Visual Abstract
Type 2 diabetes (T2D) is a global epidemic leading to excess cardiovascular (CV) mortality. CV risk factor modification does not prevent progression to non-ischemic heart failure (HF), so early detection and intervention are needed. Our group has identified preclinical cardiac dysfunction associated with central arterial stiffness and decreased cardiorespiratory fitness which is responsive to exercise training (ET) intervention.
Cardiac parameters were measured in BMI-similar participants with and without T2D, before and after a 90-day progressive aerobic ET program and compared to lean nondiabetic historical controls. Left ventricular end systolic volume (LV ESV), end diastolic volume (EDV), stroke volume, and cardiac output for both groups pre- and post-exercise training were significantly lower than those of lean controls (Table 1). ESV and EDV increased post-exercise in T2D but not in the control group. While ejection fraction did not differ between groups, decreased heart rate in people with T2D following ET suggests compensation. Pulse wave velocity (PWV) by carotid to femoral tonometry (SphygmoCor) did not change with ET, but thoracic aortic PWV from 4D flow MRI significantly improved with ET across both groups. Cardiac and central arterial function are deleteriously and differently impacted by obesity and T2D. Advanced imaging may be a useful tool to longitudinally assess function and response to intervention.
D. Enge: None. K. Jarvis: None. T. Fujiwara: None. M. Markl: None. K. S. Hunter: None. A. J. Barker: None. K. J. Nadeau: None. J. G. Regensteiner: None. J. E. Reusch: Advisory Panel; Self; Medtronic. M. Schafer: None. R. L. Scalzo: None. D. Rafferty: None. I. E. Schauer: None. L. Abushamat: None. M. O. Whipple: None. E. Johnson: None. M. B. Scott: None.
National Institutes of Health (R01DK124344, R01HL133504)
