Reflex sympathetic activation during static exercise is severely impaired in patients with myophosphorylase deficiency.
Reflex sympathetic activation during static exercise is severely impaired in patients with myophosphorylase deficiency.
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肌磷酸化酶缺乏症患者在静态运动期间反射性交感神经激活严重受损。
DOI：
10.1113/jphysiol.2003.039347
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Thomas,GailD
中科院分区：
文献类型：
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作者：
Fadel,PaulJ;Wang,Zhongyun;Tuncel,Meryem;Watanabe,Hitoshi;Abbas,Aamer;Arbique,Debbie;Vongpatanasin,Wanpen;Haley,RobertW;Victor,RonaldG;Thomas,GailD
在静态运动中，代谢物在肌肉间质中积累，刺激化学敏感传入神经，反射性地增加传出肌交感神经活动（MSNA）和血压。在实验动物中，乳酸能有效地刺激肌肉代谢反射，但它在人体中的作用更有争议。为了确定乳酸是否是人类代谢反射激活的关键介质，我们对8名肌磷酸化酶缺乏症（mccardle病）患者的MSNA进行了微电极记录，这些患者不能代谢肌内糖原，也不能在运动肌肉中产生乳酸。每位患者与三名健康对照者配对，以最大限度地提高统计效力。在对照组中，以最大自主收缩（MVC）的33%或45%进行2分钟的静态握力会产生强度依赖性的MSNA增加（分别为171±22%和379±95%）。在患者中，静态握力的MSNA反应明显减弱（33% MVC组为33±14%；45% MVC组为32±19%；与对照组相比P< 0.05）。同样，当静态握力（30% MVC）对疲劳时，对照组的MSNA增加366±73%，而患者的MSNA仅增加51±14% （P< 0.05）。与对照组相比，患者对静态握力的血压反应也有所减弱，而心率反应则相同。与运动相比，患者和对照组的MSNA对其他反射刺激（冷压试验或Valsalva动作）的反应相似。综上所述，这些数据表明，在人体静态运动中，糖原溶解途径的适当激活对于正常的代谢反射介导的交感神经兴奋是必需的。
During static exercise, metabolites accumulate in the muscle interstitium where they stimulate chemosensitive afferent nerves that reflexly increase efferent muscle sympathetic nerve activity (MSNA) and blood pressure. In experimental animals, lactic acid potently stimulates the muscle metaboreflex, but its role in humans is more controversial. To determine if lactic acid is a critical mediator of metaboreflex activation in humans, we performed microelectrode recordings of MSNA in eight patients with myophosphorylase deficiency (McArdle's disease) who cannot metabolize intramuscular glycogen and do not generate lactic acid in exercising muscles. Each patient was matched with three healthy control subjects to maximize statistical power. In controls, 2 min of static handgrip performed at 33 % or 45 % of maximal voluntary contraction (MVC) produced intensity‐dependent increases in MSNA (171 ± 22 % and 379 ± 95 %, respectively). In the patients, MSNA responses to static handgrip were markedly attenuated (33 ± 14 % at 33 % MVC; 32 ± 19 % at 45 % MVC;P< 0.05vs.controls). Likewise, when static handgrip (30 % MVC) was performed to fatigue, MSNA increased by 366 ± 73 % in controls but only by 51 ± 14 % in patients (P< 0.05). Pressor responses to static handgrip were also attenuated in patients compared to controls, whereas heart rate responses were identical. In contrast to exercise, the MSNA responses to other reflex stimuli (the cold pressor test or Valsalva's manoeuvre) were similar in patients and controls. Together these data indicate that appropriate activation of glycogenolytic pathways is obligatory for normal metaboreflex‐mediated sympathoexcitation during static exercise in humans.