The effects of voluntary exercise and prazosin on capillary rarefaction and metabolism in streptozotocin-induced diabetic male rats

Type-1 diabetes mellitus (T1D) causes impairments within the skeletal muscle microvasculature. Both regular exercise and prazosin have been shown to improve skeletal muscle capillarization and metabolism in healthy rats, through distinct angiogenic mechanisms. The aim of this study was to evaluate the independent and additive effects of voluntary exercise and prazosin treatment on capillary-to-fiber ratio (C:F) in streptozotocin (STZ)-treated diabetic rats. STZ (65mg/kg) was intraperitoneally administered to male Sprague-Dawley rats (n=36) to induce diabetes, with healthy, non-diabetic, sedentary rats (n=10) as controls. The STZ-treated rats were then divided into sedentary (SED) or exercising (EX, 24h access to running wheels) groups and then further subdivided into prazosin (Praz) or water (H₂O) treatment groups: non-diabetic-SED-H₂O, STZ-SED-H₂O, STZ-EX-H₂O, STZ-SED-Praz, and STZ-EX-Praz. After 3 weeks, untreated diabetes significantly reduced the C:F in tibialis anterior (TA) and soleus muscles in the STZ-SED-H₂O animals (both P<0.05). Voluntary exercise and prazosin treatment independently resulted in a normalization of C:F within the TA (1.86±0.12 & 2.04±0.03 vs 1.71±0.09, P<0.05) and the soleus (2.36±0.07 & 2.68±0.14 vs 2.13±0.12, P<0.05). The combined STZ-EX-Praz group resulted in the highest C:F within the TA (2.26±0.07, P<0.05). Voluntary exercise volume was negatively correlated with fed blood glucose levels (r²=-0.7015, P<0.01), and when combined with prazosin, caused further enhanced non-fasted glucose (P<0.01). Exercise and prazosin reduced circulating non-esterified fatty acids (NEFAs) more than either stimulus alone (P<0.05). These results suggest that the distinct stimulation of angiogenesis, with both regular exercise and prazosin treatment, causes a cooperative improvement in the microvascular complications associated with T1D.

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