Okay, so the next model is the energy supply or energy depletion model. It's called by both names. As you know, there is a small store of ATP in the cell. And as this ATP store is used, three energy systems replenish it almost instantaneously. These energy systems are the aerobic energy system, the anaerobic energy system, and the creatine phosphate energy system, which is also anaerobic. You are already familiar with this chart showing the power and capacity of the three ATP production mechanisms. The creatine phosphate, which is also called phosphocreatine, by the way. This energy system is very, very fast but it only has a tiny ATP replenishment capacity lasting less than six to eight seconds. Anaerobic glycolysis is slower than the CP energy system but is still quite fast. Its supply of ATP production is less than 60 seconds due to the acid byproduct that interferes with cellular activity. And the third and slowest energy system is the aerobic energy system. It supplies an enormous amount of ATP. Now, the underlying premise of the energy supply, energy depletion model, is that fatigue occurs when the muscle runs too low on ATP to support its muscle activity. And this can occur according to theory in two ways. The ATP production mechanisms cannot keep pace with the ATP demands. Or there is insufficient fuel being delivered to the ATP production mechanisms. Now, research suggests the following proof for the energy supply depletion model. First, when the liver runs low on glycogen stores, it does not adequately replenish glucose in the blood and low blood glucose is called hypoglycemia. The athlete's performance is affected because the brain relies on blood glucose. Second, when the athlete ingests glucose while training this permits their exercise to continue and they have a slight recovery. And third, carbohydrate loading improves exercise performance by supercompensating glycogen stores. A higher level of glycogen stored in muscles and the liver delays the onset of fatigue. And fourth, creatine phosphate supplementation improves the athlete's ability to produce power. Unfortunately, there is currently no really good research providing evidence that training improves glycogen or creatine phosphate storage. These athletes have higher stores of both substrates depending on whether their specialty is power or speed or endurance. However, these higher stores could also be due to genetics, and not to training. An alternative explanation is that training increases the athlete's capacity to use fat at higher exercise intensities. Theoretically, this would conserve glycogen stores and delay fatigue. Now, here's the use of glycogen as the intensity of the exercise increases and here is the use of fats. The crossover point of these two fuels is of particular interest here. This is the point where the purple and yellow lines intersect. At 60% of VO2 max the mitochondria move from using fat for fuel to a higher use of glycogen. And theory proposes that when athletes train at intensities below their crossover point they improve the ability to use fat. This is the notion of the long, slow, distance type training. And when they train at higher intensities, they improve their capacity to use glycogen. Now marathon running is an interesting phenomenon. Marathon runners typically run at around 80% of their VO2 max and at this speed, they use an awful lot of glycogen. Use of glycogen from the blood is also a factor. Blood glucose predominantly comes from the liver, although lactate is also converted back into pyruvate that is then used for fuel. The problem with the energy supply, energy depletion perspective is that the brain does not let the ATP supply in the cell go much below 60%, even during the most intense exercise. Therefore, any model claiming the muscle cell runs very low on ATP is fundamentally wrong. As well, a muscle cell with low ATP supply would not be able to relax, and the heart muscle would stop working, and this never happens in a healthy athlete. In essence, there is no evidence that the ATP used by contracting muscles and the heart muscle ever exceeds the maximum rate of ATP production mechanisms.
