Type 2 diabetes (T2D) is associated with reduced cardiac reserve and aerobic capacity. Altered myocardial autonomic nervous regulation has been demonstrated in humans with diabetes (indirectly) and animal models (directly).
To determine the chronotopic and inotropic response of the type 2 diabetic heart to β-adrenergic stimulation.
8 people with uncomplicated type 2 diabetes and 7 matched controls performed a DEXA scan and V[Combining Dot Above]O2peak test. Plasma catecholamines were determined at rest and during peak exercise. On a second visit, heart rate (HR) and left ventricular contractility was assessed using echocardiography during supine rest, parasympathetic blockade (atropine), and during incremental β-adrenergic stimulation (dobutamine).
V[Combining Dot Above]O2peak and heart rate (HR) reserve were lower in T2D (P<0.05) as expected. Both groups increased norepinephrine comparably (P=0.23) during peak exercise, however epinephrine increased less in the T2D group (P<0.05). The dobutamine dose required to achieve 85% of age predicted maximal HR was 36% higher in CON (P<0.05). Resting HR was higher (P<0.01) and stroke volumeFFM was smaller (P<0.05) in T2D. During dobutamine infusion the response (% change) in HR, end diastolic volumeFFM, stroke volume, ejection fraction and cardiac output was not different between the groups. However; HR was higher (P<0.01) and end diastolic volumeFFM (P<0.01), stroke volumeFFM (P<0.01), ejection fraction (P<0.05) and stroke work (P<0.01) were lower in T2D.
Though the type 2 diabetic heart worked at smaller volumes, the heart rate and contractile response to β-adrenergic stimulation were unaffected by diabetes. The reduced cardiac reserve observed in uncomplicated type 2 diabetes was not explained by impaired myocardial sympathetic responsiveness but may reflect changes in the loading conditions or function of the diabetic left ventricle.
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