Siegler Jason C, Marshall Paul
Sport and Exercise Science, School of Science and Health, University of Western Sydney, Sydney, NSW, Australia.
Exp Physiol. 2015 Apr 20;100(5):519-30. doi: 10.1113/EP085054.
What is the central question of this study? Does metabolic alkalosis affect central and peripheral mechanisms associated with exercise-induced muscle fatigue in humans? What is the main finding and its importance? Inducing metabolic alkalosis before exercise preserved voluntary activation, but not muscle excitation, after a 2 min maximal voluntary contraction (MVC) followed by ischaemia. An effect of pH was also observed in maximal rates of torque development, where alkalosis mitigated the reduction in maximal rates of torque development after the initial 2 min MVC. For the first time, these results demonstrate a differential effect of pH on voluntary activation as well as maximal rates of torque development after sustained, maximal voluntary knee extension in humans. The increased concentration of protons during fatiguing exercise may contribute to increased activation of group III and IV afferents and subsequently reduced central drive, but this has yet to be confirmed in exercising humans. Here, we determined whether inducing metabolic alkalosis differentially affects descending central drive after fatiguing exercise and whether this effect may, in part, be explained by attenuating group III and IV afferent firing. Eleven men performed a maximal 2 min voluntary knee extension (MVC) followed by a 2 min rest and subsequent 1 min MVC with an occlusive cuff either in placebo [PLA; 0.3 g (kg body weight)(-1) calcium carbonate] or alkalosis conditions [ALK; 0.3 g (kg body weight)(-1) sodium bicarbonate]. Femoral nerve stimulation was applied before exercise, after the 2 min MVC and at 40-60 s intervals throughout the remainder of the protocol to explore central and peripheral mechanisms associated with reductions in maximal force and rate of torque development. Although voluntary activation declined to a similar extent after the 2 min MVC, during the ischaemic period voluntary activation was higher during ALK (PLA, 57 ± 8%; ALK, 76 ± 5%). Maximal voluntary torque declined at similar rates during the task (203 ± 19 N m), but maximal rate of torque development was significantly higher in the ALK conditions after the 2 min MVC (mean difference of 177 ± 60 N m s(-1) ). These results demonstrate the effect of pH on voluntary activation as well as maximal rates of torque development after sustained, maximal voluntary knee extension in humans.
本研究的核心问题是什么?代谢性碱中毒是否会影响与人类运动诱导的肌肉疲劳相关的中枢和外周机制?主要发现及其重要性是什么?在进行2分钟最大自主收缩(MVC)后接着缺血的情况下,运动前诱导代谢性碱中毒可保留自主激活,但不能保留肌肉兴奋。在最大扭矩发展速率方面也观察到了pH值的影响,碱中毒减轻了最初2分钟MVC后最大扭矩发展速率的降低。这些结果首次证明了pH值对人类持续最大自主膝关节伸展后自主激活以及最大扭矩发展速率具有不同的影响。疲劳运动期间质子浓度的增加可能导致III和IV类传入神经的激活增加,进而导致中枢驱动降低,但这一点在运动的人类中尚未得到证实。在此,我们确定诱导代谢性碱中毒是否会对疲劳运动后的下行中枢驱动产生不同影响,以及这种影响是否部分可以通过减弱III和IV类传入神经的放电来解释。11名男性进行了2分钟的最大自主膝关节伸展(MVC),随后休息2分钟,接着在使用闭塞袖带的情况下进行1分钟MVC,分别处于安慰剂[PLA;0.3 g(体重)⁻¹碳酸钙]或碱中毒条件[ALK;0.3 g(体重)⁻¹碳酸氢钠]下。在运动前、2分钟MVC后以及在方案的其余时间每隔40 - 60秒施加股神经刺激,以探究与最大力量和扭矩发展速率降低相关的中枢和外周机制。尽管在2分钟MVC后自主激活下降到相似程度,但在缺血期,ALK期间的自主激活更高(PLA,57±8%;ALK,76±5%)。任务期间最大自主扭矩以相似速率下降(203±19 N·m),但在2分钟MVC后,ALK条件下的最大扭矩发展速率显著更高(平均差异为177±60 N·m·s⁻¹)。这些结果证明了pH值对人类持续最大自主膝关节伸展后自主激活以及最大扭矩发展速率的影响。