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5. 7. 2012.

Adaptations to aerobic training - part III

Respiratory adaptations to training

No matter how adept the cardiovascular system is at supplying adequate amounts of blood to tissues, endurance would be hindered if the respiratory system were not able to bring in enough oxygen to meet oxygen demands. Respiratory system function does not usually limit performance because ventilation can be increased to a much greater extent than cardiovascular function. But, as with the cardiovascular system, the respiratory system undergoes specific adaptations to endurance training to maximize its efficiency.

After training, pulmonary ventilation is essentially unchanged at rest. Although endurance training does not change the structure of basic psychology of the lung, it does decrease ventilation during submaximal exercise by as much as 20% to 30% at a given submaximal intensity. Maximal pulmonary ventilation is substantially increased from a rate of about 100 to 120L/min in untrained sedentary individuals to about 130 to 150L/min or more following endurance training. Pulmonary ventilation rates typically increase to about 180L/min in highly trained athletes and can exceed 200L/min in very large, highly trained endurance athletes. Two factors can account for the increase in maximal pulmonary ventilation following training: increased tidal volume and increased respiratory frequency at maximal exercise.
Ventilation is usually not considered a limiting factor for endurance exercise performance. However, some evidence suggests that at some point in a highly trained person’s adaptation, the pulmonary system’s capacity for oxygen transport may not be able to meet the demands of the limbs and the cardiovascular system. This results in what has been termed exercise-induced arterial hypoxemia, in which arterial oxygen saturation decreases below 96%. This desaturation in highly trained athletes likely results from the large right heart cardiac output directed to the lung during exercise and consequently a decrease in the time the blood spends in the lung.

Pulmonary diffusion, or gas exchange occurring in the alveoli, is unaltered at rest and at standardized submaximal exercise intensities following training. However, it increases during maximal exercise. Pulmonary blood flow(blood coming from the heart to the lungs) appears to increase following training, particularly the flow to the upper regions of the lungs when a person is sitting or standing. This increases lung perfusion. More blood is brought into the lungs for gas exchange, and at the same time ventilation increases to that more air is brought into the lungs. This means that more alveoli will be involved in pulmonary diffusion. The net result is that pulmonary diffusion increases.

The oxygen content of arterial blood changes very little with endurance training. Even though total hemoglobin is increased, the amount of hemoglobin per unit of blood is the same or even slightly reduced. The (a-ṽ)O2 difference, however, does increase with training, particularly at maximal exercise intensity. This increase results from a lower mixed venous oxygen content, which means that the blood returning to the heart(which is a mixture of venous blood from all body parts, not just the active tissues) contains less oxygen than it would in an untrained person. This reflects both greater oxygen extraction at the tissue level and a more effective distribution of blood flow to active tissue. The increased extraction results in part from an increase in oxidative capacity of active muscle fibers.
In summary, the respiratory system is quite adept at bringing adequate oxygen into the body. For this reason, the respiratory system seldom limits endurance performance. Not surprisingly, the major training adaptations noted in the respiratory system are apparent mainly during maximal exercise, when all systems are being maximally stressed.

Adaptations in muscle

Repeated use of muscle fibers with endurance training stimulates changes in their structure and function. Our main interest here is in aerobic training and the changes it produces in muscle fiber type, mitochondrial function, and oxidative enzymes.

Muscle fiber types

Aerobic activities such as jogging and low-to moderate-intensity cycling rely extensively on the slow-twitch(type I) fibers. In response to aerobic training, type I fibers become larger. That is, they develop a larger cross-sectional area, although the magnitude of change depends on the intensity and duration of each training bout and the length of the training program. Increases of up to 25% have been reported. Fast-twitch(type II) fibers, because they are not being recruited to the same extent, generally do not increase cross-sectional area.
Most early studies showed no change in the percentage of type I and type II fibers following aerobic training, but subtle changes were noted among type II fiber subtypes. Type IIx fibers are used less often than IIa fibers, and for that reason they have a lower aerobic capacity. Long-duration exercise may eventually recruit these fibers into action, demanding them to perform in a manner normally expected on the IIa fibers. This can cause some IIx fibers to take on the characteristics of the more oxidative IIa fibers. Recent evidence suggests that not only is there a transition of type IIx to IIa fibers, but there can also be a transition of type II to type I fibers. The magnitude of change is generally small, not more than a few percentage points. As an example, in the HERITAGE Family Study, a 20-week program of aerobic training increased type I fibers from 43.2% pretraining to 46.7% posttraining and decreased type IIx fibers from 20.0% to 15.1%, with type IIa remaining essentially unchanged. These more recent studies have included larger numbers of subjects and have taken advantage of improved measurement technology; both might explain why changes are now being recognized.

Capillary supply

One of the most important adaptations to aerobic training is an increase in the number of capillaries surrounding each muscle fiber. Endurance-trained men have considerably more capillaries in their leg muscles than sedentary individuals. With long periods of aerobic training, the number of capillaries has been shown to increase by more than 15%. Having more capillaries allows greater exchange of gases, heat, wastes, and nutrients between the blood ad working muscle fibers. In fact, the increase in capillary density(i.e. increase in capillaries per muscle fiber) is potentially one of the most important alterations in response to training that allows the increase in VO2max. It is now clear that the diffusion of oxygen from the capillary to the mitochondria is a major factor limiting the maximal rate of oxygen consumption. Increasing capillary density facilitates this diffusion, thus maintaining an environment well suited to energy prediction and repeated muscle contractions.

Myoglobin content

When oxygen enters the muscle fiber, it binds to myoglobin, a compound similar to hemoglobin. This iron-containing compound shuttles the oxygen molecules from the cell membrane to the mitochondria. The type I fibers contain large quantities of myoglobin, which gives these fibers their red appearance(myoglobin is a pigment that turns red when bound to oxygen). The type II fibers , on the other hand, are highly glycolitic, so they require(and have) little myoglobin-hence their whiter appearance. More important, their limited myoglobin supply limits their oxygen capacity, resulting in poor aerobic endurance for these fibers.
Myoglobin stores oxygen and releases it to the mitochondria when oxygen becomes limited during muscle action. This oxygen reserve is used during the transition form rest to exercise, providing oxygen to the mitochondria during the lag between the beginning of exercise and the increased cardiovascular delivery of oxygen.
Myoglobin’s precise contributions to oxygen delivery are not yet fully understood. But aerobic training has been shown to increase muscle myoglobin content to 75% to 80%. This adaptation would be expected only if myoglobin enhances a muscle’s capacity for oxidative metabolism.

Mitochondrial function

Aerobic(oxidative) energy production takes place in the mitochondria. Not surprisingly, then, aerobic training also induces changes in mitochondrial function that improve the muscle fibers’ capacity to produce ATP. The ability to use oxygen and produce ATP via oxidation depends on the number and size of the muscle mitochondria. Both increase with aerobic training.
During one study that involved endurance training in rats, the actual number of mitochondria increased approximately 15% during 27 weeks of exercise. Average mitochondrial size also increased by about 35% over that training period. As the volume of aerobc training increases, so do the number and size of the mitochondria.

Oxidative enzymes

Regular endurance exercise has been shown to induce major adaptations in skeletal muscle, including an increase in the number and size of the muscle fiber mitochondrial capacity. The oxidative breakdown of fuels and the ultimate production of ATP depend on the action of mitochondrial oxidative enzymes, the special proteins that catalyze(i.e., speed up) the breakdown of nutrients to form ATP. Aerobic training increases the activity of these important enzymes.
Figure below illustrates the changes in the activity of succinate dehydrogenase(SDH), a key muscle oxidative enzyme, over seven months of gradually increased swim training. While the increases in VO2max leveled off after the first two months of training, activity of this key oxidative enzyme continued to increase throughout the entire training period. This suggests that VO2max might be more influenced by the circulatory’s system limitations with respect to transporting oxygen than by the muscles’ oxidative potential.

The activities of muscle enzymes such as SDH and citrate synthase are dramatically influenced by aerobic training. This is seen in figure below, which compares the activities of these enzymes in untrained people, moderately trained joggers, and highly trained runners. Even moderate amounts of daily exercise increase these enzyme activities and thus the muscles aerobic capacity. For example, jogging or cycling for as little as 20 min per day has been shown to increase SDH activity in leg muscles by more than 25%. Training more vigorously, for example for 60 to 90 min per day, produces a two-to threefold increase in this activity.

One metabolic consequence of mitochondrial changes induced by aerobic training is glycogen sparing, a slower rate of utilization of muscle glycogen and enhanced reliance on fat as fuel source at a given exercise intensity. This increase in the oxidative enzymes with aerobic training most likely improves the ability to sustain a higher exercise intensity, such as maintaining a faster race pace in a 10km run.

Metabolic adaptations to training

Three important variables are related to metabolism:
  • Lactate threshold
  • Respiratory exchange ratio
  • Oxygen consumption.

Lactate threshold

Lactate threshold is a psychological marker that is closely associated with aerobic endurance performance – the higher the lactate threshold, the better the aerobic performance. Figure a below illustrates the difference in lactate threshold that would occur following a 6 to 12-month program of endurance training. In either case, in the trained state, one can exercise at a higher percentage of one’s VO2max before lactate begins to accumulate in the blood. Because race pace in aerobic endurance events is closely associated with lactate threshold, this translates into a much faster race pace(see figure b). The reduction in lactate values at a given rate of work to likely attributable to a combination of reduced lactate production and increased lactate clearance.

The concentration of lactate in the blood following a fixed-pace swim or run provides an excellent means of monitoring the physiological changes that occur with training. As athletes become better trained, their blood lactate concentrations are lower for the same rate of work. This suggests that they are developing greater aerobic power, a reduced reliance on the glycolytic system for energy, or perhaps both.

The respiratory exchange ratio(RER) is the ratio of carbon dioxide released to oxygen consumed during metabolism. The RER reflects the type of substrates being used as an energy source.
After training, the RER decreases at both absolute and relative submaximal exercise intensities. These changes are attributable to a greater utilization of free fatty acids instead of carbohydrate at these work rates following  training.

Resting and submaximal oxygen consumption

Oxygen consumption(VO2) at rest is unchanged following endurance training. While a few cross-sectional comparisons have suggested that training elevates resting VO2, the HERITAGE FAMILY STUDY – with a large number of subjects and with duplicate measures of resting metabolic rate both before and after 20 weeks of training – showed no evidence of an increased resting metabolic rate after training.
During submaximal exercise at a given exercise intensity, VO2 is either unchanged or slightly reduced following training. In the HERITAGE Family Study, with more than 700 participants, training reduced submaximal VO2 by 3.5% at a work rate of 50W. There was a corresponding reduction in cardiac output at 50W, reinforcing the strong interrelationship between VO2 and cardiac output. A decrease in VO2 during submaximal exercise could result from an increase in exercise economy(performing the same exercise intensity with less extraneous movement).

Maximal oxygen consumption

VO2max is the best indicator of cardiorespiratory endurance capacity and increases substantially in response to endurance training. While small and very large increases have been reported, an increase of 15% to 20% is typical for a previously sedentary person who trains at 50% to 85% of his or her VO2max three to five times per week, 20 to 60 min per day, for six months. For example, the VO2max of a sedentary individual could reasonably increase from a 35ml x kg-1 x min-1 to 42ml x kg-1 x min-1 as a result of such a program. This is far below the values we see in world-class endurance athletes, whose values generally range from 70 to 94ml x kg-1 x min-1. The more untrained an individual is when starting an exercise program, the larger the increase in VO2max.

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Thật quá tuyệt vời vì những nội dung trong bài của bạn, tôi cho rằng là sẽ có rất nhiều người tìm những nội dung này
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