what effect will endurance training have on oxidative enzymes
Endurance training Long-term endurance training induces many physiological adaptations both centrally and peripherally mediated. Central cardiovascular adaptations include decreased heart rate, increased stroke volume of the heart,[2] increased blood plasma, without any major changes in red blood cell count, which reduces blood viscosity and increased cardiac output as well as total mitochondrial volume in the muscle fibers used in the training (i.e. the thigh muscles in runners will have more mitochondria than the thigh muscles of swimmers). Mitochondria increase in both number and size and there are similar increases in myoglobin and oxidative enzymes. Adaptations of the peripheral include capillarization, that is an increase in the surface area that both the venous and arterial capillaries supply. This also allows for increased heat dissipation during strenuous exercise. The muscles heighten their glycogen and fat storing capabilities in endurance athletes in order to increase the length in time in which they can perform work. Endurance training primarily work the slow twitch (type 1) fibers and develop such fibers in their efficiency and resistance to fatigue. Catabolism also improves increasing the athletes capacity to use fat and glycogen stores as an energy source. These metabolic processes are known as glycogenolysis, glycolysis and lipolysis. There is higher efficiency in oxygen transport and distribution. In recent years it has been recognized that oxidative enzymes such as succinate dehydrogenase (SDH) that enable mitochondria to break down nutrients to form ATP increase by 2.5 times in well trained endurance athletes[2] In addition to SDH, myoglobin increases by 75-80% in well trained endurance athletes.[2]
Carbohydrate catabolism The last process in aerobic respiration is oxidative phosphorylation, also known as the electron transport chain. Here NADH and FADH2, which contain the energy in the form of electrons, deliver their electrons to the inner membranes of the mitochondrion to power the production of ATP. Oxidative phosphorylation contributes the majority of the ATP produced, compared to glycolysis and the Krebs cycle. While the ATP count is glycolysis and the Krebs cycle is two ATP molecules, the electron transport chain contributes, at most, twenty-eight ATP molecules. A contributing factor is due to the energy potentials of NADH and FADH2. As they are brought from the initial process, glycolysis, to the electron transport chain, the energy stored in them are now utilized. A second contributing factor is that cristae, the inner membranes of mitochondria, increase the surface area and therefore the amount of proteins in the membrane that assist in the synthesis of ATP. Along the electron transport chain, there are separate compartments, each with their own concentration gradient of H + ions, which are the power source of ATP synthesis. To convert ADP to ATP, energy must be provided. That energy is provided by the H+ gradient. On one side of the membrane compartment, there is a high concentration of H+ ions compared to the other. The shuttling of H+ to one side of the membrane is driven by the exergonic flow of electrons throughout the membrane. These electrons are supplied by NADH and FADH2 as they transfer their potential energy. Once the H+ concentration gradient is established, a proton-motive force is established, which provides the energy to convert ADP to ATP. The H+ ions that were initially forced to one side of the mitochondrion membrane now naturally flow through a membrane protein called ATP synthase, a protein that converts ADP to ATP with the help of H+ ions. [1]