Energy metabolism of the untrained muscle of elite runners as observed by 31P magnetic resonance spectroscopy: evidence suggesting a genetic endowment for endurance exercise.
Energy metabolism of the untrained muscle of elite runners as observed by 31P magnetic resonance spectroscopy: evidence suggesting a genetic endowment for endurance exercise.
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通过 31P 磁共振波谱观察到的精英跑步者未经训练的肌肉的能量代谢：证据表明耐力运动的遗传天赋。
DOI：
10.1073/pnas.85.23.8780
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发表时间：
1988
影响因子：
11.1
通讯作者：
Chance,B
中科院分区：
文献类型：
--
作者：
Park,JH;Brown,RL;Park,CR;Cohn,M;Chance,B
这项研究的目的是调查肌肉代谢的基因决定特性是否有助于世界级长跑运动员的卓越身体耐力。通过 31P 核磁共振波谱法定量测定优秀长跑运动员和久坐对照受试者的腕屈肌中的 ATP、磷酸肌酸、无机磷酸盐和 pH 值。两组受试者的这些肌肉都没有接受过任何特定的运动训练计划。 “未经训练的”肌肉在休息时、三个级别的运动的两个周期以及恢复时进行检查。运动员的屈肌在休息和运动时比对照组的磷酸肌酸和 ATP 浓度更高。根据以下标准，运动员的肌肉比对照受试者的肌肉具有更高的通过氧化代谢产生 ATP 的能力：(i) 在两个运动周期中更容易达到并更好地维持高力量输出，即最大自主收缩的 60%； (ii) 无机磷酸盐与磷酸肌酸的比率在运动期间上升较少，并在运动后恢复较快； (iii) 运动员肌肉中的腺嘌呤核苷酸或总磷酸盐没有损失，但对照受试者的肌肉中有显着损失； (iv) 运动期间运动员肌肉的 pH 值下降不超过 0.1 个单位，证明糖酵解相对缓慢和/或乳酸快速氧化。另一方面，在对照组受试者的肌肉中，pH 在第一个运动周期早期下降了近 0.4 个单位，表明糖酵解相对较快和/或乳酸氧化较慢。在第二个运动周期中，对照受试者肌肉的 pH 值恢复到接近正常，这反映出由于运动引起的高血流量导致糖原耗尽和乳酸流失，乳酸形成减少。到锻炼计划结束时，对照组受试者的最大自愿收缩力已降至初始值的 60% 以下。这种下降最好的解释是糖酵解对肌肉收缩的贡献耗尽。因此，如所讨论的，残余最大强度提供了支持收缩的氧化能力的量度。总之，我们认为，世界级跑步运动员未经训练的肌肉收缩支持能力相对于糖酵解能力更大，这反映了身体耐力的遗传天赋。不能完全排除培训的其他系统影响。 31P 磁共振波谱提供了一种评估这种禀赋的非侵入性方法。
The purpose of this study was to investigate whether genetically determined properties of muscle metabolism contribute to the exceptional physical endurance of world-class distance runners. ATP, phosphocreatine, inorganic phosphate, and pH were quantitatively determined by 31P nuclear magnetic resonance spectroscopy in the wrist flexor muscles of elite long-distance runners and sedentary control subjects. These muscles had not been exposed to any specific program of exercise training in either group of subjects. The "untrained" muscles were examined at rest, during two cycles of three grades of exercise, and in recovery. The flexor muscles of the athletes had higher concentrations of phosphocreatine and ATP than did those of the control subjects at rest and during exercise. The athletes' muscles possessed a higher capacity for generation of ATP by oxidative metabolism than did control subjects' muscles according to the following criteria: (i) high force output, 60% of maximum voluntary contraction, was more easily reached and better maintained in both exercise cycles; (ii) the ratio of inorganic phosphate to phosphocreatine rose less during exercise and recovered faster in the postexercise period; (iii) there was no loss of adenine nucleotides or total phosphate from the athletes' muscles but significant losses from the control subjects' muscles; and (iv) the pH decreased no more than 0.1 unit in the athletes' muscles during exercise, attesting to a relatively slow glycolysis and/or a rapid oxidation of lactate. In the muscles of the control subjects, on the other hand, the pH decreased nearly 0.4 unit early in the first exercise cycle, indicating a relatively fast glycolysis and/or slower oxidation of lactate. In the second exercise cycle, the pH returned to near normal in the control subjects' muscles, reflecting diminished lactate formation because of glycogen depletion and lactate washout by the high blood flow induced by exercise. By the end of the exercise program, the maximum voluntary contractile force for the control subjects had declined to less than 60% of the initial value. This decline could be explained best by exhaustion of the glycolytic contribution to muscle contraction. Therefore, the residual maximum strength provided a measure of the oxidative capacity to support contraction, as is discussed. In conclusion, we suggest that a greater oxidative capacity relative to glycolytic capacity for support of contraction in untrained muscle of world-class runners reflects a genetic endowment for physical endurance. Additional systemic effects of training cannot be completely excluded. 31P magnetic resonance spectroscopy provides a noninvasive method for assessing this endowment.