Francesca Saladini1, Paolo Palatini2. 1. Department of Medicine, University of Padova, via Giustiniani, 2, 35128, Padua, Italy. 2. Department of Medicine, University of Padova, via Giustiniani, 2, 35128, Padua, Italy. palatini@unipd.it.
Abstract
PURPOSE OF REVIEW: Metabolic syndrome (MetS), a cluster of risk factors including central obesity, metabolic abnormalities, and arterial hypertension, is a well-known determinant of arterial wall remodeling and stiffening. The mechanisms whereby MetS promotes arterial stiffening include increased sympathetic activity with the associated fast heart rate, enhanced activity of the renin-angiotensin-aldosterone system, increased production of inflammatory cytokines and reactive oxygen species, and reduction of nitric oxide availability. These adverse effects can explain why aerobic physical activity can retard the age-related decline in arterial elasticity in subjects with MetS. RECENT FINDINGS: A large number of studies have shown that in patients with MetS, exercise can reduce body weight and blood pressure and improve the metabolic profile. In addition, regular exercise training can counterbalance the detrimental effects of MetS by reducing sympathetic activity and improving endothelial function with a beneficial effect on arterial elasticity. Indeed, the majority of published data have shown a favorable effect of aerobic exercise on pulse wave velocity, augmentation index, central blood pressure, and small artery compliance. Special attention should be paid by clinicians to people with MetS in whom the adverse effect of metabolic disturbances on arterial structure and function can be offset by a program of physical training.
PURPOSE OF REVIEW: Metabolic syndrome (MetS), a cluster of risk factors including central obesity, metabolic abnormalities, and arterial hypertension, is a well-known determinant of arterial wall remodeling and stiffening. The mechanisms whereby MetS promotes arterial stiffening include increased sympathetic activity with the associated fast heart rate, enhanced activity of the renin-angiotensin-aldosterone system, increased production of inflammatory cytokines and reactive oxygen species, and reduction of nitric oxide availability. These adverse effects can explain why aerobic physical activity can retard the age-related decline in arterial elasticity in subjects with MetS. RECENT FINDINGS: A large number of studies have shown that in patients with MetS, exercise can reduce body weight and blood pressure and improve the metabolic profile. In addition, regular exercise training can counterbalance the detrimental effects of MetS by reducing sympathetic activity and improving endothelial function with a beneficial effect on arterial elasticity. Indeed, the majority of published data have shown a favorable effect of aerobic exercise on pulse wave velocity, augmentation index, central blood pressure, and small artery compliance. Special attention should be paid by clinicians to people with MetS in whom the adverse effect of metabolic disturbances on arterial structure and function can be offset by a program of physical training.
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