The faster rxns have less steps but are depleted fastest


The fuels used in anaerobic exercises—sprinting, for example—differ from those used in aerobic exercises—such as distance running. The selection of fuels during these different forms of exercise illustrates many important facets of energy transduction and metabolic integration. ATP directly powers myosin, the protein immediately responsible for converting chemical energy into movement (Chapter 34). However, the amount of ATP in muscle is small. Hence, the power output and, in turn, the velocity of running depend on the rate of ATP production from other fuels. As shown in Table 30.3, creatine phosphate (phosphocreatine) can swiftly transfer its high-potential phosphoryl group to ADP to generate ATP (Section 14.1.5). However, the amount of creatine phosphate, like that of ATP itself, is limited. Creatine phosphate and ATP can power intense muscle contraction for 5 to 6 s. Maximum speed in a sprint can thus be maintained for only 5 to 6 s (see Figure 14.7). Thus, the winner in a 100-meter sprint is the runner who slows down the least.

A 100-meter sprint is powered by stored ATP, creatine phosphate, and anaerobic glycolysis of muscle glycogen. The conversion of muscle glycogen into lactate can generate a good deal more ATP, but the rate is slower than that of phosphoryl-group transfer from creatine phosphate. During a ~10-second sprint, the ATP level in muscle drops from 5.2 to 3.7 mM, and that of creatine phosphate decreases from 9.1 to 2.6 mM. The essential role of anaerobic glycolysis is manifested in the elevation of the blood-lactate level from 1.6 to 8.3 mM. The release of H + from the intensely active muscle concomitantly lowers the blood pH from 7.42 to 7.24. This pace cannot be sustained in a 1000-meter run (~132 s) for two reasons. First, creatine phosphate is consumed within a few seconds. Second, the lactate produced would cause acidosis. Thus, alternative fuel sources are needed.

The complete oxidation of muscle glycogen to CO 2 substantially increases the energy yield, but this aerobic process is a good deal slower than anaerobic glycolysis. However, as the distance of a run increases, aerobic respiration, or oxidative phosphorylation, becomes increasingly important. For instance, part of the ATP consumed in a 1000-meter run must come from oxidative phosphorylation. Because ATP is produced more slowly by oxidative phosphorylation than by glycolysis (see Table 30.3), the pace is necessarily slower than in a 100-meter sprint. The championship velocity for the 1000-meter run is about 7.6 m/s, compared with approximately 10.2 m/s for the 100-meter event (Figure 30.19).

The running of a marathon (26 miles 385 yards, or 42,200 meters), requires a different selection of fuels and is characterized by cooperation between muscle, liver, and adipose tissue. Liver glycogen complements muscle glycogen as an energy store that can be tapped. However, the total body glycogen stores (103 mol of ATP at best) are insufficient to provide the 150 mol of ATP needed for this grueling ~2-hour event. Much larger quantities of ATP can be obtained by the oxidation of fatty acids derived from the breakdown of fat in adipose tissue, but the maximal rate of ATP generation is slower yet than that of glycogen oxidation and is more than tenfold slower than that with creatine phosphate. Thus, ATP is generated much more slowly from high-capacity stores than from limited ones, accounting for the different velocities of anaerobic and aerobic events.

ATP generation from fatty acids is essential for distance running. However, a marathon would take about 6 hours to run if all the ATP came from fatty acid oxidation, because it is much slower than glycogen oxidation. Elite runners consume about equal amounts of glycogen and fatty acids during a marathon to achieve a mean velocity of 5.5 m/s, about half that of a 100-meter sprint. How is an optimal mix of these fuels achieved? A low blood-sugar level leads to a high glucagon/insulin ratio, which in turn mobilizes fatty acids from adipose tissue. Fatty acids readily enter muscle, where they are degraded by β oxidation to acetyl CoA and then to CO 2 . The elevated acetyl CoA level decreases the activity of the pyruvate dehydrogenase complex to block the conversion of pyruvate into acetyl CoA. Hence, fatty acid oxidation decreases the funneling of sugar into the citric acid cycle and oxidative phosphorylation. Glucose is spared so that just enough remains available at the end of the marathon. The simultaneous use of both fuels gives a higher mean velocity than would be attained if glycogen were totally consumed before the start of fatty acid oxidation.