Adaptations in the balance between coronary blood flow and myocardial metabolism in endurance athletes

Due to the limited anaerobic capability of the myocardium, the heart is highly dependent on a continuous supply of oxygen to meet its metabolic requirements. If this need for oxygen is not met, cardiac function declines within seconds. Since resting left ventricular oxygen extraction is high (∼75%), increases in metabolic demand are met largely by increases in coronary flow. The mechanisms underlying metabolic coronary vasodilatation are not fully understood; however, recent studies have identified β-adrenoceptor ‘feedforward’ dilatation, H2O2 and ATP as potential contributors (Duncker & Bache, 2008). There are numerous conditions that affect the myocardial oxygen supply–demand balance. One such condition is endurance exercise training which has been the focus of much research, albeit with little consensus. Earlier studies in endurance athletes found either reduced or no change in baseline coronary flow while adenosine-mediated vasodilatation was either increased or unchanged compared to untrained individuals (Kalliokoski et al. 2002; Kjaer et al. 2005). Confounding factors that could contribute to these disparate findings are differences in the degree of cardiac hypertrophy and/or myocardial workload. In addition, Mizuno et al. (2005) recently documented that the expression of adenosine A2A receptors is increased in endurance-trained athletes. However, whether differences in myocardial mass, metabolism or coronary A2A receptor density could account for differences in baseline flow and/or coronary flow reserve in endurance athletes has not been delineated. In this issue of The Journal of Physiology, Heinonen et al. (2008) examined the relationship of left ventricular coronary flow at rest and during adenosine-induced vasodilatation to cardiac mass, estimates of myocardial work and adenosine A2A receptor expression in untrained and endurance-trained athletes. They found that total coronary flow under baseline conditions is elevated in athletes while flow reserve to adenosine is unchanged. The increase in baseline coronary flow is clearly related to the ∼70% increase in cardiac mass in the endurance athletes as normalization revealed a significant reduction in myocardial perfusion per gram of tissue mass. When this normalized flow is further related to an index of cardiac workload (reduced ∼45% in endurance athletes), myocardial perfusion per gram of tissue was ∼40% higher in athletes. Interestingly, this relative ‘overperfusion’ is actually constrained by an increase in coronary vascular resistance. Therefore, endurance training elicits alterations in the myocardial oxygen supply–demand balance that produce a left ventricle that is more phenotypically consistent with the more efficient right ventricle (Hart et al. 2001), i.e. lower myocardial workload and flow per gram with a relative ‘overperfusion’ as evidenced by a decrease in baseline oxygen extraction or increased oxygen extraction reserve (Hannukainen et al. 2007). Heinonen et al. (2008) found no differences in coronary flow reserve to adenosine between untrained and trained athletes. Estimates of cardiac A2A receptor density were also unchanged and were not directly coupled with changes in myocardial perfusion. The authors suggest that the degree of adenosine-induced vasodilatation declined as the level of fitness increased; however, this trend is probably related to the decrease in myocardial perfusion per gram of tissue as absolute changes in flow from baseline were similar between groups. These findings demonstrate that the vasodilatory capacity of the coronary circulation is unaltered in highly trained endurance athletes and argues against the presence of maladaptive hypertrophic cardiomyopathy. In conclusion, the present study by Heinonen et al. (2008) demonstrates important adaptations in the balance between coronary blood flow and myocardial metabolism in endurance athletes. The findings underscore the complex interaction between myocardial perfusion, mass and workload and highlight a key phenotypic switch in cardiac energy balance that occurs in highly trained endurance athletes.