Exercise attenuates the premature cardiovascular aging effects of type 2 diabetes mellitus

Type 2 diabetes mellitus (T2D) is an example of a disease process that results in decrements in function additional to those imposed by the inexorable 'primary aging' process. These decrements due to disease, rather than primary aging, can be termed 'secondary aging', and include the premature development (as early as adolescence) of asymptomatic preclinical cardiovascular abnormalities (e.g. endothelial dysfunction, arterial stiffness, diastolic dysfunction), as well as impaired exercise performance. These abnormalities are important, as they are associated with greater cardiovascular morbidity and mortality in people with and without T2D. A better understanding of the pathophysiology of secondary cardiovascular aging in people with T2D is warranted, and an evaluation of the benefits of existing treatments for these abnormalities is useful (e.g. exercise training). The focus of this review is to discuss the data relevant to the following key postulates: (a) T2D causes premature cardiovascular aging; (b) in contrast to primary cardiovascular aging, the premature cardiovascular aging of T2D may be modifiable with exercise. The exercise-focused perspective for this review is appropriate because impairments in exercise performance are markers of premature cardiovascular aging in T2D, and also because exercise training shows promise to attenuate some aspects of cardiovascular aging during the preclinical stage.