The effect of exercise intensity on ischemia/reperfusion injury and myokine profile in diabetic cardiomyopathy release_7en7sz7v5nd3hmjsrbbx5ldp4m

Abstract

<jats:title>Abstract</jats:title> Diabetes is a metabolic disorder characterised by hyperglycaemia. The diabetic heart becomes more susceptible to ischemic injury. Although exercise induces a cardioprotective phenotype, the determination of accurate protocol is crucial. We compared two different exercise intensities in the diabetes model and evaluated the role of myokines in exercise-induced cardioprotection. Male, adult, Wistar albino rats were used (n = 20 each). First, animals were divided into two groups: Non-Diabetic (ND), Diabetic (DM); then groups were further divided into subgroups: Sedentary (S), Training-1 (T1 = 10 m/min, 0° inclination), and Training-2 (T2 = 20 m/min, 10° inclination). Diabetes was induced by streptozotocin (60 mg/kg; i.p.). Animals exercised on a treadmill 5 days/a week for 6 weeks. Then, hearts were attached to the Langendorff apparatus and baseline functional parameters were measured. After 30'/120'I/R protocol, infarct size was evaluated with tetrazolium chloride staining. Interleukin-6, FNDC5, and myonectin levels were measured both in the soleus and the left ventricle. We observed cardiac hypertrophy and impaired baseline LV function in diabetes. Infarct size was significantly larger in diabetics and only T1 decreased the infarct size whereas T2 further aggravated it. Moreover, post-ischemic recovery was worst in diabetic-T2 group. Irisin and myonectin levels were decreased in the soleus muscle of diabetic animals. T1 increased the myonectin levels in the left ventricle of non-diabetics, and this effect was blunted in diabetic-T1 animals. As a conclusion, light-intensity exercise is a better approach to prevent ischemic damage in diabetes besides moderate intensity may be hazardous in diabetic population.
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