Park J H, Brown R L, Park C R, Cohn M, Chance B
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN 37232.
Proc Natl Acad Sci U S A. 1988 Dec;85(23):8780-4. doi: 10.1073/pnas.85.23.8780.
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.
本研究的目的是调查肌肉代谢的遗传决定特性是否有助于世界级长跑运动员卓越的身体耐力。通过31P核磁共振波谱法定量测定了精英长跑运动员和久坐不动的对照受试者腕部屈肌中的三磷酸腺苷（ATP）、磷酸肌酸、无机磷酸盐和pH值。两组受试者的这些肌肉均未接受任何特定的运动训练计划。在休息状态、三个运动强度等级的两个运动周期以及恢复过程中对“未经训练”的肌肉进行了检测。在休息和运动期间，运动员的屈肌中磷酸肌酸和ATP的浓度均高于对照受试者。根据以下标准，运动员的肌肉通过氧化代谢产生ATP的能力高于对照受试者的肌肉：（i）在两个运动周期中，更容易达到并更好地维持60%最大自主收缩的高力量输出；（ii）运动期间无机磷酸盐与磷酸肌酸的比率上升幅度较小，且运动后恢复较快；（iii）运动员的肌肉中腺嘌呤核苷酸或总磷酸盐没有损失，而对照受试者的肌肉中有显著损失；（iv）运动期间运动员肌肉的pH值下降不超过0.1个单位，这证明糖酵解相对较慢和/或乳酸氧化较快。另一方面，在对照受试者的肌肉中，在第一个运动周期早期pH值下降了近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值恢复到接近正常水平，这反映了由于糖原耗尽和运动引起的高血流量导致的乳酸清除，乳酸生成减少。到运动计划结束时，对照受试者的最大自主收缩力下降到初始值的60%以下。这种下降最好用糖酵解对肌肉收缩的贡献耗尽来解释。因此，如所讨论的，剩余的最大力量提供了支持收缩的氧化能力的一种度量。总之，我们认为，相对于糖酵解能力而言，世界级跑步运动员未经训练的肌肉中支持收缩的氧化能力更强，这反映了身体耐力的遗传天赋。不能完全排除训练的其他全身效应。31P磁共振波谱法提供了一种评估这种天赋的非侵入性方法。
