro BNP, myoglobin, and CK-MB) and inflammatory mediators (IL-6, IL-8, IL-10, IL12p70, IL1ß, and TNF-α) were determined one day before, immediately after, one day after, and three days after the event. Muscle damage was also determined fifteen days after race and angiotensinogen (AGT) Met235Thr, angiotensin-converting enzyme (ACE) I/D, and Bradykinin B2 receptor (BDKRB2) -9/+9 polymorphisms were determined. Marathon race participation induced an increase in all muscle damage and inflammatory markers evaluated (p < 0.0001). The muscle damage markers, troponin and pro BNP, CK and LDH and inflammatory markers, IL-6, IL-8, IL-1ß and IL-10 were also higher in ACE II genotype immediately after race, compared to DD genotype. The percentage of runners higher responders (>500U/I) to CK levels was higher for II genotypes (69%) compared to DD and ID genotypes (38% and 40%, respectively) immediately after. Troponin, pro BNP and IL-1ß, IL-8 levels were also elevated in AGT MM genotype compared to TT genotype athletes after and/or one day after race. BDKRB2 -9/-9 had pronounced response to LDH, CK, CK-MB and ALT and AST activities, myoglobin, troponin, IL-6, IL-8 levels immediately, one day and/or three days after race. The percentage of runners higher responders (>500U/I) to CK levels was greater for -9-9 and -9+9 genotypes (46 and 48%, respectively) compared to +9+9 genotypes (31%) immediately after. ACE II, AGT MM, and BDKRB2 -9-9 genotypes may increase the susceptibility to inflammation, muscle injury after endurance exercise and could be used to predict the development of clinical conditions associated with muscle damage and myocardial injury.

Impairment on Cardiopulmonary Function after Marathon: Role of Exhaled Nitric Oxide.

BACKGROUND: The endurance exercise is capable of inducing skeletal muscle, heart, and respiratory fatigue, evidenced by morphofunctional cardiac changes, release of myocardial injury biomarkers, and reduction of maximal voluntary ventilation and oxygen consumption (VO2) at peak exercise. PURPOSE: The aim of this study was to investigate whether marathoners present cardiac fatigue after marathon and whether it correlates with pulmonary levels of exhaled nitric oxide (eNO) and pulmonary inflammation. METHODS: 31 male marathoners, age 39 ± 9 years, were evaluated by cardiopulmonary exercise test three weeks before and between three and 15 days after a marathon; eNO analysis and spirometry were evaluated before, immediately after, and 24 and 72 hours after the marathon, and sputum cellularity and cytokine level were assessed before and after the marathon. RESULTS: Marathon induced an increase in the percentage of macrophages, neutrophils (from 0.65% to 4.28% and 6.79% to 14.11%, respectively), and epithelial cells and a decrease in cytokines in induced sputum, followed by an increase in eNO concentration (20 ± 11 to 35 ± 19 ppb), which presented a significant reduction 24 and 72 hours after marathon (9 ± 12 e 12 ± 9 ppb, p < 0.05). We observed a decrease in the spirometry parameters in all time points assessed after the marathon (p < 0.05) as well as in cardiopulmonary capacity, evidenced by a reduction in VO2 and ventilation peaks (57 ± 6 to 55 ± 6 mL·min-1·Kg-1 and 134 ± 19 to 132 ± 18 Lpm, respectively, p < 0.05). Finally, we observed a negative correlation between the decrease in forced expiratory volume and decrease in eNO 24 and 72 hours after marathon (r = -0.4, p = 0.05). CONCLUSION: Reduction in eNO bioavailability after marathon prevents the reduction in cardiopulmonary capacity induced by acute inflammatory pattern after marathon.

Impact of Hot Environment on Fluid and Electrolyte Imbalance, Renal Damage, Hemolysis, and Immune Activation Postmarathon.

Previous studies have demonstrated the physiological changes induced by exercise exposure in hot environments. We investigated the hematological and oxidative changes and tissue damage induced by marathon race in different thermal conditions. Twenty-six male runners completed the São Paulo International Marathon both in hot environment (HE) and in temperate environment (TE). Blood and urine samples were collected 1 day before, immediately after, 1 day after, and 3 days after the marathon to analyze the hematological parameters, electrolytes, markers of tissue damage, and oxidative status. In both environments, the marathon race promotes fluid and electrolyte imbalance, hemolysis, oxidative stress, immune activation, and tissue damage. The marathon runner's performance was approximately 13.5% lower in HE compared to TE; however, in HE, our results demonstrated more pronounced fluid and electrolyte imbalance, renal damage, hemolysis, and immune activation. Moreover, oxidative stress induced by marathon in HE is presumed to be related to protein/purine oxidation instead of other oxidative sources. Fluid and electrolyte imbalance and protein/purine oxidation may be important factors responsible for hemolysis, renal damage, immune activation, and impaired performance after long-term exercise in HE. Nonetheless, we suggested that the impairment on performance in HE was not associated to the muscle damage and lipoperoxidation.

Reduction in Post-Marathon Peak Oxygen Consumption: Sign of Cardiac Fatigue in Amateur Runners?

BACKGROUND: Prolonged aerobic exercise, such as running a marathon, produces supraphysiological stress that can affect the athlete's homeostasis. Some degree of transient myocardial dysfunction ("cardiac fatigue") can be observed for several days after the race. OBJECTIVE: To verify if there are changes in the cardiopulmonary capacity, and cardiac inotropy and lusitropy in amateur marathoners after running a marathon. METHODS: The sample comprised 6 male amateur runners. All of them underwent cardiopulmonary exercise testing (CPET) one week before the São Paulo Marathon, and 3 to 4 days after that race. They underwent echocardiography 24 hours prior to and immediately after the marathon. All subjects were instructed not to exercise, to maintain their regular diet, ingest the same usual amount of liquids, and rest at least 8 hours a day in the period preceding the CPET. RESULTS: The athletes completed the marathon in 221.5 (207; 250) minutes. In the post-marathon CPET, there was a significant reduction in peak oxygen consumption and peak oxygen pulse compared to the results obtained before the race (50.75 and 46.35 mL.kg-1 .min-1; 19.4 and 18.1 mL.btm, respectively). The echocardiography showed a significant reduction in the s' wave (inotropic marker), but no significant change in the E/e' ratio (lusitropic marker). CONCLUSIONS: In amateur runners, the marathon seems to promote changes in the cardiopulmonary capacity identified within 4 days after the race, with a reduction in the cardiac contractility. Such changes suggest that some degree of "cardiac fatigue" can occur.

Marathon Race Affects Neutrophil Surface Molecules: Role of Inflammatory Mediators.

The fatigue induced by marathon races was observed in terms of inflammatory and immunological outcomes. Neutrophil survival and activation are essential for inflammation resolution and contributes directly to the pathogenesis of many infectious and inflammatory conditions. The aim of this study was to investigate the effect of marathon races on surface molecules related to neutrophil adhesion and extrinsic apoptosis pathway and its association with inflammatory markers. We evaluated 23 trained male runners at the São Paulo International Marathon 2013. The following components were measured: hematological and inflammatory mediators, muscle damage markers, and neutrophil function. The marathon race induced an increased leukocyte and neutrophil counts; creatine kinase (CK), lactate dehydrogenase (LDH), CK-MB, interleukin (IL)-6, IL-10, and IL-8 levels. C-reactive protein (CRP), IL-12, and tumor necrosis factor (TNF)-α plasma concentrations were significantly higher 24 h and 72 h after the marathon race. Hemoglobin and hematocrit levels decreased 72 h after the marathon race. We also observed an increased intercellular adhesion molecule-1 (ICAM-1) expression and decreasedTNF receptor-1 (TNFR1) expression immediately after and 24 h after the marathon race. We observed an increased DNA fragmentation and L-selectin and Fas receptor expressions in the recovery period, indicating a possible slow rolling phase and delayed neutrophil activation and apoptosis. Marathon racing affects neutrophils adhesion and survival in the course of inflammation, supporting the "open-window" post-exercise hypothesis.

[Left ventricular hypertrophy of athletes: adaptative physiologic response of the heart]. / Hipertrofia ventricular esquerda do atleta: resposta adaptativa fisiológica do coração.

OBJECTIVE: To verify whether left ventricular hypertrophy (LVH) of elite competition athletes (marathoners) represents a purely physiological, adaptative process, or it may involve pathological aspects in its anatomical and functional characteristics. METHODS: From November 1999 to December 2000, consecutive samples from 30 under 50-year-old marathoners in full sportive activity, with previously documented LVH and absence of cardiopathy were selected. They were submitted to clinical exams, electrocardiogram, color Doppler echocardiogram and exercise treadmill test (ETT). Fifteen were assorted to be also submitted to ergoespirometric test and heart magnetic resonance imaging (MRI). RESULTS: In ETT, all of them showed good physical pulmonary capacity, with no evidences of ischemic response to exercise, symptoms or arrhythmias. In Doppler echocardiogram, values of diameter and diastolic thickness of LV posterior wall, interventricular septum, LV mass and left atrium diameter, were significantly higher when compared to non-athlete control group, with similar ages and anthropometric measurements. The mean of LV mass of athletes indexed to body surface (126 g/m2) was significantly greater than the one in control group (70 g/m2) (p < 0.001). Magnetic resonance imaging (MRI) showed there was not impairment of contractile strength or LV performance, and values of end diastolic volume, end systolic volume and EF within limits of normality. On the other hand, average ventricular parietal mass, 162.93 +/- 17.90 g, and LV parietal thickness, 13.67 +/- 2.13 mm, at the end of diastole in athlete group, differed significantly from control group: 110 +/- 14.2 g (p = 0.0001) and 8 +/- 0.9 mm, respectively (p = 0.0001). The same happened to the thickness at the end of systole, which was 18.87 +/- 3.40 mm (control group: 10 +/- 1.80 mm, p = 0.0001). CONCLUSION: Results allowed for concluding that LVH in marathoners in full sportive activity period, assessed by non-invasive methods, represents an adaptative response to intensive and prolonged physical training, with purely physiological characteristics.

Athletes with higher VO2max present reduced oxLDL after a marathon race.

BACKGROUND: During a session of prolonged and exhaustive exercise, such as a marathon race, large quantities of free radicals are produced and can oxidise (ox) several molecules, such as low-density lipoprotein (LDL). To prevent oxidative damage, athletes present higher antioxidant levels. However, the effect of marathon running on the natural IgM or IgG anti-oxLDL autoantibodies is not understood. Thus, we investigated the effect of a marathon race on oxidative stress and the mechanisms of control of this stress. METHODS: Blood samples of 20 marathon runners were collected 24 hours before, immediately and 72 hours after a marathon race to evaluate: plasma lipid profile; serum levels of oxLDL and anti-oxLDL autoantibodies (IgM and IgG isotype) and total antioxidant capacity (TAC). Maximum oxygen uptake (VO2max) was also determined. RESULTS: Immediately after the race, oxLDL and TAC levels decreased in comparison to the basal levels; however, the IgM or IgG anti-oxLDL levels remain unchanged. Whereas no differences were observed in the IgM or IgG anti-oxLDL levels 72h after the marathon, the oxLDL and TAC levels returned to the basal values. Significant positive correlations were observed between oxLDL and LDL-cholesterol before, and 72h after the marathon. Significant negative correlations were observed between oxLDL and VO2max immediately after the marathon and 72 h later, as well as between oxLDL and TAC 72 h after the race. CONCLUSIONS: Athletes with a higher VO2max and total antioxidant activity presented reduced LDL oxidation. The levels of IgM or IgG anti-oxLDL autoantibodies were not affected by running the marathon.

Sudden Cardiac Death in Sports: Not a Fatality!

Sudden cardiac death in sports is still controversial. Despite being a rare event, the death of an apparently healthy young athlete causes a major impact on the media. On the other hand, for being a rare event, it is clearly undervalued. Sports preparticipation cardiological assessment is one of the most effective preventive medical actions for professional and amateur endurance athletes. The regular and supervised practice of physical exercise does not kill. We believe that deaths are triggered by excessive physical training and use of drugs, in individuals with not diagnosed or undervalued heart diseases. It is necessary to make health professionals and athletes aware of the athletes' physiological limits, in addition to preparing the athletes properly when they try to overcome human limits

Sudden Cardiac Death in Sports: Why Its Prevalence is So Different by Gender?

Sports competition can be a trigger to fatal arrhythmias in predisposed individuals, leading to sudden cardiac death. Athletes have 2.8 fold more risk of sudden cardiac death than non-athletes. However, female athletes seem to have some cardiac protection, dying suddenly much less than men during sports. Although the mechanisms for this protection have not been well established until now, hormonal, genetic and molecular factors may play a role in it. The so-called "fair sex" might harbour the key for sudden cardiac death prevention

Relato de caso: acompanhamento cardiológico durante 26 anos de atleta de alto nível / Case report: 26-year cardiological follow-up of a high-level athlete

O coração do atleta engloba um conjunto de alterações adaptativas resultantes da prática de exercício físico intenso e prolongado, promovendo alterações clínicas, eletrocardiográficas e ecocardiográficas. As alterações mais relevantes são a hipertrofia miocárdica, o alargamento das cavidades cardíacas e o aumento da massa cardíaca. Em alguns casos, essas alterações podem ser consideradas extremas, exigindo que as condições patológicas sejam eliminadas. Por meio de um relato de caso de um atleta de basquetebol de alto nível cuja única alteração no exame físico era a presença de bradicardia sinusal, persistente ao longo de 26 anos de acompanhamento clínico, investigada através de ecocardiograma, Holter e teste de esforço, demonstrando caráter benigno e fisiológico, apresentamos e discutimos a importância da avaliação cardiovascular por médico com experiência na análise de atletas, capaz de distinguir as condições patológicas das adaptações fisiológicas frente ao exercício de alta intensidade ao qual o atleta é submetido, evitando exames invasivos ou tratamento do coração do atleta.

The athlete's heart performs a set of adaptive changes resulting from the practice of intense and prolonged physical exercise, resulting in clinical, electrocardiographic and echocardiographic alterations. The most relevant changes are myocardial hypertrophy, enlargement of the cardiac cavities, and an increase in cardiac mass. In some cases, these changes can be considered extreme, requiring the elimination of pathological con - ditions. Through a case report of a high-level basketball player, whose only change in the physical examination was the presence of sinus bradycardia, persistent over 26 years of clinical follow-up, which was investigated through echocardiogram, Holter test and stress test, demonstrating benign and physiological characteristics, we present and discuss the importance of cardiovascular evaluation by a physician with experience in analyzing athletes, capable of distinguishing pathological conditions from physiological adaptations to the high-intensity exercise to which the athlete is subjected, avoiding invasive examinations or treatment of the athlete's heart

Reduction in Post-Marathon Peak Oxygen Consumption: Sign of Cardiac Fatigue in Amateur Runners? / Redução no Consumo de Oxigênio Pico Pós Maratona: Sinal de Fadiga Cardíaca em Corredores Amadores?

Abstract Background: Prolonged aerobic exercise, such as running a marathon, produces supraphysiological stress that can affect the athlete's homeostasis. Some degree of transient myocardial dysfunction ("cardiac fatigue") can be observed for several days after the race. Objective: To verify if there are changes in the cardiopulmonary capacity, and cardiac inotropy and lusitropy in amateur marathoners after running a marathon. Methods: The sample comprised 6 male amateur runners. All of them underwent cardiopulmonary exercise testing (CPET) one week before the São Paulo Marathon, and 3 to 4 days after that race. They underwent echocardiography 24 hours prior to and immediately after the marathon. All subjects were instructed not to exercise, to maintain their regular diet, ingest the same usual amount of liquids, and rest at least 8 hours a day in the period preceding the CPET. Results: The athletes completed the marathon in 221.5 (207; 250) minutes. In the post-marathon CPET, there was a significant reduction in peak oxygen consumption and peak oxygen pulse compared to the results obtained before the race (50.75 and 46.35 mL.kg-1 .min-1; 19.4 and 18.1 mL.btm, respectively). The echocardiography showed a significant reduction in the s' wave (inotropic marker), but no significant change in the E/e' ratio (lusitropic marker). Conclusions: In amateur runners, the marathon seems to promote changes in the cardiopulmonary capacity identified within 4 days after the race, with a reduction in the cardiac contractility. Such changes suggest that some degree of "cardiac fatigue" can occur.

Resumo Fundamento: O exercício aeróbico prolongado, como correr uma maratona, produz um estresse suprafisiológico que pode ter impacto na homeostase do atleta. Algum grau de disfunção miocárdica transitória ("fadiga cardíaca") pode ser observado ao longo de vários dias após a prova. Objetivos: Verificar se ocorrem alterações na capacidade cardiopulmonar, no inotropismo e no lusitropismo cardíaco de maratonistas amadores após a realização de uma maratona. Métodos: A amostra foi composta por 6 corredores amadores masculinos. Todos realizaram teste cardiopulmonar de exercício (TCPE) uma semana antes da Maratona de São Paulo e 3 a 4 dias após a mesma. Realizaram ecocardiograma 24 horas antes e imediatamente após a prova. Todos foram orientados a não se exercitar, manter dieta regular, ingerir a mesma quantidade habitual de líquidos e descansar pelo menos 8 horas ao dia no período anterior ao TCPE. Resultados: Os atletas completaram a maratona em 221,5 (207; 250) minutos. No TCPE pós-maratona, ocorreu redução significativa no consumo de oxigênio e no pulso de oxigênio de pico em relação àqueles obtidos antes da prova (50,75 e 46,35 ml.kg-1.min-1; 19,4 e 18,1 ml.btm, respectivamente). Ao ecocardiograma, encontramos redução significativa na onda s' (marcador do inotropismo). A relação E/e' não apresentou alteração significativa após a maratona (marcador do lusitropismo). Conclusões: Em atletas amadores, a maratona parece promover alterações na capacidade cardiopulmonar identificadas pelo menos em até 4 dias após a prova, com redução na contratilidade e, portanto, no inotropismo cardíaco. Tais modificações sugerem que algum grau de "fadiga cardíaca" possa ocorrer.

Relação entre atividade física e redução dos níveis pressóricos / Relationship between physical activity and reduction in blood pressure

O exercício físico regular, como componente da mudança do estilo de vida, é recomendado como parte do tratamento da hipertensão arterial (HA). Existem diversos estudos mostrando seu benefício em reduzir, de maneira sustentada, os níveis pressóricos. O exercício isotônico (aeróbio) possui maior número de estudos e há mais conhecimento sobre os mecanismos fisiológicos, agora mais bem elucidados, relacionados ao tratamento da hipertensão. No entanto, o exercício isométrico (anaeróbio) também produz benefícios e todas as recomendações atuais já o incluem, associado ao exercício aeróbico, nos treinamentos.

Regular exercise as a lifestyle change component is recommended as part of the treatment of hypertension. There are several studies showing its benefit in reducing blood pressure levels in a sustained way. The aerobic exercise has more studies and knowledge of the physiological mechanisms related to the treatment of hypertension, now better understood. However anaerobic exercise also produces benefits and all current recommendations already include in training, associated with aerobic exercise.

Alteração de biomarcadores de lesão miocárdica em atletas após a Maratona Internacional de São Paulo / Changes in biomarkers of myocardial lesion in runners after the São Paulo International Marathon / Alteración de biomarcadores de lesión miocárdica en atletas después de Maratón Internacional de San Pablo

INTRODUÇÃO: Apesar de a prática regular de exercício físico reduzir o risco de doença cardiovascular, estudos recentes têm documentado elevações em biomarcadores relacionados com danos cardíacos após exercícios prolongados em indivíduos aparentemente saudáveis. OBJETIVO: Investigar as alterações nos níveis de brain natriuretic peptide (BNP) e troponina T cardíaca (cTnT) em atletas amadores após uma maratona, assim como verificar as possíveis relações entre as alterações, antes e depois da prova, apresentada pelos dois biomarcadores e variáveis do teste cardiopulmonar. MÉTODOS: Estudamos 38 atletas do sexo masculino (40,9 ± 6,29 anos) antes e depois da Maratona Internacional de São Paulo, SP, Brasil. Foram realizadas coletas de sangue na veia antecubital para mensurar os biomarcadores cardíacos, cTnT e BNP 24h antes, imediatamente após e 24h após a maratona. Foi realizado teste cardiopulmonar máximo nas três semanas que antecederam a prova. RESULTADOS: Os valores de BNP e cTnT aumentaram imediatamente após a maratona (p<0,001) quando comparados com os valores basais. No terceiro momento (24h) os valores de troponina tiveram uma redução significativa caracterizando um retorno aos valores basais. Não encontramos correlação entre idade e variáveis referentes a intensidade da maratona, porém encontramos correlação dos biomarcadores com o tempo de conclusão da maratona. CONCLUSÃO: Diferentes causas de liberação podem ser assumidas para cTnT e BNP e, neste caso, parecem não refletir dano miocárdico devido ao comportamento da curva destes marcadores, além de não haver relação entre a liberação dos dois biomarcadores. .

INTRODUCTION: Although the practice of physical exercises reduces the cardiovascular risk, recent studies have documented elevations in cardiac injury biomarkers after prolonged exercises in apparently healthy individuals. OBJECTIVE: We aimed to investigate the changes in brain natriuretic peptide (BNP) and cardiac troponin T (cTnT) levels after a marathon, and the correlation of these biomarkers and the variables of cardiopulmonary test. METHODS: We studied 38 male athletes (40.9 ± 6.29 years old) participants at the São Paulo International Marathon, SP, Brasil. Blood collections were performed to measure cTnT and BNP 24h before, immediately after and 24h after the marathon. Cardiopulmonary test was performed in the three weeks preceding the marathon. RESULTS: BNP and cTnT values increased significantly after the marathon (p<0.001). In the third moment (24h) the troponin values returned to the baseline values. We found no correlation between age and variables of the marathon, however, we did find a correlation between the biomarkers and time to complete the marathon. CONCLUSION: Various causes of release may be presumed for cTnT and BNP, however, they do not seem to reflect into myocardial injury, and there is no relationship between the releases of the two biomarkers. .

INTRODUCCIÓN: A pesar de que la práctica regular de ejercicio reduce el riesgo de enfermedad cardiovascular, estudios recientes han documentado elevaciones en biomarcadores relacionados con daños cardiacos después de ejercicios prolongados en individuos aparentemente saludables. OBJETIVO: Investigar las alteraciones en los niveles de BNP y troponina T cardiaca (cTnT) en atletas amateur después de maratón, así como verificar las posibles relaciones entre las alteraciones, antes y después de la prueba, presentada por dos biomarcadores y variables del test cardiopulmonar. MÉTODOS: Estudiamos 38 atletas del sexo masculino (40,9±6,29 años) antes y después de la Maratón Internacional de São Paulo, SP, Brasil. Fueron realizadas colectas de sangre en la vena antecubital para medir los biomarcadores cardiacos, cTnT y BNP, 24 horas antes, inmediatamente y 24 horas después de la Maratón. Fue realizado test cardiopulmonar máximo en las tres semanas que antecedieron a la maratón. RESULTADOS: Los valores de BNP y cTnT aumentaron inmediatamente después de la maratón (p<0,001) cuando comparados con los valores basales. En el tercer momento (24h) los valores de troponina tuvieron una reducción significativa caracterizando un retorno a los valores basales. No encontramos correlación entre edad y variables referentes a intensidad de la maratón, sin embargo encontramos correlación de los biomarcadores con el tiempo de conclusión de la maratón. CONCLUSIÓN: Diferentes causas de liberación pueden ser asumidas para cTnT y BNP y, en este caso, parecen no reflejar daño miocárdico debido al comportamiento de la curva de estos marcadores, además de no haber relación entre la liberación de los dos biomarcadores. .