Background: Myocardial dysfunction is a common development in Type I diabetes mellitus (DM). Exercise is prescribed to manage both myocardial impairments and DM, although its ability to ameliorate anatomical and functional changes typically observed in the DM heart is uncertain.

Methods: We examined the structure and function of the DM myocardium over 8-weeks and determined the effect of exercise prescribed either at the onset of, or 4-weeks following, diabetes induction. Sixty Sprague-Dawley rats were divided into DM and non-DM groups. Animals from each group (n = 10) were assigned to 1 of 3 treatments: (1) sedentary (SED); (2) 4-weeks sedentary followed by 4-weeks of exercise (EX-4); or (3) 8-weeks of exercise (EX-8). Exercise training consisted of treadmill running for 1-hour per day, 5-days per week at 27m/min (~70% VO_2max). DM was induced by a low-dose injection of streptozotocin (20mg/kg; i.p.) for 5 consecutive days. Structural and functional measures were acquired by echocardiographic imaging at 8-weeks.

Results: Heart rate (HR) was significantly reduced (P < .05) in all DM groups, while cardiac output was significantly greater (P < .05) with exercise and was independent of DM. All diabetic animals showed significantly reduced (P < .05) heart mass (standardized to tibial length), however EX-8 DM animals show significantly less (P < .05) muscle loss compared to SED and EX-4 DM animals. In contrast to the apparent beneficial effects of exercise, end-systolic volume (ESV), a general measure inversely related to healthy LV function, was elevated in DM, with EX-8 showing a significantly greater (P < .05) ESV than all other groups. In addition, LV fractional shortening, a measure of systolic function, was diminished in DM animals and was exacerbated by exercise. Moreover, LV posterior and anterior walls showed significant thinning (P < 0.05) in diabetic animals and was independent of exercise.

Conclusions: These results indicate that exercise initiated at the onset of DM was able to reduce the loss of LV mass and improve cardiac output, whereas exercise initiated 4-weeks after the onset of DM showed improved cardiac output, but could not prevent a loss of LV mass. Moreover, the present study demonstrated that certain measures of DM heart function benefit from exercise (LV mass and cardiac output), some measures were independent of exercise (wall thinning), while other measures (ESV and LV fractional shortening) appeared to be exacerbated by exercise and may have advanced diabetic cardiomyopathy. Although exercise is typically associated with both improved cardiovascular function and diabetes management there emerges a clear need to delineate exercise mechanisms in order to extract its benefits while avoiding excessive stress.