A six-month exercise intervention in subclinical diabetic heart disease: Effects on exercise capacity, autonomic and myocardial function

Objective Autonomic dysfunction may contribute to the etiology and exercise intolerance of subclinical diabetic heart disease. This study sought the efficacy of exercise training for improvement of peak oxygen uptake (VO2peak) and cardiac autonomic function in type 2 diabetic patients with non-ischemic subclinical left-ventricular (LV) dysfunction. Materials/Methods Forty-nine type 2 diabetic patients with early diastolic tissue Doppler velocity >1 standard deviation below the age-based mean entered an exercise intervention (n = 24) or usual care (n = 25) for 6-months (controlled, pre-/post- design). Co-primary endpoints were treadmill VO2peak and 5-min heart-rate variability (by the coefficient of variation of normal RR intervals [CVNN]). Autonomic function was additionally assessed by resting heart-rate (for sympathovagal balance estimation), baroreflex sensitivity, cardiac reflexes, and exercise/recovery heart-rate profiles. Echocardiography was performed for LV function (systolic/diastolic tissue velocities, myocardial deformation) and myocardial fibrosis (calibrated integrated backscatter). Results VO2peak increased by 11% during the exercise intervention (p = 0.001 vs. −1% in controls), but CVNN did not change (p = 0.23). Reduction of resting heart-rate in the intervention group (p < 0.05) was associated with an improvement in the secondary endpoint of heart-rate variability total spectral power (p < 0.05). However, baroreflex sensitivity, cardiac reflexes, and exercise/recovery heart-rate profiles showed no significant benefit. No effects on LV function were observed despite favorable reduction of calibrated integrated backscatter in the intervention group (p < 0.05). Conclusions The exercise intolerance of subclinical diabetic heart disease was amenable to improvement by exercise training. Despite a reduction in resting heart-rate and potential attenuation of myocardial fibrosis, no other cardiac autonomic or LV functional adaptations were detected.