Abstract
Nitric oxide (NO), an important endogenous pulmonary vasodilator is synthetized by the endothelial NO synthase (NOS3). Reduced NO bioavailability and thus the Glu298Asp polymorphism of NOS3 may enhance right ventricular (RV) afterload and hypertrophic remodeling and influence athletic performance. To test this hypothesis world class level athletes (water polo players, kayakers, canoeists, rowers, swimmers, n = 126) with a VO2 maximum greater than 50ml/kg/min were compared with non-athletic volunteers (n = 155). Cardiopulmonary exercise tests and cardiac magnetic resonance imaging (cMRI) were performed to determine structural or functional changes. Genotype distribution of the NOS3 Glu298Asp polymorphism was not affected by gender or physical performance. Cardiac MRI showed increased stroke volume with eccentric hypertrophy in all athletes regardless of their genotype. However, the Asp allelic variant carriers had increased RV mass index (32±6g versus 27±6g, p<0.01) and larger RV stroke volume index (71±10ml versus 64±10ml, p<0.01) than athletes with a Glu/Glu genotype. Genotype was not significantly associated with athletic performance. In the non-athletic group no genotype related differences were detected. The association between the NOS3 Glu298Asp polymorphism and RV structure and dimension in elite athletes emphasizes the importance of NOS3 gene function and NO bioavailability in sport related cardiac adaptation.
Highlights
Intensive physical conditioning results in cardiac adaptive responses known as the “athlete’s heart.” These changes include development of left- and right ventricular (LV, RV respectively) hypertrophy and increased stroke volumes, which correlate with maximal work capacity and are known to be load and sports discipline dependent [1,2,3,4].PLOS ONE | DOI:10.1371/journal.pone.0141680 October 30, 2015Athletic Heart and a Common NOS3 Gene VariantRecent recognition of the endurance training-induced disproportionate right ventricular load highlighted a more pronounced fatigue and a potentially larger damage of the right—compared to the left—heart chamber [5,6]
Weight and body mass index were higher in men versus women and in athletes versus non-athletes (Table 1)
An important value in the interpretation of cardiac magnetic resonance imaging results, was higher in athletes when compared with non-athletic controls (Table 1)
Summary
Intensive physical conditioning results in cardiac adaptive responses known as the “athlete’s heart.” These changes include development of left- and right ventricular (LV, RV respectively) hypertrophy and increased stroke volumes, which correlate with maximal work capacity and are known to be load and sports discipline dependent [1,2,3,4].PLOS ONE | DOI:10.1371/journal.pone.0141680 October 30, 2015Athletic Heart and a Common NOS3 Gene VariantRecent recognition of the endurance training-induced disproportionate right ventricular load highlighted a more pronounced fatigue and a potentially larger damage of the right—compared to the left—heart chamber [5,6]. Intensive physical conditioning results in cardiac adaptive responses known as the “athlete’s heart.”. These changes include development of left- and right ventricular (LV, RV respectively) hypertrophy and increased stroke volumes, which correlate with maximal work capacity and are known to be load and sports discipline dependent [1,2,3,4]. Diminished right ventricular contractile reserve and limited pulmonary vascular response put an almost ten-fold stress on the RV wall during exercise [5]. Chronic RV overload evokes structural, electrical and functional changes, which may result in the development of exercise-induced arrhythmogenic RV cardiomyopathy and increase the incidence of ventricular arrhythmias [6,7]
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