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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.

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.

Objectives The genotypes of α-actinin-3 (ACTN3), angiotensin I-converting enzyme (ACE), bradykinin B2 receptor (BDKRB2) and angiotensinogen (AGT) genes have been associated to skeletal muscle efficiency, strength, resistance and power. Therefore, the aim of this study was associate the ACE ID, ACTN-3 RX, AGT MT and B2BRK -9 + 9 polimorphisms and power genotype score to myocardial and muscle injury induced by endurance exercise. Methods Sixty male endurance runners participated in this study. Blood samples (30 mL) were collected 24 h before, immediately after, 24 h after, 72 h after, 15 days after the Sao Paulo International Marathon 2015 (60 runners, 15-17°C and relative humidity of 82%). The power genotype score was based on ACE ID, ACTN-3 RX, AGT MT and B2BRK -9 + 9 polimorphisms. To quantify the combined influence of all 4 polymorphisms currently associated with power phenotypes, an algorithm was created to incorporate the 4 genotype. The total score was then transformed mathematically to lie within the range 0–100 (to be intuitively meaningful) and labelled the power genotype score. The following parameters were carried out to evaluate muscle injury: pro-BNP, creatine kinase (CK), CK-MB, lactate dehydrogenase (LDH), troponin, myoglobin, aspartate aminotransferase (AST) from muscle and of alanine aminotransferase (ALT). Results The demographic data for these subjects are summarised as follows: age, 34 ± 6 years; height, 174 ± 0 cm; body mass, 74 ± 1 kg;% of fat mass, 20 ± 0.5; body mass index, 25 ± 0.2 kg/m2; average training race 56 ± 2,2 km/week; frequency of training 4,4 time/week; time on 10 km race 46 ± 0.7 minutes. Marathon race induced an increase on myoglobin (21-fold, p Conclusion The power genotype score are associated with endurance exercise-induced muscle injury suggesting less injury on runners with high power genotype score. Acknowledgment This work was supported by Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [Project Number 2014/21501-0].