Association between basketball playing position and ACTN3 R577X polymorphism in athletes of first division Brazilian Basketball League.

INTRODUCTION: Genetic-association studies have shown that some polymorphisms are associated with different aspects of athletic performance, including very specific features, such as players' position in team sports, like soccer, rugby, and Australian football. However, this type of association has not been investigated in Basketball yet. The present study analyzed the association of ACTN3 R577X, AGT M268T, ACE I/D and BDKRB2+9/-9 polymorphisms with the position of basketball players. METHODS: One hundred fifty-two male athletes from 11 teams of the first division of Brazilian Basketball League and 154 male Brazilian controls were genotyped. The analyses of the ACTN3 R577X and AGT M268T were performed by the allelic discrimination method, while ACE I/D and BDKRB2+9/-9 by conventional PCR followed by electrophorese in agarose gel. RESULTS: The results showed a significant effect of height on all positions and an association between the genetic polymorphisms analyzed and basketball positions. In addition, a significantly higher frequency of ACTN3 577XX genotype was observed in Point Guards. Also, compared to Point Guard, ACTN3 RR and RX were more prevalent in the Shooting Guard and Small Forward group and RR genotype was also more prevalent in the Power Forward and Center group. CONCLUSION: The main finding of our study was the positive association of ACTN3 R577X polymorphism and basketball playing position, and a suggestion of genotypes related to strength/power performance with post players and genotypes related to endurance performance with point guard players.

Exercise Induced-Cytokines Response in Marathon Runners: Role of ACE I/D and BDKRB2 +9/-9 Polymorphisms.

Renin-angiotensin system (RAS) and kallikrein-kinin system (KKS) have a different site of interaction and modulate vascular tone and inflammatory response as well on exercise adaptation, which is modulated by exercise-induced cytokines. The aim of the study was to evaluate the role of ACE I/D and BDKRB2 +9/-9 polymorphism on exercise-induced cytokine response. Seventy-four male marathon finishers, aged 30 to 55 years, participated in this study. Plasma levels of exercise-induced cytokines were determined 24 h before, immediately after, and 24 h and 72 h after the São Paulo International Marathon. Plasma concentrations of MCP-1, IL-6 and FGF-21 increased after marathon in all genotypes of BDKRB2. IL-10, FSTL and BDNF increased significantly after marathon in the genotypes with the presence of the -9 allele. FSTL and BDNF concentrations were higher in the -9/-9 genotype compared to the +9/+9 genotype before (p = 0.006) and after the race (p = 0.023), respectively. Apelin, IL-15, musclin and myostatin concentrations were significantly reduced after the race only in the presence of -9 allele. Marathon increased plasma concentrations of MCP1, IL-6, BDNF and FGF-21 in all genotypes of ACE I/D polymorphism. Plasma concentrations of IL-8 and MIP-1alpha before the race (p = 0.015 and p = 0.031, respectively), of MIP-1alpha and IL-10 after the race (p = 0.033 and p = 0.047, respectively) and VEGF 72 h after the race (p = 0.018) were lower in II homozygotes compared to runners with the presence of D allele. One day after the race we also observed lower levels of MIP-1alpha in runners with II homozygotes compared to DD homozygotes (p = 0.026). Before the marathon race myostatin concentrations were higher in DD compared to II genotypes (p = 0.009). Myostatin, musclin, IL-15, IL-6 and apelin levels decreased after race in genotypes with the presence of D allele. After the race ACE activity was negatively correlated with MCP1 (r = -56, p < 0.016) and positively correlated with IL-8, IL-10 and MIP1-alpha (r = 0.72, p < 0.0007, r = 0.72, p < 0.0007, r = 0.47, p < 0.048, respectively). The runners with the -9/-9 genotype have greater response in exercise-induced cytokines related to muscle repair and cardioprotection indicating that BDKRB2 participate on exercise adaptations and runners with DD genotype have greater inflammatory response as well as ACE activity was positively correlated with inflammatory mediators. DD homozygotes also had higher myostatin levels which modulates protein homeostasis.

Chronic Low or High Nutrient Intake and Myokine Levels.

Inadequate nutrient availability has been demonstrated to be one of the main factors related to endocrine and metabolic dysfunction. We investigated the role of inadequate nutrient intakes in the myokine levels of runners. Sixty-one amateur runners participated in this study. The myokine levels were determined using the Human Magnetic Bead Panel from plasma samples collected before and after the marathon. Dietary intake was determined using a prospective method of three food records. The runners with lower carbohydrate and calcium intakes had higher percentages of fat mass (p < 0.01). The runners with a sucrose intake comprising above 10% of their energy intake and an adequate sodium intake had higher levels of BDNF (p = 0.027 and p = 0.031). After the race and in the recovery period, the runners with adequate carbohydrate intakes (g/kg) (>5 g/kg/day) had higher levels of myostatin and musclin (p < 0.05). The runners with less than 45% of carbohydrate of EI had lower levels of IL-15 (p = 0.015) and BNDF (p = 0.013). The runners with higher cholesterol intakes had lower levels of irisin (p = 0.011) and apelin (p = 0.020), and those with a low fiber intake had lower levels of irisin (p = 0.005) and BDNF (p = 0.049). The inadequate intake influenced myokine levels, which promoted cardiometabolic tissue repair and adaptations to exercise.

Time Course and Role of Exercise-Induced Cytokines in Muscle Damage and Repair After a Marathon Race.

Endurance exercise induces an increase in the expression of exercise-induced peptides that participate in the repair and regeneration of skeletal muscles. The present study aimed to evaluate the time course and role of exercise-induced cytokines in muscle damage and repair after a marathon race. Fifty-seven Brazilian male amateur marathon finishers, aged 30-55 years, participated in this study. The blood samples were collected 24 h before, immediately after, and 24 and 72 h after the São Paulo International Marathon. The leukogram and muscle damage markers were analyzed using routine automated methodology in the clinical laboratory. The plasma levels of the exercise-induced cytokines were determined using the Human Magnetic Bead Panel or enzyme-linked immunosorbent assays [decorin and growth differentiation factor 15 (GDF-15)]. A muscle damage was characterized by an increase in plasma myocellular proteins and immune changes (leukocytosis and neutrophilia). Running the marathon increased interleukin (IL)-6 (4-fold), IL-8 (1.5-fold), monocyte chemoattractant protein-1 (2.4-fold), tumor necrosis factor alpha (TNF-α) (1.5-fold), IL-10 (11-fold), decorin (1.9-fold), GDF-15 (1.8-fold), brain-derived neurotrophic factor (BDNF) (2.7-fold), follistatin (2-fold), and fibroblast growth factor (FGF-21) (3.4-fold) plasma levels. We also observed a reduction in musclin, myostatin, IL-15, and apelin levels immediately after the race (by 22-36%), 24 h (by 26-52%), and 72 h after the race (by 25-53%). The changes in BDNF levels were negatively correlated with the variations in troponin levels (r = -0.36). The variations in IL-6 concentrations were correlated with the changes in follistatin (r = 0.33) and FGF-21 (r = 0.31) levels after the race and with myostatin and irisin levels 72 h after the race. The changes in IL-8 and IL-10 levels had positive correlation with variation in musclin (p < 0.05). Regeneration of exercise-induced muscle damage involves the participation of classical inflammatory mediators, as well as GDF-15, BDNF, follistatin, decorin, and FGF-21, whose functions include myogenesis, mytophagia, satellite cell activation, and downregulation of protein degradation. The skeletal muscle damage markers were not associated to myokines response. However, BDNF had a negative correlation with a myocardial damage marker. The classical anti-inflammatory mediators (IL-10, IL-8, and IL-6) induced by exercise are associated to myokines response immediately after the race and in the recovery period and may affect the dynamics of muscle tissue repair.

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.

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.

Angiotensin-converting enzyme related-polymorphisms on inflammation, muscle and myocardial damage after a marathon race

ABSTRACT: 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. (AU)

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.

Association between hematological parameters and iron metabolism response after marathon race and ACTN3 genotype

αlpha-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, na 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 protective role of the XX genotype on hematological and renal changes induced by long-distance exercise. Therefore, these findings should be further replicated.(AU)

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.

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.

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.

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.

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 resolutionand contributes directly to the pathogenesis of many infectious and inflammatory conditions.nThe aim of this study was to investigate the effect of marathon races on surface moleculesrelated 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 raceinduced 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 significantlyhigher 24 h and 72 h after the marathon race. Hemoglobin and hematocrit levels decreased72 h after the marathon race. We also observed an increased intercellular adhesion molecule-1(ICAM-1) expression and decreasedTNF receptor-1 (TNFR1) expression immediatelyafter 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 possibleslow rolling phase and delayed neutrophil activation and apoptosis. Marathon racing affectsneutrophils adhesion and survival in the course of inflammation, supporting the “openwindow”post-exercise hypothesis...