Habitual exercise attenuates myocardial stiffness in diabetes mellitus in rats.

The effects of regular voluntary (habitual) exercise on left ventricular (LV) diastolic performance, as well as on those hemodynamic, LV geometric and myocardial interstitial changes that influence myocardial diastolic function, were examined in streptozocin (50 mg/kg)-induced diabetes mellitus (DM) in male rats. After 16 wk of regular exercise on voluntary running wheels, cardiac performance was measured in anesthetized open-chest ventilated rats. Rats with DM developed a decrease in LV end-diastolic (LVED) chamber and myocardial wall compliance associated with an increase in myocardial collagen fluorescence (a measure of collagen advanced glycosylation end product concentrations), an increase in systemic blood pressure, and a dilated LV. However, LV end-systolic elastance and total myocardial hydroxyproline concentration were unchanged. Habitual exercise prevented the augmented LVED chamber stiffness (slope of linearized LVED pressure-strain relation, DM vs. exercise DM, P < 0.01) and myocardial wall stiffness (slope of linearized LVED stress-strain relation, DM vs. exercise DM, P < 0.001) produced by DM. However, neither markers of blood glucose control, blood pressure, LV geometry, myocardial hydroxyproline concentration, nor collagen fluorescence were altered by the exercise program. A reduced LVED chamber and myocardial wall stiffness, as noted in euglycemic control rats in response to regular exercise, was also not associated with hemodynamic or myocardial interstitial alterations. Therefore, regular voluntary exercise opposes the decrement in myocardial diastolic performance produced by DM in male rats without influencing the accumulation of myocardial advanced glycosylation end products thought to be partly responsible for the stiff myocardium after chronic hyperglycemia. The beneficial effects of regular exercise on myocardial compliance are likely to be a consequence of changes in active as opposed to passive properties of the myocardial wall.