AEROBIC TRAINING

Training Increases the Resistance to Fatigue

Aerobic conditioning increases the resistance to fatigue at all exercise intensities. As already noted, training increases VO2max (p. 1248) as well as the body's ability to eliminate excess heat that is produced during

exercise (see Fig. 58-5).

The increased VO2max that occurs with training has obvious practical benefits. As the requirement for

energy release in active muscle approaches VO2max, anaerobic processes become increasingly important

in maintaining ATP production. Increasing one's VO2max allows a given rate of ATP production to occur

relatively more aerobically, all other factors being equal. When VO2 is less than 50% of the maximum,

essentially all of the net energy release in active muscle is aerobic. In this condition, the O2 transport via

the pulmonary and circulatory systems matches the O2 demand in the muscle, avoiding disturbances in

acid-base balance.

When O2 uptake exceeds 60% of VO2max, muscle anaerobiosis increases roughly in proportion to the

increase in relative power output. In addition, the muscle produces excess lactic acid and protons, and these byproducts diffuse into the bloodstream. The body partially compensates for the resulting decrease in blood pH by hyperventilation (p. 723). Increasing the VO2max thus raises the threshold of exercise intensity

at which lactic acid appears, suggesting that physical training alters both the O2-transport and

O2-acceptance systems.

Aerobic Training Increases Maximal O2 Delivery By Increasing Plasma Volume, Thereby Increasing

Maximal Cardiac Output

Maximal O2 uptake could increase as the result of either optimizing O2 delivery to active muscle or

optimizing O2 extraction by active muscle, as demonstrated in the following modification of Equation 59-6:

In fact, aerobic training improves both O2 delivery and extraction; the problem for physiologists has been to

determine to what extent each system contributes to the whole-body response. For example, an increase in the circulatory system's capacity to deliver O2 could reflect an increase in either the maximal arterial O2

content or the maximal cardiac output, or both.

MAXIMIZING ARTERIAL O2 CONTENT.

Several factors could theoretically contribute to maximizing CaO2:

Increasing the maximal alveolar ventilation enhances the driving force for O2 uptake by the lungs

(see Fig. 30-4).

1.

Increasing the capacity for gases to diffuse across the alveolarcapillary barrier in the lungs could enhance O2 uptake at very high cardiac output, particularly at high altitude (see Fig. 26-8).

2.

Improving the matching of pulmonary ventilation to perfusion increases arterial PO2 and increases

the saturation of hemoglobin (p. 705).

3.

Increasing the concentration of hemoglobin enables a given volume of arterial blood to carry a greater amount of O2 (p. 656).

4.

In nearly all conditions of exercise, the pulmonary system maintains alveolar PO2 at levels that are

sufficiently high to ensure nearly complete (i.e., ∼97%) O2 saturation of hemoglobin, even at maximal

power output. Thus, it is unlikely that an increase in the maximal alveolar ventilation or pulmonary diffusing

capacity could explain the large increase in VO2max that occurs with training.

CaO2 would be increased by elevating the blood's hemoglobin concentration. However, there is no evidence

that physical training induces such an increase. To the contrary, [hemoglobin] tends to be slightly lower in endurance athletes, a phenomenon called "sports anemia," which reflects an expansion of the plasma compartment (see later). Whereas increasing [hemoglobin] provides a greater O2-carrying capacity in

blood, the maximal O2 transport does not necessarily increase accordingly because blood viscosity, and

therefore total vascular resistance, would also increase. The heart would be required to develop a higher arterial pressure to generate an equivalent cardiac output. The resultant increased cardiac work would thus be counterproductive to the overall adaptive response.

MAXIMIZING CARDIAC OUTPUT.

Factors that contribute to increasing maximal cardiac output include optimizing the increases in heart rate and cardiac stroke volume so that their product (i.e., cardiac output) is maximal (see Equation 59-7).

Figure 59-8 illustrates how conditioning affects cardiac output and the arteriovenous difference for O2

content. Compared with a control situation (blue curves), prolonged bed rest (red curves) has little effect on maximal heart rate, diminishes maximal stroke volume, and greatly reduces maximal cardiac output. However, training (green curves) increases maximal stroke volume, slightly decreases maximal heart rate, but greatly increases maximal cardiac output. Neither training nor bed rest has a substantial effect on (CaO2

- CvO2)max (i.e., maximal O2 extraction).

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Figure 59-8 Effect of training on various cardiovascular parameters. The four graphs show changes in four cardiovascular parameters at

different levels of O2 uptake (i.e., different intensities of exercise). The four blue curves represent mean values for five untrained subjects. The

purple curves summarize similar data for the same five subjects after 20 days of bed rest. The green curves summarize data after 50 days of physical training. (Data from Saltin B, Blomqvist G, Mitchell JH, et al: Response to submaximal and maximal exercise after bed rest and

training. Circulation 38(Suppl. 7):1968.)

Because training produces no dramatic increase in either maximal heart rate or maximal O2 extraction,

nearly all of the increase in VO2max that occurs with training must be due to an increase in maximal cardiac

output, the product of optimal heart rate and optimal stroke volume in Equation 59-7. The athlete achieves

this increased cardiac output by increasing maximal cardiac stroke volume. Maximal cardiac output can increase by approximately 40% during physical conditioning that also increases maximal aerobic power by 50%. The difference between 40% and 50% is accounted for by an increased extraction, (CaO2 - CvO2)max.

The latter is the consequence of capillary proliferation and of elevating key oxidative enzymes in the mitochondria of type I muscle fibers, creating a greater O2 sink under maximal conditions (see the next

section).

Maximal cardiac stroke volume increases during aerobic training because expansion of the plasma compartment increases the heart's preload (p. 528). An increase in preload increases ventricular filling and proportionally increases stroke volume (Starling's law of the heart), elevating maximal cardiac output accordingly. An additional benefit is that a trained athlete achieves a given cardiac output at a lower cardiac frequency, both at rest and during moderate exercise. Because it is more efficient to increase stroke volume than heart rate, increasing stroke volume reduces the myocardial metabolic load for any particular level of activity.

The expansion of plasma volume probably reflects an increase in albumin content (1 g albumin is dissolved in 18 g of plasma H2O). This increase appears to be due both to translocation (by an unknown mechanism)

from the interstitial compartment and to increased synthesis by the liver. The result is increased colloid osmotic pressure in the capillaries, promoting a shift of fluid from the interstitium to the blood. Although the total volume of red blood cells increases with aerobic training, the plasma-volume expansion is greater than

the red-cell expansion, thus reducing the hemoglobin concentration; hence, the sports anemia.

The increased blood volume has another beneficial effect: it enhances the ability to maintain a high skin blood flow in potentially compromising conditions (e.g., heavy exercise in the heat), thus providing a greater heat transport from core to skin and thus a relatively lower storage of heat (p. 1233).

Training Enhances Diffusion of O2 into Muscle

Whereas an increase in maximal cardiac output accounts for most of the increased delivery of O2 to

muscle with training, a lesser fraction reflects increased O2 extraction from blood. Fick's law describes the

diffusion of O2 between the alveolar air and pulmonary capillary blood (see Equation 29-7). A similar

relationship, shown in Equation 58-8, describes the diffusion of O2 from the systemic capillary blood to the

mitochondria.

The factors that contribute to DO2 are analogous to those that affect the diffusing capacity in the lung.

Trained muscle can accommodate a greater maximal blood flow (and therefore an increased blood volume) because of the growth of new capillaries. Indeed, well-conditioned people have a 60% greater number of capillaries for a given cross-sectional area of muscle fiber than sedentary people do. This increased capillary density increases DO2, thus providing a greater surface area for diffusion. Increased capillary

density also reduces the diffusion distance for O2 between the capillary and muscle fibers (see Fig. 19-4).

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Another consequence of increased capillary density (and perhaps increased capillary length as well) is that at a given blood flow the mean transit time of blood in muscle increases. Because the blood lingers for a longer time in the muscle capillaries, O2 extraction increases. However, training also increases maximal

skeletal-muscle blood flow, reflecting an increase in maximal cardiac output and the greater number of parallel vessels in muscle. The increase in blood flow through active skeletal muscle minimizes the decay in capillary PO2 that tends to occur along the vessel as the result of increased DO2 and capillary density. This

preservation of capillary PO2 maintains the blood-to-mitochondrion PO2 gradient, enhancing O2 diffusion.

Aerobic Training Also Increases the Expression of Key Mitochondrial Enzymes

Another factor that accounts for the increased uptake of O2 by muscle in trained people is elevated

oxidative enzyme activity in the muscle mitochondria (Fig. 59-9). Levels of mRNA increase for specific enzymes, implying increased transcription owing to signals associated with the exercise stimulus (e.g., elevated hormones, altered plasma osmolality). Prolonged aerobic conditioning increases levels of succinic dehydrogenase, NADH dehydrogenase, and cytochrome oxidase.

Increased oxidative enzyme activity increases the muscle PO2 sink (i.e., decreases PO2 mito as illustrated in

Equation 59-8), enhancing O2 diffusion from capillary to mitochondrion. This increased diffusion is also the

reason why (CaO2 - CvO2)max in Equation 59-7 remained approximately constant with training, even though

blood flow increased markedly. If O2 diffusion had not increased, [O2]V would have risen, and (CaO2 -

CvO2)max would have decreased.

Figure 59-9 Enzyme adaptation during training. Training causes a slow increase in the level of several enzymes, as well as in the number of capillaries, maximal O2 uptake, and size of muscle fibers. These changes reverse rapidly on the cessation of training. (Data from Saltin B,

Henriksson J, Nygaard E, Andersen P: Fiber types and metabolic potentials of skeletal muscles in sedentary man and endurance runners. The Marathon: Physiological, Medical, Epidemiological, and Psychological Studies. Ann NY Acad Sci 301:3-29, 1977.)

Trained athletes mobilize free fatty acids more rapidly during exercise. Increasing mitochondrial oxidative enzyme activity provides an increased ability to oxidize these free fatty acids during a demand for fuel delivery. This change is accompanied by an adaptive decrease in the activity of glycolytic rate-limiting enzymes. These adaptations conserve muscle glycogen and thus delay glycogen depletion during a given demand for fuel.

Aerobically trained people have a decreased tissue sensitivity to insulin during exercise, in contrast to the increase that occurs during exercise in the general (untrained) population. A decreased insulin sensitivity slows glucose transport into muscle, increasing the reliance on the oxidation of free fatty acids, and further sparing muscle glycogen.

References

REFERENCES

Books and Reviews

Booth FW, Thomason DB: Molecular and cellular adaptation of muscle in response to exercise: Perspectives of various models. Physiol Rev 71:541-585, 1991.

Fitts RH: Cellular mechanisms of muscle fatigue. Physiol Rev 74:49-94, 1994.

Jones JH, Lindstedt SL: Limits to maximal performance. Annu Rev Physiol 55:547-569, 1993.

Lehmann MJ, Lormes W, Opitz-Gress A, et al: Training and overtraining: An overview and experimental results in endurance sports. J Sports Med Phys Fitness 37:7-17, 1997.

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Nadel ER: Physiological adaptations to aerobic training. Am Scientist 73: 334-343, 1985.

Saltin B, Strange S: Maximal oxygen uptake: Old and new arguments for a cardiovascular limitation. Med Sci Sports Ex 24:30-37, 1992.

Wagner PD: Determinants of maximal oxygen transport and utilization. Annu Rev Physiol 58:21-50, 1996.

Journal Articles

Gollnick PD, Armstrong RB, Saubert CW IV, et al: Enzyme activity and fiber composition in skeletal muscle of untrained and trained men. J Appl Physiol 33:312-319, 1972.

Nadel ER, Bussolari SR: The Daedalus Project: Physiological problems and solutions. Am Scientist 76:351-360, 1988.

Saltin B, Blomqvist G, Mitchell JH, et al: Response to submaximal and maximal exercise after bed rest and training. Circulation 38(Suppl 7): 1-78, 1968.

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