There is evidence that aerobic exercise improves endothelial function in healthy subjects as well as in patients with chronic heart failure. However, it is unknown whether this effect occurs in patients with recent myocardial infarction (AMI).

Fifty-two patients with a recent first uncomplicated AMI underwent endothelial function evaluation before and after 3 months of moderate aerobic exercise training. We measured brachial artery vasomotor reactivity using flow-mediated dilation (FMD), a cold pressor (CP) test, and sublingual nitroglycerin. Patients were randomized into 2 groups: 28 patients (G1) underwent training, while 24 patients (G2) served as controls. Brachial artery vasomotor reactivity was reassessed after 1 month of detraining (DT).

At baseline the FMD was 1.66% ± 4.11% in G1 and 2.04% ± 3.4% in G2 (P = NS) and vasoconstriction was evident after a CP test. The diameter reduction was −4.1% ± 3.89% in G1 and −4.39% ± 5.67% in G2 (P = NS). At follow-up the FMD had increased to 9.39% ± 4.87% in G1 (P < .01) and to 4.4% ± 3.9% in G2 (P < .01 vs G1). Vasoconstriction during a CP test was observed only in G2. Endothelium-independent vasodilation was unchanged in both groups. Effort tolerance increased by 32% in G1 patients (P < .01 versus G2) and was correlated with FMD change (R = 0.51, P < .01). After detraining the FMD was significantly reduced in G1 (P < .01) and a further vasoconstriction was evident after CP testing.

Exercise training improves endothelium-dependent vasodilation in post-AMI patients. This improvement is associated with a significant increase in exercise tolerance. These benefits disappeared after detraining.