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首页> 外文期刊>American Journal of Physiology >Neural and metabolic mechanisms of excessive muscle fatigue in maintenance hemodialysis patients.
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Neural and metabolic mechanisms of excessive muscle fatigue in maintenance hemodialysis patients.

机译：维持性血液透析患者过度肌肉疲劳的神经和代谢机制。

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Dialysis patients have severe exercise limitations related to metabolic disturbances, but muscle fatigue has not been well studied in this population. We investigated the magnitude and mechanisms of fatigue of the ankle dorsiflexor muscles in patients on maintenance hemodialysis. Thirty-three dialysis patients and twelve healthy control subjects performed incremental isometric dorsiflexion exercise, beginning at 10% of their maximal voluntary contraction (MVC) and increasing by 10% every 2 min. Muscle fatigue (fall of MVC), completeness of voluntary activation, and metabolic responses to exercise were measured. Before exercise, dialysis subjects exhibited reduced strength and impaired peripheral activation (lower compound muscle activation potential amplitude) but no metabolic perturbation. During exercise, dialysis subjects demonstrated threefold greater fatigue than controls with evidence of central activation failure but no change in peripheral activation. All metabolic parameters were significantlymore perturbed at end exercise in dialysis subjects than in controls, including lower phosphocreatine (PCr) and pH, and higher P(i), P(i)/PCr, and H(2)PO(4)(-). Oxidative potential was markedly lower in patients than in controls [62.5 (SD 27.2) vs. 134.6 (SD 31.7), P < 0.0001]. Muscle fatigue was negatively correlated with oxidative potential among dialysis subjects (r = -0.52, P = 0.04) but not controls. Changes in central activation ratio were also correlated with muscle fatigue in the dialysis subjects (r = 0.59, P = 0.001) but not the controls. This study provides new information regarding the excessive muscular fatigue of dialysis patients and demonstrates that the mechanisms of this fatigue include both intramuscular energy metabolism and central activation failure.
机译：透析患者的运动受限与代谢紊乱有关，但对该人群的肌肉疲劳尚未进行充分研究。我们调查了维持性血液透析患者的踝背屈肌的疲劳程度和机制。 33位透析患者和12位健康对照受试者进行了增量等距背屈运动，从最大自愿收缩（MVC）的10％开始，每2分钟增加10％。测量了肌肉疲劳（MVC的下降），自发激活的完成以及运动的代谢反应。运动前，透析对象的力量降低，外周激活受损（复合肌肉激活电位幅度降低），但没有代谢紊乱。在运动过程中，透析对象的疲劳程度是对照组的三倍，有中枢激活失败的迹象，但外周激活没有变化。与对照组相比，透析受试者在结束运动时所有代谢参数的干扰明显更多，包括较低的磷酸肌酸（PCr）和pH值以及较高的P（i），P（i）/ PCr和H（2）PO（4）（- ）。患者的氧化潜能明显低于对照组[62.5（SD 27.2）与134.6（SD 31.7），P <0.0001]。透析受试者中的肌肉疲劳与氧化电位呈负相关（r = -0.52，P = 0.04），而对照组则没有。中枢激活率的变化也与透析对象的肌肉疲劳有关（r = 0.59，P = 0.001），但与对照组无关。这项研究提供了有关透析患者过度肌肉疲劳的新信息，并证明了这种疲劳的机制包括肌肉内能量代谢和中枢激活衰竭。

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