"Endothelial Dysfunction and Exercise Responses in Type 1 Diabetes" by Ruby A. Nyarko, Ashlesha D. Dalve et al.
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Abstract

Type 1 diabetes (T1D) is associated with widespread hyperglycemia-induced vascular damage, which affects both conduit and resistance arteries. This damage has been demonstrated by impaired vasodilatory responses to a 5-minute ischemic stimulus (flow-mediated dilation) and infusion of pharmacological vasodilators in patients with T1D. However, whether this vascular impairment affects blood flow regulation during steady-state exercise in T1D remains unclear. PURPOSE: Herein, we tested the hypothesis that adults with T1D would exhibit blunted forearm blood flow (FBF) and forearm vascular conductance (FVC) during steady-state rhythmic handgrip exercise (RHG), compared to age-matched healthy controls. METHODS: We studied 27 adults (15 Control (7 men); 12 T1D (5 men)) [age (Control: 27 ± 9; T1D: 29 ± 10 years; mean ± SD, p = 0.54); BMI (Control: 24.0 ± 2.3; T1D: 23.8 ± 3.3 kg/m²; p = 0.86)]. FBF (duplex Doppler ultrasound) and mean arterial pressure (MAP; finger photoplethysmography) were measured at baseline and during RHG performed at 3 workloads for 3 minutes each (15%, 30%, and 45% of maximal voluntary contraction (MVC)). FVC was calculated as FBF/MAP. Participants were also assessed for flow-mediated dilation (FMD) to evaluate conduit artery dilation at rest. RESULTS: Baseline FBF (Control: 56.7 ± 28.2 and T1D: 61.3 ± 28.5 ml/min; p = 0.68), FVC (Control: 67.7 ± 33.6 and T1D: 71.6 ± 30.6 ml/min/100 mmHg; p = 0.59), and MVC (Control: 64.4 ± 20.4 and T1D: 61.7 ± 17.8 kg; p = 0.72) were similar between groups. Both groups exhibited intensity-dependent increases in FBF and FVC; however, no significant differences were observed between groups [two-way repeated measures ANOVA; %Δ FBF (group effect p = 0.50, intensity effect p < 0.001, interaction p = 0.31) and %Δ FVC (group effect p = 0.53, intensity effect p < 0.001, interaction p = 0.39)]. For instance, in response to RHG at 45% MVC, the Control group showed a 548 ± 195% increase in FBF from baseline, whereas the T1D group showed a 475 ± 196% increase (p = 0.35). Baseline MAP and changes in MAP during RHG at each intensity were not different between the groups (e.g., ΔMAP at 45% MVC: Control = 13 ± 8 mmHg and T1D = 14 ± 11 mmHg; p = 0.77). Lastly, FMD responses were significantly lower in T1D participants compared to healthy controls (Control: 9.5 ± 2.3% and T1D: 6.1 ± 3.0%; p = 0.002) and remained significantly reduced after normalization to shear rate area under the curve (p = 0.006). CONCLUSION: Our preliminary findings suggest that while endothelial dysfunction is present, it may not impair blood flow during steady-state submaximal exercise in T1D.

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