Abstract
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.
Highlights
Iron deficiency is associated with impairment in the transport and use of oxygen, and increases the risk to sports anemia and may affect athletic performance (Peeling et al, 2008, 2014)
Our findings indicate that marathon running induces hemolysis and hematuria and that the body compensates for this by producing erythropoietin and elevating mean corpuscular hemoglobin concentration (MCHC) and mean corpuscular hemoglobin (MCH) in the recovery period
We show in our preliminary results that marathoners with the ACTN3 XX genotype have reduced susceptibility to hematuria and iron deficiency
Summary
Iron deficiency is associated with impairment in the transport and use of oxygen, and increases the risk to sports anemia and may affect athletic performance (Peeling et al, 2008, 2014). The potential mechanisms involved in iron deficiency induced by long-distance exercise are intravascular and extravascular hemolysis, hematuria, and sweat and gastrointestinal iron loss and inflammation (Kobayashi et al, 2014; Peeling et al, 2014). Our hypothesis is that the metabolic efficiency attributed to XX genotype may improve parameters of oxygen transport and utilization system (red blood cells and iron metabolism) after long-distance exercise. Blood flow and oxygen demand increase in muscle cells during exercise, promoting changes in some metabolites such as 2,3-diphosphoglycerate (2,3-DPG) and adenosine triphosphate (ATP), H+, CO2, Cl−, and/or leading to hypoxia that modulates oxygen transport and utilization system and hematuria (renal hypoxia) (Mairbaurl, 2013)
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