Aerobic high-intensity interval training (HIIT) has demonstrated benefits for ventricular remodeling after myocardial infarction (MI) through various mechanisms. Despite this, the optimal training volume is not well known. The present study aimed to assess the effects of different (low vs. high volume) aerobic HIIT compared to an attentional control (AC) group on echocardiographic and biochemical indicators of left ventricular (LV) remodeling in adults after MI. Randomized clinical trial conducted on post-MI patients with preserved ventricular function. Participants were assigned to three study groups. Two groups performed HIIT 2 d/week, one group with low-volume HIIT (20 min, n = 28) and another with high-volume HIIT (40 min, n = 28). A third group was assigned to AC (n = 24) with recommendations for unsupervised aerobic training. Left ventricular echocardiographic parameters and cardiac biomarker levels (N-terminal pro-b-type natriuretic peptide, NT-proBNP; soluble growth stimulation expressed gene 2, ST2; troponin T; and creatine kinase) were assessed at baseline and after the intervention (16 weeks). Eighty participants (58.4 8.3 yrs, 82.5% male) were included. Both low- and high-volume HIIT showed increases (p 0.05) in left ventricular end-diastolic diameter (1.2%, 2.6%), and volume (1.1%, 1.3%), respectively. Interventricular septal and posterior walls maintained their thickness (p = 0.36) concerning the AC. Significant (p 0.05) gain in diastolic function was shown with the improvements in E (-2.1%, -3.3%), e' waves (2.2%, 5.5%), and the deceleration time (2.1%, 2.9%), and in systolic function with a reduction in global longitudinal strain (-3.2%, -4.7%), respectively. Significant (p 0.05) reductions of N-terminal pro-B-type natriuretic peptide (NT-proBNP) (-4.8%, -11.1%) and of ST2 (-21.7%, -16.7%)were found in both HIIT groups respectively compared to the AC group. Creatine kinase elevation was shown only in high-volume HIIT (19.3%, p 0.01). Low-volume HIIT is proposed as a clinically time-efficient and safer strategy to attenuate dysfunctional remodeling by preventing wall thinning and improving LV function in post-MI patients.