Augmented pressor and sympathetic responses to skeletal muscle metaboreflex activation in type 2 diabetes patients

Augmented pressor and sympathetic responses to skeletal muscle metaboreflex activation in type 2 diabetes patients
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DOI:
10.1152/ajpheart.00636.2015
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发表时间:
2016-01-15
影响因子:
4.8
通讯作者:
Fadel, Paul J.
Fadel, Paul J.
中科院分区:
医学2区
文献类型:
--
作者:
Holwerda, Seth W.;Restaino, Robert M.;Fadel, Paul J.

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先前的研究报告了2型糖尿病(T2 D)患者在运动期间动脉血压的过度升高。然而,关于所涉及的潜在神经机制知之甚少。我们假设T2 D患者会表现出增强的肌肉代谢反射激活,这有助于在运动过程中更大的升压和交感神经反应。测量16例T2 D患者(8例正常血压和8例高血压)和10例健康对照者的平均动脉压(MAP)、心率(HR)和肌肉交感神经活动(MSNA)。在30%和40%最大随意收缩(MVC)下进行静态握力后,通过运动后缺血(PEI)实现肌肉代谢反射的分级隔离。冷加压试验(CPT)也进行了广泛的交感神经兴奋性刺激。与对照组相比,T2 D患者在30%和40% MVC手柄期间的MAP和MSNA增加增加(P < 0.05),并且这些差异在PEI期间维持(MAP:30% MVC PEI:T2D,Delta 16 +/- 2 mmHg vs.对照,Delta 8 +/- 1 mmHg; 40% MVC PEI:T2 D,Delta 26 +/- 3 mmHg vs.对照,Delta 16 +/- 2 mmHg,均P < 0.05)。正常血压组与高血压组T2 D患者对握力和PEI的MAP和MSNA反应无显著性差异(P > 0.05)。有趣的是,在CPT期间,与对照组相比,T2 D患者的MSNA反应也更大(P < 0.05)。总的来说,这些研究结果表明,肌肉代谢反射激活增强T2 D患者,这有助于,部分,增强升压和交感神经反应,在这个患者群体中的运动。更大的CPT反应表明,可能涉及到一个高度的中枢交感神经反应。
Previous studies have reported exaggerated increases in arterial blood pressure during exercise in type 2 diabetes (T2D) patients. However, little is known regarding the underlying neural mechanism(s) involved. We hypothesized that T2D patients would exhibit an augmented muscle metaboreflex activation and this contributes to greater pressor and sympathetic responses during exercise. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were measured in 16 patients with T2D (8 normotensive and 8 hypertensive) and 10 healthy controls. Graded isolation of the muscle metaboreflex was achieved by postexercise ischemia (PEI) following static handgrip performed at 30% and 40% maximal voluntary contraction (MVC). A cold pressor test (CPT) was also performed as a generalized sympathoexcitatory stimulus. Increases in MAP and MSNA during 30 and 40% MVC handgrip were augmented in T2D patients compared with controls (P < 0.05), and these differences were maintained during PEI (MAP: 30% MVC PEI: T2D, Delta 16 +/- 2 mmHg vs. controls, Delta 8 +/- 1 mmHg; 40% MVC PEI: T2D, Delta 26 +/- 3 mmHg vs. controls, Delta 16 +/- 2 mmHg, both P < 0.05). MAP and MSNA responses to handgrip and PEI were not different between normotensive and hypertensive T2D patients (P > 0.05). Interestingly, MSNA responses were also greater in T2D patients compared with controls during the CPT (P < 0.05). Collectively, these findings indicate that muscle metaboreflex activation is augmented in T2D patients and this contributes, in part, to augmented pressor and sympathetic responses to exercise in this patient group. Greater CPT responses suggest that a heightened central sympathetic reactivity may be involved.