Department of Applied Design, Cape Peninsula University of Technology, Cape Town 8000, South Africa.
Nutrients. 2022 Feb 18;14(4):862. doi: 10.3390/nu14040862.
The introduction of the needle muscle biopsy technique in the 1960s allowed muscle tissue to be sampled from exercising humans for the first time. The finding that muscle glycogen content reached low levels at exhaustion suggested that the metabolic cause of fatigue during prolonged exercise had been discovered. A special pre-exercise diet that maximized pre-exercise muscle glycogen storage also increased time to fatigue during prolonged exercise. The logical conclusion was that the athlete's pre-exercise muscle glycogen content is the single most important acutely modifiable determinant of endurance capacity. Muscle biochemists proposed that skeletal muscle has an obligatory dependence on high rates of muscle glycogen/carbohydrate oxidation, especially during high intensity or prolonged exercise. Without this obligatory carbohydrate oxidation from muscle glycogen, optimum muscle metabolism cannot be sustained; fatigue develops and exercise performance is impaired. As plausible as this explanation may appear, it has never been proven. Here, I propose an alternate explanation. All the original studies overlooked one crucial finding, specifically that not only were muscle glycogen concentrations low at exhaustion in all trials, but hypoglycemia was also always present. Here, I provide the historical and modern evidence showing that the blood glucose concentration-reflecting the liver glycogen rather than the muscle glycogen content-is the homeostatically-regulated (protected) variable that drives the metabolic response to prolonged exercise. If this is so, nutritional interventions that enhance exercise performance, especially during prolonged exercise, will be those that assist the body in its efforts to maintain the blood glucose concentration within the normal range.
20 世纪 60 年代，针式肌肉活检技术的引入使得人们首次能够从运动中的人体中采集肌肉组织样本。研究发现，肌肉糖原含量在力竭时降至极低水平，这表明人们已经发现了长时间运动中疲劳的代谢原因。一种特殊的运动前饮食可以最大限度地增加运动前肌肉糖原的储存，从而延长长时间运动中的疲劳时间。逻辑结论是，运动员的运动前肌肉糖原含量是耐力能力的唯一最重要的急性可调节决定因素。肌肉生物化学家提出，骨骼肌对高肌肉糖原/碳水化合物氧化率有强制性依赖，尤其是在高强度或长时间运动期间。如果没有来自肌肉糖原的强制性碳水化合物氧化，最佳的肌肉代谢就无法维持；疲劳会发展，运动表现会受到损害。尽管这个解释似乎很合理，但它从未得到证实。在这里，我提出了一个替代解释。所有最初的研究都忽略了一个关键发现，即在所有试验中，不仅在力竭时肌肉糖原浓度很低，而且低血糖总是存在。在这里，我提供了历史和现代证据，表明血糖浓度——反映了肝糖原，而不是肌肉糖原含量——是调节（保护）变量，它驱动了长时间运动的代谢反应。如果是这样，那么那些有助于身体努力将血糖浓度维持在正常范围内的营养干预措施将能够提高运动表现，尤其是在长时间运动中。
