| Autor: |
Bock, Joshua M., Hughes, William E., Ueda, Kenichi, Feider, Andrew J., Satoshi Hanada, Kruse, Nicholas T., Erika Iwamoto, Casey, Darren P. |
| Předmět: |
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| Zdroj: |
American Journal of Physiology: Heart & Circulatory Physiology; Oct2020, Vol. 319 Issue 4, pH797-H807, 11p |
| Abstrakt: |
Patients with type 2 diabetes mellitus (T2DM) exhibit diminished exercise capacity likely attributable to reduced skeletal muscle blood flow (i.e., exercise hyperemia). A potential underlying mechanism of the impaired hyperemic response to exercise could be inadequate blunting of sympathetic-mediated vasoconstriction (i.e., poor functional sympatholysis). Therefore, we studied the hyperemic and vasodilatory responses to handgrip exercise in patients with T2DM as well as vasoconstriction to selective a-agonist infusion. Forearm blood flow (FBF) and vascular conductance (FVC) were examined in patients with T2DM (n = 30) as well as nondiabetic controls (n = 15) with similar age (59±9 vs. 60±9 yr, P = 0.69) and body mass index (31.4±5.2 vs. 29.5±4.6 kg/m², P = 0.48). Intra-arterial infusion of phenylephrine (a1-agonist) and dexmedetomidine (a2-agonist) were used to induce vasoconstriction: [(FVCwith drug - FVCpredrug)/FVCpredrug × 100%]. Subjects completed rest and dynamic handgrip exercise (20% of maximum) trials per a-agonist. Patients with T2DM had smaller increases (from rest) in FBF (147±71 vs. 199±63 ml/min) and FVC (126±58 vs. 176±50 ml·min-1·100 mmHg-1, P < 0.01 for both) during exercise compared with controls, respectively. During exercise, patients with T2DM had greater a1- (-16.9±5.9 vs. -11.3±3.8%) and a2-mediated vasoconstriction (-23.5±7.1 vs. -19.0±6.5%, P < 0.05 for both) versus controls. The magnitude of sympatholysis (in %vasoconstriction between exercise and rest) for PE was lower (worse) in patients with T2DM versus controls (14.9±12.2 vs. 23.1±8.1%, P < 0.05) whereas groups were similar during DEX trials (24.6±12.3 vs. 27.6±13.4%, P = 0.47). Our data suggest patients with T2DM have attenuated hyperemic and vasodilatory responses to exercise, which could be attributable to greater a1-mediated vasoconstriction in contracting skeletal muscle. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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