THE METABOLIC CAUSES OF SLOW RELAXATION IN FATIGUED HUMAN SKELETAL-MUSCLE
THE METABOLIC CAUSES OF SLOW RELAXATION IN FATIGUED HUMAN SKELETAL-MUSCLE
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DOI：
10.1113/jphysiol.1989.sp017843
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发表时间：
1989-11-01
影响因子：
5.5
通讯作者：
MOLL, A
中科院分区：
文献类型：
--
作者：
CADY, EB;ELSHOVE, H;MOLL, A
在人骨骼肌中，在疲劳的发展和随后的恢复过程中，松弛的减缓与细胞内pH和磷代谢物的变化之间的关系已经被研究。与正常受试者获得的结果进行了比较，从一个主题与肌磷酸化酶缺乏症（MPD）谁不产生H+糖酵解在运动过程中，因此提供了机会，评估的作用H+在减缓放松。受试者疲劳的第一背侧骨间肌在一个逐步的方式在缺血的条件下，与之间的时间间隔，在此期间，从短暂的强直cocontractions和肌肉磷代谢和pH值测定的松弛率的疲劳收缩。在缺血条件下21 s最大自主收缩后，MPD受试者的松弛减慢至约50%的新鲜肌肉中的速率，此时肌内pH值没有变化。这表明，有一种机制，导致弛豫的放缓，是独立的H+积累。当循环恢复时，与MPD受试者相比，正常受试者显示出缓慢的松弛恢复。此时MPD和正常受试者之间细胞内代谢物浓度的主要差异在于，对于后者，在循环恢复后至少60 s内pH值保持较低（约6.5）。结果表明，缓慢恢复是持续酸中毒的结果，即存在pH依赖性减缓机制。对于正常受试者，对于类似的细胞内磷酸肌酸浓度，恢复肌肉的松弛约为疲劳肌肉的一半，这一事实进一步表明存在pH依赖性机制。这是在恢复肌肉的pH值比部分疲劳肌肉的pH值低0.3-0.4单位的时候。结果表明，在正常肌肉中，至少有两个过程导致疲劳肌肉的缓慢松弛：一个是由于H+积累，另一个是独立的H+。
The relationship between slowing of relaxation and changes of intracellular pH and phosphorous metabolites has been examined in human skeletal muscle during the development of fatigue and subsequent recovery. Results obtained with normal subjects have been compared with those from a subject with myophosphorylase deficiency (MPD) who produced no H+ from glycolysis during exercise and therefore afforded the opportunity of assessing the role of H+ in the slowing of relaxation. Subjects fatigued the first dorsal interosseous muscle in a stepwise fashion under ischaemic conditions, with intervals between the fatiguing contractions during which the relaxation rate was measured from brief tetanic coontractions and the muscle phosphorous metabolities and pH were measured by nuclear magnetic resonance spectroscopy. After 21 s maximal voluntary contraction under ischaemic conditions, relaxation in the MPD subject slowed to approximately 50% of the rate in the fresh muscle at a time when the intramuscular pH had not changed. This demonstrates that there is a mechanism causing slowing of relaxation that is independent of H+ accumulation. The normal subjects showed a slow recovery of relaxation compared to the MPD subject when the circulation was restored. The main difference in the intracellular metabolite concentrations between MPD and normal subjects at this time was that, for the latter, the pH remained low (around 6.5) for at least 60 s after the circulation was restored. The results suggest that the slow recovery is a consequence of continuing acidosis, i.e. the existence of a pH-dependent mechanism of slowing. The existence of a pH-dependent mechanism was further indicated by the fact that for the normal subjects, for a similar intracelluar concentration of phosphocreatine, relaxation of the recovering muscle was approximately half that of the fatiguing muscle. This was at a time when the pH of the recovering muscle was 0.3-0.4 units less than in the partially fatigued muscle. The results show that in normal muscle there are at least two processes that lead to slow relaxation in fatigued muscle: one due to H+ accumulation, the other being independent of H+.