Metabolic Interrelationships (pdf file) Medical Biochemistry from Univ. of Illinois at Chicago
Fuel usage (light exercise)
The best examples of light exercise are walking and light jogging. The muscles that are recruited during this type of exercise are those that contain a large amount of type I muscle cells, and, because these cells have a good blood supply, it is easy to for fuels and oxygen to travel to the muscle. ATP consumption makes ADP available for new ATP synthesis.
The presence of ADP (and the resulting synthesis of ATP) simulates the movement of hydrogen (H+) into the mitochondria; this, in turn, reduces the proton gradient and thus stimulates electron transport. The hydrogen on the reduced form of nicotinamide adenine dinucleotide (NADH) is used up, nicotinamide adenine dinucleotide (NAD) becomes available, and fatty acids and glucose are oxidized. Incidentally, the calcium released during contraction stimulates the enzymes in the Krebs cycle and stimulates the movement of the glucose transporter 4 (GLUT-4) from inside of the muscle cell to the cell membrane. Both these exercise-induced responses augment the elevation in fuel oxidation caused by the increase in ATP consumption.
Fuel usage (moderate exercise)
An increase in the pace of running simply results in an increased rate of fuel consumption, an increased fatty acid release, and, therefore, an increase in the rate of muscle fatty acid oxidation. However, if the intensity of the exercise increases even further, a stage is reached in which the rate of fatty acid oxidation becomes limited.
The reasons why the rate of fatty acid oxidation reaches a maximum are not clear, but it is possible that the enzymes in the beta-oxidation pathway are saturated (ie, they reach a stage in which their maximal velocity [Vmax] is less than the rate of acetyl-coenzyme A [acetyl-CoA] consumption in the Krebs cycle). Alternatively, it may be that the availability of carnitine (the chemical required to transport the fatty acids into the mitochondria) becomes limited.
Whatever the reason, the consequence is that as the pace rises, the demand for acetyl-CoA cannot be met by fatty acid oxidation alone. The accumulation of acetyl-CoA that was so effective at inhibiting the oxidation of glucose is no longer present, so pyruvate dehydrogenase starts working again and pyruvate is converted into acetyl-CoA. In other words, more of the glucose that enters the muscle cell is oxidized fully to carbon dioxide. Therefore, the energy used during moderate exercise is derived from a mixture of fatty acid and glucose oxidation.
Fuel usage (strenuous exercise)
As the intensity of the exercise increases even further (ie, running at the pace of middle-distance races), the rate at which the muscles can extract glucose from the blood becomes limited. In other words, the rate of glucose transport reaches Vmax, either because the blood cannot supply the glucose fast enough or the number of GLUT-4s becomes limited. ATP generation cannot be serviced completely by exogenous fuels, and ATP levels decrease. Not only does this stimulate phosphofructokinase, it also stimulates glycogen phosphorylase. This means that glycogen stored within the muscle cells is broken down to provide glucose. Therefore, the fuel mix during strenuous exercise is composed of contributions from blood-borne glucose and fatty acids and from endogenously stored glycogen.
Fuel usage in individuals who are unfit
Being fit (biochemically speaking) means that the individual has a well-developed cardiovascular system that can efficiently supply nutrients and oxygen to the muscles. Fit people have muscle cells that are well perfused with capillaries (ie, they have a good muscle blood supply). Their muscle cells also have a large number of mitochondria, and those mitochondria have a high activity of Krebs cycle enzymes, electron transport carriers, and oxidation enzymes.
Individuals who are unfit must endure the consequences of a poorer blood supply, fewer mitochondria, less electron transport units, a lower activity of the Krebs cycle, and poorer activity of beta-oxidation enzymes. To generate ATP in the mitochondria, a steady supply of fuel and oxygen and decent activity of the oxidizing enzymes and carriers are needed. If any of these components are lacking, the rate at which ATP can be produced by mitochondria is compromised. Under these circumstances, the production of ATP by aerobic means is not sufficient to provide the muscles with sufficient ATP to sustain contractions. The result is anaerobic ATP generation using glycolysis. Increasing the flux through glycolysis but not increasing the oxidative consumption of the resulting pyruvate increases the production of lactate.