Exercise oxidative phosphorylation

Glycolysis produces NADH from NAD in Reaction 6 (G3P <=> 1,3BPG). In aerobic glycolysis, NADH is converted to NAD+ by the processes of electron transport and oxidative phosphorylation, which occur in the mitochondria. If oxygen is limiting (such as during heavy exercise), oxidative phosphorylation does not occur and NADH is not converted to NAD+. This could be disastrous if there were no other way to produce NAD... 

Creatine supplementation has been shown to increase the rate of PCr resynthesis in the recovery period after ischemic exercise (Greenhaff et al., 1993a). This could be attributed to an acceleration of oxidative phosphorylation by increased free creatine content available to the mitochondrial fraction of the creatine kinase enzyme, as previously suggested (Bessman and Fonyo, 1966). 

During the recovery period from exercise, ATP (newly produced by way of oxidative phosphorylation) is needed to replace the creatine phosphate reserves — a process that may be completed within a few minutes. Next, the lactic acid produced during glycolysis must be metabolized. In the muscle, lactic acid is converted into pyruvic acid, some of which is then used as a substrate in the oxidative phosphorylation pathway to produce ATP. The remainder of the pyruvic acid is converted into glucose in the liver that is then stored in the form of glycogen in the liver and skeletal muscles. These later metabolic processes require several hours for completion. 

During periods of recovery following exercise, creatine phosphate is regenerated at the expense of ATP synthesized from mitochondrial oxidative phosphorylation energy currency is paid into a reserve account, or reservoir, for the next period of sustained exercise. 

DNOC is an uncoupler of oxidative phosphorylation. In DNOC exposed humans or animals, a portion of the energy formed from the Krebs cycle is therefore not stored as ATP, but is given off as heat. This usually results in signs and symptoms, such as hyperthermia, perspiration, and fatigue, in humans exposed to DNOC. High doses of DNOC, elevated environmental temperatures, or physical exercise tends to exaggerate these effects and can result in death. 

Mitochondrial oxidative ADP phosphorylation is the primary source of ATP in skeletal muscle during aerobic exercise. Thus, to maintain the tree-energy state of the cytoplasmic phosphoenergetic compounds ATP, ADP, and inorganic phosphate (PI), oxidative phosphorylation is modulated to match the rate of ATP utilization during exercise. The mitochondrial components of Wu et a/. s model are illustrated in Figure 7.13. Additional components include ATP hydrolysis, adenylate kinase,... 

ATP is synthesized by mitochondrial oxidative phosphorylation (Jpop) and glycolysis. The latter contribution may be disregarded for a muscle engaging little or moderate exercise. Exerted power by a muscle P is directly related to the rate of ATP hydrolyzed by the myosin ATPases. /p. and we have... 

Spectral Analysis. - A new method of analysis of ATP utilisation and resynthesis has been developed which simulates cellular ATP flux, mitochondrial oxidative phosphorylation and creatine kinase kinetics. The model was used to examine previously published P NMR data of changes in PCr and Pi in resting muscle, muscle exercising during ischaemia and muscle in aerobic recovery. The model allowed estimation of the maximal velocity of oxidative... 

Otto Shape had difficulty losing weight because human fuel utilization is too efficient. His adipose tissue fatty acids are being converted to acetyl CoA, which is being oxidized in the TCA cycle, thereby generating NADH and FAD(2H). The energy in these compounds is used for ATP synthesis from oxidative phosphorylation. If his fuel utilization were less efficient and his ATP yield were lower, he would have to oxidize much greater amounts of fat to get the ATP he needs for exercise. 

If the pace of exercise increases from a walk to a light jog, the rate of fatty acid oxidation by the muscles also increases. This is a consequence of Krebs cycle flux increasing in response to elevated rates of NADH consumption and oxidative phosphorylation. Increased activity of P-oxidation is dependent on both an adequate supply of fatty acids to the mitochondrial matrix and responsive P-oxidation enzymes. 

Metabolism, the sum of all cellular reactions, involves the breakdown (catabolism) and synthesis (anabolism) of molecules. Objective 6 (Section 12.6), Exercise 12.26. There are three stages in the catabolism of foods to provide energy. In Stage I, digestion converts foods into smaller molecules. In Stage II, these smaller molecules are converted into two-carbon acetyl units that combine with coenzyme A, forming acetyl CoA. Stage HI, which is called the common catabolic pathway, consists of the citric acid cycle followed by the electron transport chain and oxidative phosphorylation. The main function of catabolism is to produce ATP molecules. 

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