Exercise Training Across the Hypertensive Heart Disease Continuum: Clinical Evidence and Implications for Prescription.

Arterial hypertension is the leading driver of hypertensive heart disease (HHD), the cardiac structural or functional injury attributable to sustained pressure overload, which promotes left ventricular hypertrophy and provides the substrate for incident heart failure, especially heart failure with preserved ejection fraction (HFpEF). Antihypertensive pharmacotherapy lowers blood pressure (BP) and regresses hypertrophy, yet residual cardiovascular risk persists, and exercise training may add to what drug therapy achieves. HHD progresses through interwoven autonomic, vascular, structural, and diastolic mechanisms, and the benefits of training are uneven across them: functional capacity, BP, endothelial function, and autonomic indices improve within typical trial durations, whereas resting diastolic indices, left ventricular mass, and myocardial fibrosis markers change inconsistently. Carotid-femoral pulse wave velocity is itself sensitive to distending pressure, so a fall does not by itself establish structural arterial remodeling. Small hypertensive trials support favorable geometry, and animal models support antifibrotic mechanisms, but in predominantly hypertensive HFpEF cohorts, capacity gains often occur without durable resting diastolic reversal or mortality benefit. By pairing each hypertension-specific mechanism with the corresponding human evidence, the present narrative review concludes that exercise training is a beneficial adjunct to antihypertensive therapy and to broader risk-factor management, while reverse remodeling and clinical-event reduction remain incompletely proven. Phenotype-guided trials with sensitive imaging, exercise-load endpoints, and hard outcomes are needed.