Myocardial perfusion (MP) may differ in physiologic and pathologic left ventricular hypertrophy (LVH). We compared MP in LVH in elite athletes and patients with hypertension with healthy, age-matched subjects. We included 12 rowers with LVH, 19 patients with hypertension with LVH, and 2 age-matched groups of healthy subjects (n = 11 and n = 12). The left ventricular mass index was determined echocardiographically. MP was measured by N-13 ammonia positron emission tomography. The maximal perfusion and perfusion reserve were studied using dipyridamole, and endothelial function was assessed by a cold pressor test. The degree of LVH was similar in athletes and those with hypertension. Compared with controls, athletes had 20% lower baseline MP (p <0.05), a similar response to the cold pressor test, and a higher perfusion reserve (31%, p <0.05). The patients with hypertension had a 25% higher baseline MP (p <0.05), a reduced increase during the cold pressor test (12% vs 25% in controls, p <0.05), and a reduced perfusion reserve (27% lower, p <0.001). The peak global perfusion (MP × left ventricular mass index) was 62% higher in athletes (p <0.05) than in controls, but the peak global perfusion in patients with hypertension did not differ from that of controls. In conclusion, physiologic LVH in athletes is suited for a high peak workload at the cost of only a small increase in basal myocardial oxygen consumption. In contrast, LVH in the presence of hypertension is a good adaptation to the increased baseline workload with maintained maximal cardiac performance. Endothelial dysfunction may contribute to the reduced perfusion reserve seen in hypertensive LVH.