Abstract
BackgroundIt is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy against diabetes mellitus; however, the precise mechanism remains unknown. The aim of this study was to investigate the cardioprotective effect of voluntary exercise in the Goto-Kakizaki type 2 diabetic rat heart against ischemia–reperfusion injury and to clarify its biochemical background, focusing on the nitric oxide synthase/heme oxygenase system.MethodsOne group of male Goto-Kakizaki rats were allowed voluntary exercise, whereas others were kept sedentary for 6 weeks. At the end of the 6th week the hearts were isolated from both groups and subjected to 45-min coronary occlusion followed by 120-min reperfusion. The infarct size was evaluated by means of triphenyltetrazolium chloride staining. The cardiac and aortic nitric oxide synthase/heme oxygenase activities, plasma leptin and glucose concentrations were also assessed.ResultsThe sedentary state prior to the ischemia–reperfusion injury was associated with a significantly higher infarct size (24.56 ± 2.21 vs. 16.66 ± 1.87 %) as compared with that in the voluntary wheel-running group. Exercise altered the constitutive nitric oxide synthase activity; an enhancement was evident in the cardiac (42.5 ± 2.72 vs. 75.6 ± 13.34 pmol/min/mg protein) and aortic tissues (382.5 ± 66.57 vs. 576.9 ± 63.16 pmol/min/mg protein). Exercise lead to a higher heme oxygenase activity (0.68 ± 0.08 vs. 0.92 ± 0.04 nmol bilirubin/h/mg protein) in the diabetic rat hearts. Exercise was associated with lower plasma leptin (192.23 ± 7.22 vs. 169.65 ± 4.6 ng/L) and blood glucose (19.61 ± 0.76 vs. 14.58 ± 0.88 mmol/L) levels.ConclusionsThese results indicate the beneficial role of exercise against myocardial ischemia–reperfusion injury in diabetic rats. These observations in experimental diabetes suggest that the cytoprotective mechanism of exercise involves modulation of the nitric oxide synthase/heme oxygenase system and metabolic parameters that may be responsible for cardioprotection.Electronic supplementary materialThe online version of this article (doi:10.1186/s13098-015-0080-x) contains supplementary material, which is available to authorized users.
Highlights
It is well established that physical exercise continues to be one of the most valuable forms of nonpharmacological therapy against diabetes mellitus; the precise mechanism remains unknown
Animal studies confirm that regular bouts of aerobic exercise protect the heart from IR injury [3], while convincing evidence indicates that both short-term (3–5 consecutive days) and long-term endurance exercise improves the myocardial tolerance to IR injury in both male and female and both young and old animals [4], there is no clear understanding of the cardioprotective effect of exercise in the presence of comorbidities such as diabetes mellitus (DM)
We set out to evaluate the effects of exercie on IR injury, heme oxygenase (HO), and nitric oxide synthase (NOS) in Gioto Kakizaki (GK) rats, undergoing 6 weeks of Voluntary exercise (Wheelrunning) followed by acute myocardial infarction (MI)
Summary
It is well established that physical exercise continues to be one of the most valuable forms of nonpharmacological therapy against diabetes mellitus; the precise mechanism remains unknown. The aim of this study was to investigate the cardioprotective effect of voluntary exercise in the Goto-Kakizaki type 2 diabetic rat heart against ischemia–reperfusion injury and to clarify its biochemical background, focusing on the nitric oxide synthase/heme oxygenase system. To the best of our knowledge, there have been no studies that have evaluated the influence of exercise on the infarct size-limiting effect, and mediators responsible for exercise-induced cardioprotection in rats with spontaneous type 2 DM (T2DM). We set out to evaluate the effects of exercie on IR injury, heme oxygenase (HO), and nitric oxide synthase (NOS) in Gioto Kakizaki (GK) rats, undergoing 6 weeks of Voluntary exercise (Wheelrunning) followed by acute MI
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