HFE Genotype and Endurance Performance in Competitive Male Athletes.

Introduction Hereditary hemochromatosis can cause individuals to absorb too much iron from their diet. Higher tissue iron content, below the threshold of toxicity, may enhance oxygen carrying capacity and offer a competitive advantage. Single nucleotide polymorphisms (SNPs) in the homeostatic iron regulator (HFE) gene have been shown to modify iron metabolism and can be used to predict an individual's risk of hemochromatosis. Several studies have shown that HFE genotypes are associated with elite endurance athlete status; however, no studies have examined whether HFE genotypes are associated with endurance performance. Purpose The objectives of this study were to determine whether there was an association between HFE risk genotypes (rs1800562 & rs1799945) and endurance performance in a 10km cycling time trial as well as maximal oxygen uptake (VO2peak), an indicator of aerobic capacity. Methods Competitive male athletes (n=100; age = 25 ± 4 years) completed a 10km cycling time trial. DNA was isolated from saliva and genotyped for the rs1800562 (C282Y) and rs1799945 (H63D) SNPs in HFE. Athletes were classified as low risk (n=88) or medium/high risk (n=11) based on their HFE genotype for both SNPs using an algorithm. ANCOVA was conducted to compare outcome variables between both groups. Results Individuals with the medium/high risk genotype were ~8% (1.3 minutes) faster than those with the low risk genotype (17.0 ± 0.8 vs. 18.3 ± 0.3 min, P = 0.05). VO2peak was ~17% (7.9 kg*ml/min) higher in individuals with the medium/high risk genotype compared to those with the low risk genotype (54.6 ± 3.2 vs. 46.7 ± 1.0 kg*ml/min, P = 0.003). Conclusion Our findings show that HFE risk genotypes are associated with improved endurance performance and increased VO2peak in male athletes.