Metaboreflex-Induced Flow Improvement is Absent in Older Males With Type II Diabetes
Bravo, Michael Francis
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Background: Exercise is widely recognized as the cornerstone of management of type II diabetes (T2D). However, it is also known that people with T2D have poor adherence to exercise regimens, which is largely thought to be because of poor exercise tolerance. Recent studies have suggested that this exercise intolerance may be caused by a reduction in exercising muscle blood flow. One physiological mechanism which could potentially contribute is the muscle metaboreflex (MMR). This mechanism is thought to be a pressure-based flow-improving mechanism, but as a result of reduced efficacy of vasodilators and sympatholytic agents, might in fact be restraining the flow-improvement in persons with T2D. Hypothesis: Persons with T2D would not improve exercising muscle blood flow upon MMR activation. This absence of flow-improvement will be due to an augmented vasoconstriction in the exercising muscle. Methods: T2D (n=7) and CTL (n=6) participants performed rhythmic forearm handgrip exercise at an intensity equivalent to 20% MVC for 9 minutes with and without the application of ischemic plantar flexion (IPF). Forearm blood flow (FBF), mean arterial pressure (MAP), cardiac output (CO), heart rate (HR), total peripheral resistance (TPR) and forearm vascular conductance (FVK) were quantified for the last thirty seconds of each of four time points during the protocol. Plasma norepinephrine was measured via deep venous and arterialized venous blood sampling. Results: Steady state exercising FBF was increased in CTL but not in T2D during MMR activation (mean ± SE mL/min: CTLControl 161.16 ± 5.95, CTLMMR 212.72 ± 9.49, T2DControl 156.71 ± 13.08, T2DMMR 144.22 ± 10.55). This occurred despite similar increases in MAP, CO, HR, and TPR (across groups and treatment conditions, NS). FVK increased in CTL during the MMR protocol compared to the Control protocol, but decreased in the T2D group using the same comparison (mean ± SE mL/min/100 mm Hg: CTLControl 144.74 ± 5.63, CTLMMR 176.76 ± 11.99, T2DControl 143.29 ± 13.44, T2DMMR 103.53 ± 8.44). Conclusions: In the exercise model utilized, persons with T2D do not demonstrate the MMR-induced flow improvement seen in CTL. This impaired muscle blood flow in T2D is the result of MMR induced exercising limb vasoconstriction.