乳酸生成延缓而非引起酸中毒:体育学生的实用方法。

F. C. Silva, F. L. Lazarim, L. S. Tessutti, R. Hohl, M. F. Sarraipa, D. Macedo
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引用次数: 0

摘要

人们普遍认为,剧烈运动会导致乳酸的产生,从而导致酸中毒,这是错误的。这种由体育教育和其他专业人士推行的信念干扰了训练方法,并提出了乳酸肌是运动疲劳的罪魁祸首的观点。对于理论方法,我们展示了所有糖酵解反应的结构说明,重点是磷酸甘油酸激酶反应,其中包括从1,3双磷酸甘油酸的第一个碳到ADP的简单磷酸转移,形成ATP。磷酸甘油酸3的羧基在糖酵解的剩余中间体中保持未质子化。从这个生化事实来看,产生引起质子释放的乳酸是不可能的。实际上,糖酵解释放2个质子乳酸生成消耗2个质子。在此生化解释之后,我们提出了三种说明的运动情况:低强度,无氧阈值和高强度运动。从这一点上,学生可以理解质子主要来自ATP水解,当线粒体呼吸满足肌肉收缩所需的ATP时,细胞内没有质子积累,因为线粒体利用质子来维持膜间空间的质子梯度。当ATP水解超过线粒体的缓冲能力,并且ATP需求由非线粒体来源提供时,细胞内的质子增加,引起酸中毒。在这些细胞条件下,乳酸产量增加,以防止丙酮酸积累,并为糖酵解提供NAD+。乳酸也通过与由乳酸转运体(MCT)介导的质子(来自ATP水解而不是来自乳酸生成)的同质转运来延缓酸化。因此,血乳酸检测的增加是酸中毒的结果而不是原因。学生们必须明白,如果肌肉不产生乳酸,酸中毒和疲劳就会更快发生,从而影响高强度运动的表现。在他们的培训计划中必须考虑到这些信息。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lactate production retards, not causes, acidosis: a practical approach for physical education students.
The  widespread  belief that intense  exercise causes the  production  of lactic  acid that contributes to acidose is erroneous.  This belief, carried  out by physical  education  and other  professionals,  interferes on methods of training and raise the opinion that muscle lactate is the vilain of exercise fatigue.  For a theorical  approach  we show a structural illustration of all the glycolysis reactions  with enphasis  to phosphoglycerate kinase reaction  wich envolves a simple phosphate transfer  from the  first carbon  of1,3 bisphosphoglycerate to  ADP,  forming  ATP.  The  carboxyl  group  of 3 phosphoglycerate remains unprotonated for the remaining  intermediates of glycolisis. From this biochemical fact it is impossible the production of acid lactic causing the release of a proton.  Actually,  glycolysis releases 2 protons  and lactate formation  consumes 2 protons.  After this biochemical explanation we present three  illustrated exercises situations: low intensity, anaerobic threshold  and high intensity exercise. From this point the students can understand that the protons  came mainly  from the ATP  hydrolysis  and when the ATP demand  for muscle contraction is met by mithocondrial respiration, there  is no proton  accumulation in the  cell as protons  are  used  by mithocondria to  maintain the  proton  gradient in the  intermem- branous  space.  When the ATP  hydrolysis exceeds mithocondria buffering capacity  and ATP  demand is supplied  by nonmithocondrial sources,  protons  increase  inside  the  cell causing  acidoses. Lactate production  increases  under  these  cellular  conditions  to  prevent  pyruvate accumulation and  supply the  NAD+  for glycolysis.  Lactate also retards the acidoses by the  symport with protons  (from ATP hydrolysys  not  from lactate production) mediated  by Lactate Transporters (MCT).  Thus,  increased blood  lactate detection  is the  effect  not  the  cause  of acidosis. The  students  must  understand that if muscles do not  produce  lactate, acidoses and fatigue  would accour faster,  impairing  high intensity exercise performance.  This information must be considered  in their  training schedules.
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